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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1003_en.txt

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+In this report, we present a 26-year-old male with a past medical history of Behcet's disease who developed progressive vision loss and severe hypotonia. He had received 15 mg of methotrexate weekly and 7.5 mg of prednisolone daily as well as multiple injections of subtenon triamcinolone acetonide (TA; 40 mg). He had also undergone phacoemulsification and posterior chamber intraocular lens placement for cataract in his both eyes. Pars plana vitrectomy with silicone oil injection was performed in his right eye for hypotony. Visual acuity was 20/400 in his right eye and “hand motion” in his left eye. Ocular hypotony persisted despite all these treatments in the absence of active inflammation. Corneal folds and band keratopathy were noted after few weeks. Fundus was poorly visible but it was remarkable for cystic changes in the macular region. B-scan showed a significant serous choroidal detachment due to severe hypotony in both eyes. To increase the IOP, multiple injections of 40 mg of subtenon and 4 mg of intravitreal TA were administered; however, no improvement was observed in vision, IOP status, and serous choroidal detachment. Visual acuity deteriorated because of persistent hypotony maculopathy. Ibopamine (a dopamine agonist) eye drops were used for three months with an increase in IOP of 2 mm Hg in both the eyes, but no change in vision was detected.
+We discussed the details of our experimental treatment based on published studies with the patient and proceeded with the treatment after obtaining a written consent. Subsequently, high-dose latanoprost eye drops (XALATAN, 0.005%, Pfizer) were administered every 6 hours in both eyes.
+One month later, IOP increased to 4 mm Hg, and at two months, to 7 mm Hg. After two months of latanoprost treatment, we performed a drug rechallenge test by discontinuing latanoprost for four weeks and then resuming the drug to prove its effect on IOP. After 6 months, IOP was stable at 7 mm Hg and remained unchanged even after 24 months. B-scan showed significant improvement in hypotony maculopathy and fluid resolved subretinally . The patient's vision improved to 20/200 in his right eye and “finger counting” at 1.5 m in his left eye.

data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1008_en.txt

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+A 46-year-old male was brought to the emergency department (ED) with complaints of two weeks of cough, fever, generalized myalgias, sore throat, with progressively worsening of shortness of breath, and night sweats. He was initially treated with amoxicillin-clavulanate for pneumonia for seven days as prescribed by his primary care physician. On day eight he began to have tremors without fevers, which resulted in difficulty ambulating. He denied any nausea, vomiting, diarrhea, constipation, chest or abdominal pain. He had no other relevant medical history, denied taking any other medications, and denied history of alcohol use. Before going into self-quarantine he noted that some of his co-workers were having flu-like symptoms but he was unaware whether they had been tested for COVID-19.
+On physical examination in the ED his vital signs were blood pressure 130/87 millimeters of mercury, temperature 36.6° Celsius (97.9° Fahrenheit), pulse rate 108 beats per minute, respiratory rate 22 breaths per minute, and oxygenating at 96% on room air. On respiratory exam, he had clear and equal breath sounds bilaterally. Neurologic exam revealed intact mental status that was oriented to self, date, and place. He had no dysarthria, aphasia, or neglect. His cranial nerves exam was significant for saccadic intrusions with smooth pursuit. A generalized tremor was noted when the patient was lying down, which worsened with movement, and there was a postural tremor in all extremities. Heel-to-shin exam was non-dystaxic although tremulous, and there was a bilateral intention tremor. On motor exam, he had normal tone and five out of five strength of all muscle groups in the upper and lower extremities. He was noted to have a wide-based gait with unsteadiness, but there was no dysmetria, pronator drift or truncal ataxia. His sensation was intact to light touch. No other abnormalities were noted on physical exam.
+In the ED he was evaluated by neurology due to the constant tremors. Computed tomography (CT) of the head and CT angiogram did not reveal any significant findings, toxicology report came back negative, and thyroid-stimulating hormone, thiamine, and folate levels were normal. Chest radiograph showed clear lungs without any focal consolidation. Magnetic resonance imaging (MRI) done during his hospital stay showed hyperintense foci in the bifrontal subcortical and deep white matter on scattered T2-weighted, fluid-attenuated inversion recovery. These findings likely represent sequalae of microangiopathic ischemic changes. His hospital course was uncomplicated, and respiratory status improved with supportive measures. Final impression by neurology was that these were essential tremors, and the decision was made to treat with propranolol from which patient reported some mild improvement of symptoms.

data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1022_en.txt

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+An 82-year-old lady was referred to gynaecology outpatients in June 2007 with a one month history of post menopausal bleeding. Her past gynaecological history included a negative hysteroscopy in 1998, and previous use of hormone replacement therapy. She had previously given birth to two children. The patient was fit and well, with no significant past medical history apart from hypertension for which she took bendroflumethiazide and atenolol.
+Physical examination revealed a bulky uterus with no adnexal masses. A pipelle biopsy demonstrated only tiny fragments of blood clot. A subsequent transvaginal ultrasound scan showed a large endometrial mass with calcification . The ovaries appeared normal. She underwent a hysteroscopy in July 2007 when a 6 cm uterine fibrotic polyp, which filled the uterine cavity, was removed.
+Microscopy demonstrated polypoid tissue with a variably cellular and fibrotic stroma, focal adipose and possible chondroid metaplasia, but no malignant features. The glands showed focal mucinous and keratinising sqaumous epithelial metaplasia. There was focal nuclear atypia, focal mitotic activity and occasional cribriform gland fusion. These features were in keeping with either atypical complex hyperplasia within an endometrial polyp associated with metaplastic changes, or a polypoid uterine teratoma.
+Immunohistochemistry showed positive staining of the small crowded epithelium for the epithelial marker cytokeratin (CK)-7 and the thyroid and lung marker TTFI. There was positive staining of the chondroid area for S100 protein, focal staining of dilated gland epithelium and stromal cells for oestrogen receptor and progesterone receptor, and staining of stromal cells for smooth muscle α-actin (SMA). Thyroglobulin, desmin, CK20 and CDX2 staining was negative. A diagnosis of benign teratoma with thyroid gland and cartilaginous elements was therefore made.
+Following hysteroscopy, the bleeding continued. A repeat ultrasound scan revealed that the teratoma had grown back almost completely filling the uterine cavity. A magnetic resonance imaging (MRI) scan in November 2007 showed the tumour filling and distending the endometrial cavity and extending down into the cervix . There was evidence of posterior wall myometrial invasion but there was no lymphadenopathy and the ovaries appeared normal. Tumour markers including alpha-fetoprotein (AFP), carcinoembryonic antigen (CEA) and Ca19-9 were within normal limits. Serum Ca125 was slightly elevated at 42 U/ml (normal range 0–35 units (U)/ml) and lactate dehydrogenase (LDH) raised at 372 IU/L (normal range 125–250 U/ml).
+The patient proceeded to a total abdominal hysterectomy and bilateral salpingo-oophorectmy in December 2007. At operation, the uterus was found to contain a haemorrhagic polypoid tumour (110 × 80 × 70 mm) arising from the posterior aspect of the endometrial cavity . Uterine size was equivalent to that of a 12-week gestation uterus.
+Microscopically the tumour was a teratoma containing mature and immature elements with mixed malignant transformation . The tissue types found included squamous and glandular epithelium, thyroid parenchyma, smooth muscle, connective and adipose tissue. In addition there were areas of immature bone, invasive adenocarcinoma, and papillary thyroid carcinoma. There was extensive lymphovascular invasion and deep myometrial, but not serosal, involvement. The omentum, cervix, fallopian tubes and ovaries were free of tumour. Immunohistochemistry showed that the malignant epithelial components were positive for CK-7 and TTF-1, but negative for CK20 and thyroglobulin. One area of the tumour stained positive for desmin but not for SMA, S100 or CD10, suggesting that this is likely to be a small focus of myogenic sarcoma.
+The histopathological conclusion was of a poorly differentiated adenocarcinoma and a focal myogenic sarcoma arising in a polypoid uterine teratoma with mature and immature elements. A post-operative computer tomography (CT) scan of the thorax, abdomen and pelvis found no evidence of distant disease giving an overall International Federation of Gynaecology and Obstetrics disease stage 1C.
+The patient recovered well from surgery and was referred for oncological follow up. Given her age and performance status a surveillance approach was taken with regular clinical examinations, serial tumour markers and routine CT scans. Initially in remission, six months post-operatively para-aortic lymphadenopathy was detected on CT although she remained asymptomatic with an Eastern Cooperative Oncology Group (ECOG) performance status of 0. In view of her age and wishes for a treatment with acceptable toxicity, the patient was commenced on an initial dose of cisplatin (20 mg/m2) and etoposide (100 mg/m2). This was well tolerated so one week later treatment was continued with a fortnightly alternating regimen of paclitaxel (135 mg/m2) and etoposide (150 mg/m2), followed by paciltaxel (135 mg/m2) and cisplatin (60 mg/m2). This treatment was chosen based on our experience of its effectiveness and tolerability in the treatment of relapsed germ cell tumours and gestational trophoblastic disease [,].
+After three cycles of chemotherapy there was a reduction in the size of the para-aortic mass, but an increase in the cystic component suggesting possible differentiation towards a mature teratoma. Consequently she underwent a retro-peritoneal lymph node dissection in October 2008. Histology from this confirmed the presence of metastatic teratoma. Unfortunately she had a turbulent post-operative course and, although she recovered well enough to return home a month later, she sadly died shortly thereafter.

data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1034_en.txt

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+A 40-year-old African American female presented in 2014 with complaints of a right neck mass that was first appreciated 9 months earlier. The appearance of the neck mass coincided with a constellation of symptoms: frequent severe headaches, periods of lightheadedness, vertigo and tinnitus, hoarseness, dysphagia, blurred vision and tearing of the right eye. On physical examination, a non-pulsatile, non-tender mass was palpated, deep to the right sternocleidomastoid muscle. The patient underwent CT neck imaging, which revealed a 6.1 × 4.0 × 4.1 cm right neck mass extending to the base of the skull and encompassing the internal and external carotid artery . Upon further evaluation, the tumor was felt to be a Shamblin II lesion because there was some carotid arterial attachment, but the tumor did not entirely encase the carotid arteries, so the tumor was deemed as reasonable for resection. A cerebral arteriogram showed no intracranial arterial vascular abnormality, so an extracranial embolization was performed. Transcervical resection of the right carotid body tumor was performed the following day, and pathology showed a paraganglioma measuring 4.9 cm with areas of infarct and multiple vessels with intravascular thrombi, consistent with prior embolization procedure. The transcervical resection of the right carotid body paraganglioma was a gross total resection, but a microscopic surgical margin assessment on the surgical pathology was not performed. Following surgery, the patient continued to remain symptomatic with headaches, right neck and ear soreness, Horner’s syndrome symptoms, and right vocal cord paralysis. She received right vocal fold injection medialization. Over time, the patient reported improvement in most of her symptoms.
+The patient was routinely followed in office and via imaging. MRI in 2017 showed a small mass measuring about 1 cm in the vicinity of the carotid bifurcation, but it was unclear if this was recurrent disease, so the decision was made to continue to observe the mass. In 2018, a subsequent MRI showed interval enlargement of the mass from 1.4 × 1 × 1.2 cm to 2.5 × 1.7 × 2.4 cm. Due to the disease progression, the patient received Stereotactic Body Radiation Therapy of 25 Gy in 5 fractions to the presumed recurrent right paraganglioma in 2018. For the next two years, the patient’s imaging and clinical symptoms remained stable. In 2021, the patient re-presented with six months of new onset thoracic radiculopathy and weight loss, and one month of progressive bilateral lower extremity weakness, dysmetria, and paresthesias and numbness from the umbilicus down. Upon physical examination, the patient's strength was 4 + /5 in her bilateral lower extremities, she had decreased sensation to light touch and pin-prick from her naval to her distal bilateral lower extremities, she had intact sensation to light perineal touch, her bilateral patellar reflexes were 2 + , and her bilateral ankle reflexes had single beat clonus. She had a mildly ataxic gait with dysmetria on heel to toe walk and heel walk. While her finger to nose testing was intact, her heel to shin testing revealed dysmetria. During rectal examination, the patient demonstrated brisk voluntary anal contraction. MRI of the T spine showed a spinal mass arising from the posterior elements at T6-T7 with at least Bilsky grade 2 posterior to anterior cord compression as well as a mass in the T11 vertebral body . This compressive pathology localized to the patient’s acute symptoms, and it was determined that she would require surgical intervention. She underwent T6-T7 laminectomy, T5-T7 tumor resection, and T5-T9 posterior fixation in 2021 with pathology showing metastatic paraganglioma . She subsequently completed radiation therapy of 30 Gy in 10 fractions to the thoracic spine from T4 to T11 to encompass both the surgical field as well as the T11 metastasis in 2021.
+Following completion of radiation therapy to the thoracic spine, restaging DOTATATE PET in mid-2021 showed multifocal uptake in the right carotid body surgical bed as well as uptake in T4, T11, and the right iliac. Genetic evaluation showed no evidence of pathogenic mutations. The patient was evaluated for 131Iodine-Iobenguane but she was not felt to be a candidate. The patient was started on systemic therapy with sunitinib complicated by mucositis. The patient’s sunitinib dose was decreased to help alleviate the mucositis. Interval DOTATATE PET in late 2021 showed decreased size and uptake of the right neck masses and osseous metastases consistent with treatment response. The patient reported 2–3 months of dull, burning right hip pain. An MRI was obtained showing a well marginated lesion within the right iliac bone in the area of PET avidity consistent with metastatic disease. The right iliac lesion was treated with 8 Gy of radiation therapy in a single fraction for right hip pain attributed to bony metastatic disease. DOTATATE PET in mid 2022 showed two areas of focal uptake in the right carotid body surgical bed, small volume mild uptake in the C5 and T11 vertebral bodies and the right iliac, and a left adrenal nodule without PET uptake. Therefore, the patient’s systemic therapy was switched to capecitabine and temozolomide. At the time of her last follow up in 2022—a total of 13 months since completing thoracic spinal surgery and radiotherapy and 4 months since completing palliative right hip radiotherapy—the patient was ambulatory, her previously reported neurologic deficits had resolved, and she had no right hip pain. Upon physical examination at last follow up, the patient's strength was 5/5 throughout, her sensation was normal to light touch, and her reflexes were 2 + throughout. She ambulated independently with intact heel to toe walking, heel walking, and toe walking.

data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1039_en.txt

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+A 31-year-old woman, gravidity three, parity zero, was admitted because of a suspected intramural pregnancy after IVF-ET.
+The patient was completely asymptomatic. She had regular menstruation, a moderate amount of menstruation and no dysmenorrhea. Her last menstrual period was November 17, 2020. The endometrium was prepared using hormone replacement therapy following 1.875 mg of subcutaneous gonadotropin-releasing hormone agonist (Leuprorelin Acetate, Livzon Pharmaceuticals, China) on day 3 of the menstrual cycle. In addition, 90 mg of vaginal progesterone (Crinone, Merck Serono, United Kingdom) once a day and 10 mg of dydrogesterone three times daily were administered (P + 0). A frozen day 6 embryo which had undergone preimplantation genetic screening was transferred on the 7th day of progesterone exposure (P + 6) under sonographic guidance.
+She received laparoscopic salpingotomy in 2014 due to a right tubal pregnancy. She had suffered secondary infertility since December 2015 and her hysterosalpingography results showed an obstruction in the right fallopian tube and adhesion of the distal end of the left fallopian tube in June 2016. As spontaneous pregnancy did not subsequently occur, she was referred to the reproductive center of our hospital for IVF-ET in June 2018. The patient underwent laparoscopic bilateral salpingectomy for bilateral tubal pregnancy after two frozen day 3 embryos were transferred in December 2018. Of the other three frozen-thawed embryo transfer cycles, a total of 5 embryos were transferred, but pregnancy was not achieved. In addition, the patient had a history of hysteroscopy three times to remove endometrial polyps and separate uterine adhesions.
+Her personal history and family history were unremarkable.
+The patient’s vital signs were normal. Physical examination revealed a 7-week sized uterus with no tenderness and no abnormalities in the uterine cervix and abdomen. There was no vaginal bleeding or fluid.
+At day 14 after ET, her serum β-human chorionic gonadotropin (β-hCG) level was 111.54 mIU/mL and then increased from 290 mIU/mL to 1759 mIU/mL. On day 32 after ET, her serum β-hCG level was 3819 mIU/mL.
+A transvaginal ultrasound examination revealed a suspected intramural pregnancy. When admitted on day 33 after ET, three-dimensional transvaginal ultrasound indicated a heterogeneous echogenic area measuring 1.40 cm × 1.26 cm in size arising from the uterine fundus which had a 0.48 cm × 0.37 cm anechoic region inside and was surrounded by myometrium . Color Doppler ultrasound showed abundant blood flow. This region seemed to have a slender and extremely hypoechoic area stretching to the uterine cavity . In addition, a hypoechoic structure with an indistinct boundary measuring 2.74 cm × 1.61 cm in size was observed in the anterior myometrium near the uterine fundus, which was thought to be a uterine adenomyoma.

data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1047_en.txt

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+The proband (II-2 in Fig. ) is a 45-year old woman, who first presented to our university hospital at the age of 35 and was referred to us because of her pregnancy. She has congenital deafness, first experienced syncope at the age of 3, and was diagnosed with epilepsy. She was treated with anti-epilepsy medications; however, she subsequently experienced several instances of syncope. At the age of 13, she had a syncope event, and was suspected of having JLNS because of her congenital deafness and prolonged QT interval. Her syncope was diagnosed as an arrhythmic episode when she was aware of tachycardia and as epilepsy when she was not. She also had a subarachnoid hemorrhage at the age of 29.
+When she first presented at our hospital, she was not taking beta-blockers, because of a history of asthma, but was taking mexiletine in addition to phenytoin. Her QTc was found to be prolonged (584 ms) at presentation and administration of atenolol was initiated. She delivered her baby (III-1 in Fig. ) through Caesarean operation at our hospital at the age of 35. At 37, she delivered her second baby (III-2 in Fig. ) through Caesarean operation at our hospital. Despite administration of beta-blockers, her QTc remained prolonged (600 msec at the age of 37, 780 msec at 44) , which is not unexpected because treatment with beta-blockers in LQTS1 is not expected to overtly reduce QTc . However, she continued to experience occasional syncope and finally underwent an implantable cardioverter defibrillator (ICD) operation at 38 years of age. Subsequently, she is in a stable clinical condition. Because the proband was suspected of JLNS and both infants had a measured QTc of 500 ms or greater within 1 month after birth, beta blockers were initiated and both children remain in stable condition at ages 10 and 8 . QTc of the son (III-1 in Fig. ) was measured as 500 ms one month after birth, while the QTc of his sister (III-2) was 530 ms at birth.
+The father (I-1) and mother (I-2) of the proband were first cousins. There is no history of sudden unexplained syncope or death of children or adults in the immediate family members, despite the prolonged QTc of the children.
+Clinical evaluation and consultation of the proband and her family members were performed at Chiba University Hospital. Clinical phenotypes were deduced from the clinical history, physical examinations, and ECG. Blood samples were collected from the proband and her family members following genetic counseling, and written informed consent was obtained prior to sample collection.
+Genomic DNA was isolated from peripheral blood lymphocytes according to established protocols at our laboratory . Entire coding exons, including the intronic boundaries of the genes, of KCNQ1 (NCBI ref: NM_000218) and other LQT causative genes (KCNH2, SCN5A, KCNE1, KCNE2, KCNJ2, SCN4B, KCNJ5) were amplified by polymerase chain reaction (PCR), according to established protocols in our laboratory. Briefly, 30–100 ng of genomic DNA was subjected to PCR amplification with DNA polymerase (PrimeSTAR GXL DNA Polymerase; Takara Bio Inc., Kusatsu, Japan) and primer sets.
+The amplicons were subjected to conventional sequencing with Sanger sequencers (Applied Biosystems 3730/3130 DNA analyzers; Thermo Fisher Scientific, Waltham, MA, USA). The sequence data were processed with Gene Codes Sequencher Software (Takara Bio Inc.) and mapped to the human genome sequence (build GRCh37/hg19).
+Genetic analysis was performed to screen all coding exons and the exon–intron boundaries of the KCNQ1 gene (NCBI ref: NM_000218.2, NP_000209.2) with concurrent screening of other LQT causative genes (KCNH2, SCN5A, KCNE1, KCNE2, KCNJ2, SCN4B, KCNJ5). We detected a novel homozygous nonsense variant, NM_000218.2:c.115G > T (p.Glu39X, in exon 1a), in the KCNQ1 gene of the proband, as well as a homozygous common variant (NM_000218.2:c.1343C > G, p.Pro448Arg) (Additional file : Table S1). Genetic screening of her mother (I-2) and children (III-1 and III-2) revealed that they were heterozygous for the nonsense variant . Her husband (II-3) was also screened and found to be heterozygous for the common variant (NM_000218.2:c.1343C > G, p.Pro448Arg). The proband is a child from a first-cousin marriage, and we have concluded the homozygous nonsense variant in the proband is the cause of her JLNS1. The proband was negative for pathogenic variants in other LQT causative genes, including the KCNE1 gene (Additional file : Table S1).

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+A 82-year old lady presented to the Department of General Surgery at the University of Heidelberg, Germany with recurrent attacks of hypoglycemia and a large abdominal mass. While diagnostic tests repeatedly documented glucose levels below 40 mg/dl (normal levels 80 – 120 mg/dl), a computed tomography (CT) scan of the abdomen revealed a large lesion of around 5 to 6 cm in relation to the pancreatic body and tail. There were also large masses of about 3–5 cm in the retroperitoneum and in the area of the celiac trunk and around the mesenteric artery. Furthermore, in the pancreatic body there was a hypervascularized area , that was suspicious for an insulinoma. Clinically this lady, who was not thriving, reported a weight loss of 12 kilograms over the previous 4 months. A somatostatin receptor scintigraphy showed an enhanced uptake in the region of the pancreatic body/tail as well as in the right axilla (a palpable mass was also noted there) and excluded the possibility of other involved areas.
+She gave a past history of an operation done on the right eyebrow 2 years prior for a 0.8 × 0.8 cm lesion that was reported as a Merkel cell carcinoma. Histopathology showed rather uniform tumor cells in a trabecular growth pattern with monomorphous pale-stained nuclei and many mitoses . There was invasion of dermal lymphatics and blood vessels . Immunohistochemistry revealed strong positivity for cytokeratin 20 and neurofilament (not shown) in the characteristic dot-like pattern and a weak expression of chromogranin A . After excision, radiation therapy was also administered only at the site of the primary lesion, the draining lymphatic vessels and the first lymph node station. A year later, a large abdominal mass was noted of uncertain origin and an ultrasound guided biopsy showed an unspecified small cell cancer. In view of the large mass with additional suspicious areas being noted in the spleen, left adrenal gland and axilla, she had been subjected to palliative radiotherapy of 30 Gray over 2 months. However no definitive diagnosis of metastasis in these areas was established. With a working clinical diagnosis of symptomatic insulinoma not responding to medical measures, a decision for surgical resection of this large lesion was inevitable, the age of the patient and the previous history of palliative radiation just 6 months prior notwithstanding.
+Surgical exploration revealed a large mass of about 5 cm in the tail of the pancreas, in close proximity to the spleen and the splenic flexure of the transverse colon. However there was no evidence of any metastatic disease to the liver, peritoneum and the adnexae. After a careful and meticulous mobilization, a distal pancreatectomy, splenectomy, and adrenalectomy along with resection of the splenic flexure of the colon were performed.
+Pathological examination revealed a tumor with manifestations in the pancreatic tail, the adrenal gland, the peripancreatic tissue, and the surrounding soft tissue. Grossly, the mass displayed a whitish and glassy cut surface, containing extended areas of haemorrhage and necrosis. Histologically, the tumor displayed endocrine architecture with mostly solid formations of rather monomorphic cells. The tumor was mitotically highly active (mitotic count >10 per high power field) and contained abundant areas of necrosis. Immunohistochemically, the tumor cells were strongly positive for the endocrine marker synaptophysin and for cytokeratin 20 while there was no expression of insulin. The proliferative activity (MIB-1) reached approximately 80% .
+Furthermore, gross examination of the resected specimen revealed a well demarcated, brownish tumor of the pancreatic body, measuring 1.2 cm in diameter. This tumor microscopically displayed endocrine architecture with trabecular arrangements of uniform tumor cells, showing no mitotic activity. Immunohistochemistry revealed strong positivity for synaptophysin as well as focal positivity for insulin. The proliferative activity (MIB-1) was approximately 1% . The diagnosis of a poorly differentiated endocrine carcinoma (Merkel cell carcinoma) along with that of benign pancreatic insulinoma was thus made.
+The patient had a smooth postoperative recovery, the bouts of hypoglycaemia completely disappeared, and she was discharged home within 3 weeks of surgery. She is presently asymptomatic and remains on regular follow up.

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+A 37-year-old Chinese woman presented to our department four years and 11 months ago with bilateral lower limb crush injuries sustained in a traffic accident. The lower limb injuries were at different anatomic levels . On the right side, her lower limb was crushed from her hip joint to 16cm below her knee joint, but the bones and soft tissues of the lower one-third of her leg were intact with only slight injury to the skin. On the left side, the distal portion of her leg was crushed. Our patient was in serious hypovolemic shock on arrival, with a heart rate of 150 beats per minute and blood pressure of 80/60mmHg.
+After rapid infusion of intravenous fluids, our patient rapidly recovered from shock and did not develop acute renal failure or acute respiratory distress syndrome. Emergency surgery was performed. Bilateral lower limb amputations were necessary. Her lower left leg was unsalvageable, but her lower right leg was suitable for replantation to the left leg stump after debridement. We decided to perform crossover replantation of her right lower leg to the left leg stump to provide our patient with a sensate weight-bearing extremity. Her amputated right lower leg was wrapped in sterile dressings, placed on a sterile tray and stored in the refrigerator at 4°C during fixation of the left leg fracture.
+After amputation and debridement of her right hip joint, her right lower tibia was fixed to her left upper tibia . The fibula was not fixed. The tendons, blood vessels and nerves of her left leg were anastomosed to the amputated lower right leg structures. The anterior tibial artery and posterior tibial artery were anastomosed crosswise, and the ends of the great saphenous vein, small saphenous vein and four deep veins were anastomosed without crossover. The sural nerve and saphenous nerve were anastomosed crosswise, and the anterior and posterior tibial nerves were anastomosed without crossover. Heterotopic replantation of her right lower leg to the left leg stump was thus completed. A stump was created on the right side at her hip joint. Routine antibiotic, anti-coagulant, and anti-angiospasm treatments were administered post-operatively. In a second operation, a soft tissue defect of the replanted limb was covered by a microvascular-free latissimus dorsi muscle flap. The post-operative anti-coagulation regime was as follows: dextran 40 (500mL) twice a day for seven days; aspirin (100mg) orally three times a day for three days; narceine (30mg) four times a day for seven days; and tolazoline (25mg) three times a day for seven days. Routine post-operative blood tests, including coagulation tests, were performed for seven days.
+The replantation was successful and our patient was discharged after two months . She was rehabilitated with a contralateral prosthesis and ambulates with a walking stick. One year post-operatively, X-ray examination showed perfect union of the tibia . There was no ulceration of the replanted extremity or the right-sided amputation stump at 39 months post-operatively. The sole of her foot on the left side regained complete protective sensation . Our patient described the functional result of the replantation as satisfying, and found that the prosthesis on the right side caused more problems than the replanted left lower limb. She had no complaints about the cosmetic result. In addition, she experienced restoration of perceived body height with the crossover replantation.

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+A 23-year-old male initially presented in our emergency department with symptoms suggestive of angina pectoris. The patient reported the sudden onset of chest pain radiating to the left arm as well as headache 1 day after vaccination with the second dose of the mRNA-1273 (Moderna) COVID-19 vaccine. Dyspnoea, fever, or excessive sweating were denied. Further examination revealed a relevant past-history of perimyocarditis in 2018 and 2019 (possibly post-infectious). The patient was not on medication at the time of presentation.
+The clinical examination of the patient was unremarkable. The body temperature recording was 37.5°C. The heart rate on admission was 96 beats/min and the blood pressure was 110/60 mmHg. The oxygen saturation was 99% on room air. An electrocardiogram (ECG) showed sinus rhythm with mild concave ST-elevations in II, III, and aVF. Laboratory data (see ) revealed leucocytosis, elevated levels of creatine kinase, C-reactive protein, and high-sensitivity troponin I levels. The nasopharyngeal SARS-CoV-2 PCR test was negative, and the patient denied any history of infection with COVID-19. The patient was admitted to our intensive care unit (ICU) for observation and further clinical management.
+The troponin I level peaked on the second day (10.923 μg/L; normal range 0–0.045 μg/L) and NT-proBNP levels showed moderate elevation (1,970 ng/L; normal range 0–125 ng/L). A thoracic CT revealed no obvious pulmonary infiltrates and no evidence of coronary plaques or significant stenoses in the coronaries. An echocardiogram performed in the ICU revealed a moderately reduced left ventricular ejection fraction (LVEF) with hypokinetic inferolateral and apical segments.
+The echocardiographic findings were confirmed using a cardiac MRI (CMR) (3T MAGENTOM SKYRA, Siemens Healthineers, Erlangen, Germany). Considering the medical history of the patient, images from the CMR scan during the earlier bout of myocarditis were compared to the present . The contrast enhanced images showed comparable subepicardial late gadolinium enhancement (LGE) in the lateral and apical myocardial wall during the qualitative assessment. A definitive diagnostic conclusion based on LGE alone could not be drawn due to inter-scanner and inter-study differences. Cine images from the current CMR revealed a dilated left ventricle (end-diastolic diameter-−64 mm) and a moderately reduced LVEF (38%) vs. a mildly reduced LVEF (51%) in the examination 2 years ago. Additionally, in the current CMR, native T1 maps revealed a diffuse increase in relaxation times in all myocardial segments [1,344 ± 74 ms; normal range <1,228 ms (1,181 ± 47 ms) for this 3T machine] . As example, the elevation of T1 mapping indices in the mid-ventricular myocardial inferoseptal segment has been shown in , although there is no evidence of any LGE in this segment. There was evidence of a mild pericardial effusion (3 mm). This could suggest renewed involvement of affected myocardium with spread of acute inflammation in other segments too. These findings support the diagnosis of acute myocarditis according to the updated Lake Louise criteria .
+The patient was started on a therapy with Ibuprofen 400 mg (twice daily), beta-blockers (Bisoprolol 2.5 mg once daily) as well as an ACE-Inhibitor (Ramipril 2.5 mg once daily). There was rapid improvement of clinical symptoms and a repeat echocardiogram performed on day 6 showed only a mildly reduced LVEF (52%) thus facilitating a timely discharge. The patient was stable throughout the course of hospital stay and no complications were documented. A follow-up CMR performed after 3 months revealed a markedly improved LVEF (57%). Videos documenting this improvement have been added as . LGE was comparable to the previous studies. T1 mapping indices had normalized (1,194 ms) except for myocardial segments corelating to chronic myocarditis (also evident in past CMR images) .

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+A 56-year-old Caucasian male with a past medical history of hypertension, acute coronary syndrome and atrial fibrillation presented to the emergency department (ED) with acute epigastric pain. His complaints had started 2 weeks earlier and had worsened 1 day prior to ED presentation. The pain was associated with nausea and increased on inspiration. Defecation and micturition were normal. In addition to fenprocoumon and sotalol, he was on antihypertensives, a statin and a proton-pump inhibitor. There was no history of trauma. Physical examination showed a pale, sweating and obese man in pain. His blood pressure was 113/73 mmHg, with a heart rate of 72 beats/min, oxygen saturation of 95% on room air and a respiratory rate of 13 breaths/min. The abdomen was not distended, and there were normal bowel sounds. He had epigastric tenderness without muscular defence or hepato-splenomegaly. His initial haemoglobin was 8.5 mmol/l. White blood cell count was 8.5 × 109/l with a c-reactive protein of 26 mg/l. The international normalised ratio (INR) was 2.4. Abdominal ultrasound showed an inhomogeneous aspect of the spleen without free fluid. Contrast-enhanced computed tomography (CT) imaging of the abdomen revealed splenic haemorrhage with subcapsular hematoma .
+An acute operation was deemed unnecessary because his vital signs remained stable. Oral anticoagulation was reversed with 10 mg vitamin K. The patient was admitted to the hospital for observation and was discharged in good condition after 3 days.

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+An 8-year-old Japanese boy presented with recurrent headache. He had a medical history of hypothyroidism and Down syndrome confirmed by a 47,XY, +21 karyotype. No thyroid peroxidase or anti-thyroglobulin antibody were detected . There was no family history of cerebrovascular disease. Magnetic resonance imaging and angiography showed old cerebral infarction in the left temporal lobe and bilateral occlusion of the terminal portions of the internal carotid arteries with development of collateral arteries consistent with moyamoya syndrome . Based on the asymptomatic stage and the lack of perfusion defects as revealed by 123I-iodoamphetamine single-photon emission computed tomography (SPECT) , we initiated antiplatelet therapy with aspirin, not revascularization.
+At 9 years old, he developed altered consciousness and slurred speech. Hypoperfusion was identified in the left cerebral hemisphere on 123I-iodoamphetamine SPECT . To prevent further stroke, the patient underwent left-sided indirect revascularization consisting of encephalo-duro-arterio-synangiosis and encephalo-myo-synangiosis. No perioperative complications were observed. After the bypass surgery, ischemic symptoms regressed. Postoperatively, 123I-iodoamphetamine SPECT and cerebral angiography demonstrated improved cortical perfusion . However, cerebral angiography showed left choroidal anastomosis and residual moyamoya vessels .
+At 13 years old, the patient was admitted to our center with sudden onset of severe headache and recurrent vomiting, with a Glasgow Coma Scale of 14 and blood pressure of 127/81 mmHg. Computed tomography (CT) of the brain revealed left thalamic hemorrhage with left intraventricular hemorrhage , considered as a cerebral hemorrhage attributable to the left dilated anterior choroidal artery . Aspirin therapy was discontinued and blood pressure was managed using an intravenous calcium channel blocker for 7 days to achieve a systolic blood pressure under 120 mmHg (<95th percentile for age and sex) . Four days after the onset of cerebral hemorrhage, he again complained of headache. Brain CT at this point revealed expansion of intracerebral hemorrhage to the right ventricle, suggesting rebleeding. Eight days after onset, clinical symptoms improved and magnetic resonance imaging demonstrated decreased intracerebral hemorrhage. The patient developed bacterial aspiration pneumonia and gastric ulcer and was therefore started on intravenous ampicillin and famotidine. Twenty days after onset, brain CT detected no findings of post-hemorrhagic hydrocephalus and he was discharged with no neurological deficits. Four months later, cerebral angiography showed spontaneous regression of the dilated left anterior choroidal artery .
+Genomic DNA was extracted from the peripheral blood sample of the patient and targeted Sanger sequencing confirmed a heterozygous RNF213 R4810K variant (GenBank accession number, NM_001256071.3), as a major susceptibility gene for MMD . Follow-up angiography detected the development of a contralateral right choroidal anastomosis and the patient therefore underwent right-sided direct revascularization to prevent future hemorrhagic stroke six months after onset of the left hemorrhagic stroke. Four months after revascularization, angiography showed regression of the right choroidal collateral vessels. No ischemic or hemorrhagic stroke was observed as of the time of writing, 22 months postoperatively.

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+In 2006, a 52-year old female patient was admitted to a neurological department due to sudden difficulties with swallowing and speech, ophthalmoparesis with a vertical and horizontal eye movement disorder, dysesthesia of the hands with a quality of “pins and needles” and a glove-like distribution, as well as generalized areflexia. Muscle strength was normal. A Miller Fisher syndrome was diagnosed. Under treatment with 150 g intravenous immunoglobulins the symptoms completely remitted within a few days. In the following years, the patient consulted the general practitioner and several gastroenterologists because of unspecific abdominal pain, from which she has been suffering since childhood. Diagnostics including computer tomography (CT), magnetic resonance imaging (MRI) and gastroscopy were normal.
+In October 2017 the meanwhile 63-year old patient was hospitalized with generalized epileptic seizures with prolonged postictal confusion. Cerebral MRI showed no pathological findings, and therapy with levetiracetam was started.
+In December 2017 the patient was admitted to our clinic for internal medicine because of persisting diarrhea, abdominal pain, renal failure and a reduced general state of health. Again, the patient had generalized epileptic seizures with postictal confusion and significantly reduced vigilance, accompanied from a lactic acidosis (serum-lactate 26.0 mmol/l (reference 0.55–2.2 mmol/l), pH 6.863), leading to admission to the neurological intensive care unit. Moreover, a slight, presumably residual ophthalmoparesis as vertical gaze palsy with conjugate, bilateral limitation of the eye movements in upgaze was evident. The anticonvulsive therapy with levetiracetam (3 g/day) was extended by lacosamide (400 mg/day). A mechanical ventilation was necessary due to the sudden and massive metabolic acidosis as well as a respiratory failure during an epileptic seizure (serum-lactat 14.7; 10.6; 16.0 mmol/l). In CSF, lactate (12.01 mmol/l (reference 1.12–2.47 mmol/l) and protein level (67 mg/dl (reference 15–45 mg/dl) were significantly increased. There were no signs for an infectious origin in CSF (polymerase chain reaction for neurotrophic germs, including Tropheryma whippelii). CT and MRI of the brain as well as abdominal- and thorax-CT were normal. The electroneurography revealed a slight mixed axonal-demyelinating polyneuropathy, the electromyography was normal. Besides a sinus-tachycardia with 140 bpm and a mild pericardial effusion, no signs of a Wolff–Parkinson–White syndrome, that would be common in mitochondriopathies, were present.
+Attempted extubation failed as another severe epileptic seizure occurred with life-threatening lactic acidosis and hyperkalemia (lactate 26.0 mmol/l; pH 6.925; potassium 7.8 mmol/l (referece 3.6–5.2 mmol/l). EEG showed an alpha rhythm, with intermittent slow waves and tendency to generalize. In cerebral follow-up MRI, multiple fat embolies were detected. CT-angiography of the lung revealed a pulmonary embolism. As a reason for the fat embolies, multiple vertebral fractures were verified in CT, presumably as a result of severe epileptic seizures. A surgical fixation of vertebral fractures was performed. Intensive care therapy including ventilation was necessary for more than eight weeks. Weaning was successful after dilatative tracheostomy and nutrition via percutaneous endoscopic gastrostomy (PEG) tube. Vitamin-B6 was supplemented. Subsequently, a rehabilitative therapy was performed. After five months, the patient returned to her normal life. Tracheostomy and PEG were removed.
+Taking into account all the symptoms (abdominal pain, relapsing remitting course, neurological deficits, epileptic seizures, peripheral neuropathy, lactic acidosis, cardiac disturbance), two main differential diagnosis were discussed: porphyria and a mitochondrial disease (MERRF syndrome). None of both diagnoses could be verified: Laboratory test revealed no hints of porphyria (Porphyria Specialist Center of the European Porphyria Network University Hospital Düsseldorf, Germany). A muscle biopsy gave no hint of a mitochondrial disease and revealed only a slight unspecific atrophy that was very likely due to immobility (Institute of Neuropathology of the University Hospital Essen, Germany). In terms of differential diagnosis, other metabolic diseases came into consideration. Comprehensive diagnostic for diseases of copper metabolism, lead poisoning or adrenoleukodystrophy remained inconspicuous. Finally, the analysis of the amino acids in the urine, CSF and serum showed a strong abnormality with ubiquitously increased amino acids, especially proline (proline in serum 3085 μmol/l (reference 90-342 μmol/l), in urine 46,531 μmol/g Crea (reference < 100 μmol/g Crea), in CSF 104 mg/dl (reference < 6 mg/dl), Hydroxyproline in urine 1395 μmol/g Crea (reference <100) Table ). Furthermore, vitamin-B6 was decreased with 3.3 μg/l (reference > 4.9 μg/l). We supplemented vitamin B6 with 200 mg/d.
+Therefore, a hyperprolinemia type I or type II was most likely. The targeted genetic analyses by Sanger sequencing revealed no pathogenic variant within the PRODH-gene (hyperprolinemia type I) but identified two novel variants within the ALDH4A1-gene . In combination, both heterozygous variants within the ALDH4A1 gene could lead to a compound heterozygosity (variants in trans), that would cause the described disease phenotype. Since the patient’s son had only one of the two heterozygous variants of his mother, the compound heterozygous state of both variants in our patient was proven.

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+A 38-year-old male complained of palpitation and exertional dyspnea on his first visit to a local hospital in February. He never had a fever, arthralgias, weight loss or fatigue, nor did he have a personal or relevant family history of cardiovascular disease or neoplasms. A grade II/6 pansystolic heart murmur was heard during physical examination. Transthoracic echocardiography (TTE) revealed a large mass in the left ventricle, attached to the anterolateral papillary muscle and chordae tendineae. The local doctor made a preliminary diagnosis of suspected intracardiac fibroelastoma or myxoma, and suggested surgical resection for this intracardiac neoplasm through conventional median sternotomy. However, the patient was deterred by the invasiveness of sternotomy, and refused to have surgery in his local hospital. In May, as he learned about our experience in minimally invasive cardiac surgery, he came to our center.
+We reexamined the patient. The TTE confirmed a mobile round cystic mass inside the left ventricle. The mass had a hyperechogenic wall and hypoechogenic content and was attached to the anterior mitral leaflet . In systole, the mass prolapsed into the left ventricular outflow tract (LVOT) with accelerated peak velocity (2.5 m/s), which led to mitral regurgitation . The LVOT appeared normal without subvalvular ridge or asymmetric septal hypertrophy. Complementary thoracic and abdominal computed tomographic (CT) scans did not show any evidence of the existence or potential spread of noncardiac neoplasms. All laboratory examinations including tumor markers were unremarkable.
+Non-invasively distinguishing aggressive from non-aggressive intracardiac tumors is an important clinical challenge. Preoperative biopsy for histopathological diagnosis is inapplicable to intracardiac tumors. In this case, fortunately, the TTE provided significant information on morphology, localization, biological characteristics, as well as tumor vascularity-perfusion. The mass had a smooth surface, clear border, and low echodensity. No imaging evidence showed any features of malignancy like vascularity-perfusion, invasion or filtration into the cardiac structure, permeation to the great vessels, or pericardial effusion. So, there was a fairly high probability that this mass would be benign. We made a diagnosis of a primary intracardiac cystic tumor according to the obtained information, and decided to resect the tumor.
+Generally, a benign intracardiac tumor in this location and size can be accessed via trans-aortic or mitral orifice approach through mini-thoracotomy. Since we have enough experience of totally endoscopic mitral surgery, we decided to perform the operation in a totally thoracoscopic approach, and manage the possible deformation and dysfunction of the cardiac structure if necessary.
+Tumor resection was planned and performed through a totally endoscopic, video-assisted approach with thoracoscopy and femoral cannulation (Supplemental Video). The cardiopulmonary bypass and the surgical approach were established as the conventional endoscopic mitral surgery . A 35-mm working port was made in the fourth interspace, lateral to the midclavicular line. After deflation of the right lung, two additional ports were then placed: a camera port through the anterior axillary line in the fourth interspace, and an 8-mm port in the lateral fifth interspace for a transthoracic Chitwood clamp (Scanlan International, Minneapolis, Minn). We used the Chitwood clamp to occlude the ascending aorta and administrated the antegrade cardioplegia. A left atriotomy was performed, and the atrial retractor was applied. The mitral orifice and the mass were then clearly visualized . The mass was oval and reddish, partly attached to the chordate structure of anterior papillary muscle and A1 area of anterior mitral leaflet via two pedicles . We completely excised the mass through the roots of the pedicles, and then carefully cauterized the margin of excision. The size and structure of the mitral leaflets and subvalvular apparatus appeared to be normal. No surgical injuries were found during further exploration . The saline test showed no mitral regurgitation.
+The excised mass was 25 mm*20 mm*20 mm in size . Pathologic diagnosis confirmed a simple blood cyst, consistent with blood-filled space lined with a single layer of endothelium. The patients had an uneventful recovery. He was able to walk on the first postoperative day and was discharged three days after the operation. The patient was symptom-free and working full time during follow-up.

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+A 70-year-old man, without any particular pathological history, referred by family physician, to emergency with a 48h evolving abdominal pain, important abdominal distension, nausea, vomiting, and a last bowel movement reported 2 days ago. On examination, his vital signs were: temperature: 37.3 °C, pulse rate: 110/minute, respiratory rate: 24/minute and blood pressure: 110/60 mmHg. The abdominal examination revealed an abdominal sensibility at the right illiac fossa, a distension of the abdomen and an empty rectal ampula on rectal examination. The biological checkup showed hyperleukocytosis at 15700/mm3, hemoglobin at 11g/dl, platelets count at 159,000/mm3 and C-reactive protein at 180 mg/liter, the hepatic and renal check-ups were normal. An abdominal X-ray revealed the presence of hydro-aeric levels at the ileum segments without pneumoperitoneum. The abdomino-pelvic CT-scan objectified a distension of the terminal ileum measured at 30mm, upstream of a transitional level in which seats a rectangular and plane foreign body (, ). Considering these findings, the patient was diagnosed with intestinal perforation caused by a foreign body. After optimization of his general condition with a Naso-Gastric tube suction and intravenous fluids resuscitation, a decision was taken to proceed with an emergency laparotomy, under general anesthesia with endotracheal intubation. Performed by a 5th year and a 4th year surgical resident. Preoperative prophylactic antibiotics were administered. The exploration revealed a sharp foreign body (fish bone) measuring 3 cm/2cm at the 15 proximal centimeters of the terminal ileum, which penetrated through the wall of the ileum. The foreign body was removed and we noticed that it is a fish bone (, ). The margins of the perforation were excised and primary closure was performed. The patient recovered well and was discharged on the 6th postoperative day. On interrogation, the patient acknowledged that he incidentally swallowed the fish bone 5 days ago. The postoperative course was uneventful: improvement of the general condition of the patient.

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+An 18-year-old man was referred for painful bilateral testicular tumors confirmed with scrotal ultrasonography. MRI revealed a 2.5 cm tumor and a 3.0 cm tumor in the rete testis regions of the right and left testicles, respectively . CBC, LH (4.9 mIU/mL, normal 1.5–9.3 mIU/mL), FSH (5.1 mIU/mL, normal 1.6–8.0 mIU/mL), and total testosterone (398 ng/dL, normal 249–836 ng/dL) were normal. Tumor marker beta-HCG, AFP, and LDH were also normal. Both tumors subjectively progressed in size during the time between initial evaluation and surgery. Bilateral partial orchiectomies were attempted . The right was converted to a radical orchiectomy with prosthesis due to intraoperative concerns regarding testis viability. A partial orchiectomy was successfully completed on the left. Intraoperative frozen sections were not conclusive for germ cell, Leydig cell, or another histology. Pathologic evaluation of both tumors revealed the proliferation of tumor cells throughout the testicular parenchyma and rete testis, with nodules ranging from <1 to 10 mm, a low proliferation index (Ki67 positive in 1% of cells) and negative p53. No features of malignancy such as necrosis, mitotic figures, or pleomorphism were present . A presumptive diagnosis of Leydig cell tumors vs TARTs was suggested.
+CT scans of the abdomen and pelvis revealed a soft tissue density measuring 2.1 × 1.7 cm in the left para-aortic region . Also noted were slightly enlarged inter-aortocaval nodes and a small left adrenal nodule. An image-guided biopsy of the para-aortic mass was nondiagnostic.
+A postoperative endocrine evaluation revealed markedly elevated ACTH levels (4322 pg/mL) yet normal cortisol levels. The patient’s clinical and radiographic findings, testis pathology, and elevated ACTH level, all supported a diagnosis of NCAH and the presence of TARTs. The postoperative endocrine evaluation also revealed an LH level of 21.5 mIU/mL, FSH of 22.9 mIU/mL, and a low testosterone level (81 ng/dL). Borderline adrenal insufficiency and moderate hypogonadism were effectively managed with hydrocortisone and testosterone supplementation. Larger than average doses of hydrocortisone were necessary to maintain the ACTH at a desired level (under 100 pg/mL).
+Follow-up scrotal U/S and CT scans 2 years post-surgery revealed a right testicular prosthesis, a partial left testicle containing no new masses, and a stable para-aortic soft tissue mass .

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+An immunocompetent 28-year-old male was empirically diagnosed with a primary tectal tumor at an outside hospital; his history was negative for intravenous drug use or significant systemic bacterial infection. He presented initially with progressive intermittent headache for more than 6 months. Initial magnetic resonance imaging (MRI) showed a 10 mm × 9 mm left midbrain tectum ring-enhancing lesion with associated surrounding edema and mild hydrocephalus . At the other hospital, he underwent placement of a ventriculoperitoneal shunt (VPS) for obstructive hydrocephalus.
+Eight weeks later, he started to have worsening headache, nausea, and intermittent vomiting. He was readmitted with a VPS infection and an abdominal pseudocyst. He was transferred to our institution where the VPS was removed, an external ventriculostomy was placed, and he was started on intravenous ceftriaxone and vancomycin. Cerebrospinal fluid (CSF) profile showed elevated white blood cell (WBC) count of 482 with lymphocyte predominance, suggesting a chronic infection; CSF culture revealed A. aphrophilus. His other workup including blood cultures and transthoracic echocardiogram were negative for infectious etiologies. He slowly improved with antibiotic treatment and was weaned off the ventriculostomy after 14 days, without any subsequent recurrence of hydrocephalus. Vancomycin was stopped after 10 days when the culture finalized A. aphrophilus sensitive to ceftriaxone. The tectal lesion completely resolved after 15 weeks of intravenous ceftriaxone . At the 4-month follow-up, he had no headache or any other clinical sequelae.

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+We report on an 81-year-old woman with no relevant comorbidities and a smoking history of 5 pack years. In 2006 she was diagnosed with a pT2a, pN0 (0/5), cM0, UICC stage IB squamous cell carcinoma of the left upper lung lobe, for which she underwent a double-sleeve lobectomy with lymphadenectomy. During 5 years of follow-up, no relapse occurred. In April 2019, the patient presented with a post-stenotic pneumonia. Computed tomography of the chest showed a mass in the left lung. Radiological staging with whole-body 18F-FDG-PET/CT and brain MRI showed metastatic disease with a strongly metabolically active primary tumor (SUVmax 16.7), pleural carcinomatosis on the left side (SUVmax 9.4), periclavicular lymph node metastases on the left side (SUVmax 9.9), and bone metastases in the 12th thoracic and 4th lumbar vertebra (SUVmax 5.0 and 4.6, respectively) . Histology of bronchoscopic biopsy specimens revealed squamous cell carcinoma, which could be interpreted as recurrence or as a second lung cancer, taking into consideration the 13-year-long disease-free interval. The immunohistochemistry for programmed cell death ligand 1 (PD-L1) revealed an expression in 20% of tumor cells and in < 10% of immune cells. In order to complete our internal lung cancer diagnostic algorithm (Treichler G, manuscript in preparation), we performed next-generation sequencing using the FDA-approved FoundationOne®CDx assay. We found a structural aberration on the long arm of chromosome 3 (3q) with amplifications of the genes , SOX2, and FGF12; mutations of TP53, ATRX1, RB1, and, subclonally, PIK3CA; a stable microsatellite state (MSS), and a low tumor mutational burden (5 Muts/Mb).
+Based on the recommendation by our multidisciplinary tumor board, a therapy regimen consisting of pembrolizumab, carboplatin and paclitaxel in analogy to the KEYNOTE-407 study was suggested. The patient declined systemic treatment. She was thus referred for radiotherapy in order to achieve local control, due to the central localization of the tumor with associated risk of post-stenotic pneumonia and bleeding. The patient underwent conventionally fractionated radiotherapy of the principal pulmonary tumor bulk with palliative intention with 3 Gy in 12 fractions, resulting in a total dose of 36 Gy, using Volumetric Modulated Arc Therapy (VMAT, RapidArc™). Radiotherapy was well tolerated, with esophagitis grade 2 according to the Common Terminology Criteria for Adverse Events (CTCAE) version 5.0. Four weeks after the last day of radiotherapy, restaging was performed with 18F-FDG-PET/CT. A partial remission of the tumor bulk, the nodal metastases and, surprisingly, also of the vertebral lesions was shown . Of note, the supraclavicular lymph nodes and the two bone metastases in the spinal column had not been included in the irradiation field with scatter doses of 0.201 Gy, 0.093 Gy, and 0.021 Gy on the lymph nodes, vertebra Th12, and L4, respectively . Furthermore, no antiresorptive medication had been administered. Due to the remission and the lack of tumor-related symptoms, systemic treatment—although no longer refused by the patient—was withheld. The patient underwent radiological follow-up, during which further decrease in tumor size and complete metabolic remission of the bone, pleural and lymph node metastases was seen . Currently, 25 months after radiotherapy, the patient is still free of symptoms and has an Eastern Cooperative Oncology Group (ECOG) Performance Status of 0.

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+A 25 year-old Caucasian woman presented with a four-day history of acute onset of blurred vision in both eyes. She reported a viral upper respiratory tract infection for seven to 10 days, for which she had taken two Excedrin® Migraine (acetaminophen 250 mg, aspirin 250 mg and caffeine 65 mg) tablets. She used Midrin (acetaminophen 325 mg, dichloralphenazone 100 mg, isometheptene mucate 65 mg) as needed for her headaches concurrently. Additionally, she smoked half-pack cigarettes and consumed four to five 12-ounce cans of a caffeinated drink, Mountain Dew (caffeine 54 mg/can) per day.
+Her uncorrected Snellen visual acuity was 20/20 in both eyes and Amsler testing revealed bitemporal paracentral scotomas. She correctly identified 10 and nine out of 14 Ishihara color plates, in her right and left eye, respectively. No afferent pupillary defect was noted and the anterior segment was unremarkable. Fundus examination revealed bilateral hyperpigmentary changes in the papillomacular bundle . Fundus autofluorescence revealed a normal autofluorescence pattern. IR imaging disclosed classic wedge-shaped lesions with their apices oriented towards the fovea. SD-OCT exhibited changes at the inner segment-outer segment (IS-OS) junction, with a thickened OPL overlying these areas . Humphrey visual field (HVF) 30-2 demonstrated bilateral paracentral scotomas. Fluorescein and indocyanine green angiography did not demonstrate any perfusion defects or any other abnormality.
+Five months after initial presentation, her color vision improved to 14 of 14 Ishihara color plates correctly identified in each eye. Repeat HVF testing demonstrated interval improvement in the scotomas, more in her right eye than left. Similarly, SD-OCT showed a corresponding small improvement at the IS-OS junction in her right eye and no change in her left eye . Microperimetry using an MP-1 (Nidek, Japan) demonstrated focal elevation in threshold correlating with the wedge-shaped defects in both her eyes .

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+A 79-year-old male presented to the dermatology clinic with a new rash. He had a past medical history of chronic kidney disease stage 3, gout, and papillary and invasive urothelial carcinoma, extravesical high-grade invading into the lamina propria and muscularis propria Stage IVA (pT4b, pN0, cM0) diagnosed by transurethral resection of bladder tumor 05/2020 on pembrolizumab. Of note, his urothelial carcinoma biomarkers were programmed death-ligand 1 negative (immune cell 5%, tumor <1%), Tempus XF (liquid) = IDH1 GOF, xT = ERBB2, RB1, TP53, CDKN2A, GATA-3, MTAP, TMB 4.2 m/MB, MS-S. He was treated with neoadjuvant Gemcitabine/Cisplatin ×3 cycles complicated by sepsis. The patient underwent cystoprostatectomy 09/2020. In 07/2021, he was found to have metastasis to the rectum after sigmoidoscopy biopsies show rectal mucosa and submucosa containing rare foci of malignant cells in lymphatic spaces. GATA-3 immunostaining was positive in these cells, compatible with a spread from the patient's known urothelial primary carcinoma. Surgery was offered at this time, but the patient declined. He was then started on pembrolizumab. Recent CT and sigmoidoscopy were concerning for the progression of rectal mass. After receiving 15 cycles of pembrolizumab, the patient was started on enfortumab vedotin plus pembrolizumab. On cycle 3 day 1, he presented to dermatology with a rash of the right inguinal region for 5 weeks which was painful and pruritic. He had previously been treated with oral valacyclovir and topical clotrimazole cream with no improvement. The patient denied a history of fevers or night sweats.
+His physical exam was notable for firm papulonodules, several of which formed confluent, hyperpigmented to violaceous plaques involving the right inguinal fold . Similar lesions also extended onto the proximal anterior thigh. A punch biopsy was performed which revealed a dermal proliferation of neoplastic cells in irregular nests with retraction artifact and focal glandular differentiation. The cells show high-grade nuclear features with background apoptosis. There was no involvement of the overlying epidermis. Immunohistochemistry revealed that the tumor cells were positive for CK20 and GATA3 and negative for CK7 . The presence of a glandular proliferation in the dermis, without overlying connection to the epidermis, and with a staining pattern consistent with the patient's known urothelial carcinoma, led to the diagnosis of cutaneous metastasis. Of note, the papillary dermis showed edema and perivascular inflammation that corroborated the clinical appearance of the rash and can be seen in metastatic lesions, adding to diagnostic challenge on clinical grounds. After confirmation of skin metastasis, the patient received one fraction of intensity-modulated radiation therapy to the right pelvis/groin. He was continued on enfortumanb vedotin plus pembrolizumab at that time. Significant decline in CA19-9 and ctDNA had stabilized. The newest CT imaging demonstrates a decrease in abdominal/pelvic lymphadenopathy with no new findings.

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+A 7-month-old Chinese boy was referred to the pediatric nephrology and immunology department of our hospital with eyelid edema for more than 2 months and limb swelling for 1 week. In the medical history, there had been recurrent cough that continued for some days. He had a pale complexion, with periorbital and bilateral pitting pedal edema on clinical examination, but no jaundice, petechiae, purpura, or lymphadenopathy. There was no history of tachycardia or tachypnea. There was no hepatosplenomegaly. His blood pressure (81/62 mmHg) was in the normal range at admission. The child had a history of amniotic fluid contamination at birth and no history of asphyxia. Neither the boy nor his family had a significant history of conditions such as kidney-related diseases or autoimmune diseases. However, the grandmother died of hematological disease.
+Investigations 3 days prior at clinics of another hospital showed a hemoglobin (Hb) level of 62 g/L without thrombocytopenia (platelet count 396 × 109/L). Serum lactate dehydrogenase (LDH) was elevated (579 U/L) (normal <382 U/L). An elevated serum cholesterol of 5.38 mmol/L was noted at that time, along with range proteinuria (1+) and hypoalbuminemia (serum albumin 28.8 g/L). There was no gross or microscopic hematuria. The serum C3 and C4 levels were normal. The laboratory values with reference values are shown in the . The boy was immediately referred to our hospital with a referral diagnosis of “nephrotic syndrome (NS)”.
+The patient presented with likely NS with anemia for five days after admission but no proteinuria or hypoalbuminemia. The direct Coombs test was negative. On hospital day 6, the patient presented with “hemolytic uremic syndrome (HUS)” following episodes of vomiting and diarrhea with fever. There were systemic pitting pedal edema, oliguria, petechiae, and soy sauce-colored urine at that time, along with hypertension (129/89 mmHg). Laboratory workup revealed normocytic hemolytic anemia with an Hb level of 62 g/L, mean corpuscular volume (MCV) of 86 fL, elevated reticulocyte count of 9.3%, schistocytes count of 3% on the peripheral smear, thrombocytopenia (platelet count 23 × 109/L), a serum creatinine (SCr) level of 0.62 mg/dl, blood urea nitrogen (BUN) level of 5.66 mmol/L, cystine (C) level of 1.57 mg/L, C3 level of 0.89 g/L, C4 level of 0.21 g/L, a markedly increased lactate dehydrogenase (LDH) level of 585.1 U/L, hematuria (red blood cells 4,627.9/µl), and proteinuria (3+). Coagulation function, including prothrombin time (PT), activated partial thromboplastin time (APTT) and fibrinogen, was elevated (36.2 s, 58.6 s and 4.26 g/L, respectively). The serum bilirubin, AST, ALT, and serum electrolyte levels were within normal limits. The activity of a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13), was normal. The stool rotavirus test was positive. Stool culture grew Streptococcus and Escherichia coli (E. coli), and stool multiplex polymerase chain reaction (PCR) showed that Shigella, Salmonella, E. coli O157, and pathogenic Vibrio were not detected. The infectious workup was notable for a negative respiratory viral panel, negative special viral panel (human parvovirus B19, EB virus, cytomegalovirus, rubella virus, herpes simplex virus, hepatitis virus), negative Mycobacterium tuberculosis, and negative blood culture. Antinuclear antibodies were negative. The chest x-ray was negative. B-ultrasound showed a small amount of abdominal effusion . Abdominal computed tomography (CT) showed that the kidney, liver and spleen increased in volume with a low-density image . The echocardiogram showed a central atrial septal defect (2.3 mm) with a normal ejection fraction (EF 66%). The 24 h urine protein quantification was not performed due to the difficulty in collecting 24 h urine. Moreover, due to his uncontrolled hypertension and thrombocytopenia, the patient could not undergo a kidney biopsy.
+Given the concern for HUS, broad-spectrum antibiotics and fresh frozen plasma infusions were given to treat his gastrointestinal infection and TMA. The following other treatments were employed: intravenous immunoglobulin (IVIg) infusions, human prothrombin complex infusions, albumin infusions (due to a decreased level of albumin), red blood cell infusions, platelet infusions, intramuscular injection of vitamin K1, low-dose methylprednisolone for anti-inflammatory treatment, antihypertensive treatment (nifedipine and metoprolol), and symptomatic treatment.
+The patient was diagnosed further with aHUS, had been administered plasma infusions (PIs) discontinuously and had required plasma exchange (PE) 2 times during the PICU hospital stay. Given the trend of acute respiratory distress syndrome (ARDS) with worsening pneumonedema and pneumorrhagia, mechanical ventilation (MV) was given for 7 days. There was a transient remission of respiratory symptoms. However, given the trend of worsening renal function [elevated levels of blood urea nitrogen (BUN)], progressing edema, and worsening hypertension, continuous renal replacement therapy (CRRT) and hemodialysis (HD) on alternating days were given to treat his acute kidney injury (AKI) for 13 days and 15 days, respectively. The patient's renal function and hematologic parameters (stage 3 AKI with gross hematuria) worsened during the 6th–7th week of the hospital stay while HD and PI therapy was continued, as depicted in . Subsequently, the patient developed a hypertensive emergency with features of intracranial hypertension leading to right temporoparietal hematoma and subarachnoid hemorrhage, as depicted in . He required multiple drugs (furosemide, nitrate, glycerin fructose) for the control of hypertension and intracranial hypertension. Ultimately, he still had a recurrence of ARDS and deteriorated to a stage of involuntary respiration requiring high ventilatory settings with pulmonary hemorrhage, gastrointestinal hemorrhage, and multiorgan dysfunction. Chest CT displayed both lung pneumonia and partial atelectasis of the upper lobe of the right lung . Head CT showed that the subarachnoid hemorrhage was more extensive than before . The patient's parents decided to withdraw the patient from further management. The patient died during the 8th week of his hospital stay.
+We obtained 2 ml of peripheral blood from the patient, his parents and older brother respectively. Whole exome sequencing was performed on the patient, his parents and brother. Sanger sequencing was used to verify the mutation site. CNVnator software was used for CNV analysis, and QPCR was used for family analysis. Two heterozygous variations in the DGKE exon region: NM_003647.2, c.610dup, p.Thr204Asnfs*4 and deletion of exons 4–6 were identified. The first variant was classified as de novo compared with the results obtained in the conventional in the Sanger sequencing of the parents and the older brother . The second variant was a deletion of DGKE exons 4–6, which was also detected in the asymptomatic father, but absent in both the mother and the older brother . The patient in this case had aHUS, consistent with recessive transmission with the 100% penetrance.

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+A 71-year-old female with a past medical history of undifferentiated connective tissue disease (UCTD) presented to an acute care hospital in December, 2020 after experiencing sudden onset of lower extremity weakness over 8-10 min, sensory loss from the lower trunk down, urinary retention, and worsening hypotension.
+This individual had recently been exposed to COVID-19 through a household member and subsequently tested positive, with COVID cycle thresholds suggestive of recent infection. She demonstrated cough and fever before hospitalization, but did not require supplemental oxygen beyond the first few hospital days. She was issued 5 d of IV methylprednisolone and remdesivir, followed by an oral prednisone taper of 5 additional days. Neurological exam in acute care found incomplete sensory deficits T3-8 but complete absence of sensation from T9 and below.
+During inpatient rehabilitation, we did acquire some key historical information about her UCTD, which to date had never progressed to a defined connective tissue disorder such as mixed connective tissue disease (MCTD). This condition is characterized by the presence of certain antibodies, particularly presence of the U1 small nuclear ribonucleoprotein particles (snRNP). Notes received indicate a negative titer for U1snRNP in 2020 when she had acute COVID-19, similar to her level when last tested in 2016. No lab quantification of U1-anti RNP titer was listed among lab results, other than a note stating it was not present. She had no clinical features of MCTD other than presence of sclerodactyly and stated history of Raynaud’s, which was not active during rehabilitation. She had myalgias but no evidence of synovitis or myositis that would prompt us to request a muscle biopsy. At the time of her admission to rehabilitation, this individual’s discomfort and spasms, as well as pain were in the middle and upper trunk and mid-back. However, during past UCTD exacerbations, she had endured aching and often sharp pain specifically in the posterior cervical spine and shoulders and during more significant attacks, pain and swelling in her fingers. Except during practice with wheelchair transfers, she reported no shoulder, arm, or hand pain with physical or occupational therapies.
+The possibility exists that some of the pain and spasms she was feeling was a different manifestation of her usual UCTD flare. In the past, such instances had always affected more proximal areas of the body, specifically neck, shoulders and hands. In her 2.5 years since discharge from her second inpatient rehabilitation stay, she has only experienced two significant UCTD exacerbations, both during an acute hospital admission for secondary complications of her NTSCI. The first occurred in the summer of 2022 when septic from a severe UTI. Her antibiotics for that condition included first intravenous cephalosporins and then ciprofloxacin. Both agents may have impaired absorption of hydroxychloroquine prescribed daily for chronic UCTD. In addition, several doses of this long-term medication were missed due to acute illness. During this hospitalization, she became weaker and had increased joint pain, neck pain, and hand swelling. However, the only serology that was abnormal among rheumatologic indices was an elevated ESR of 3 points beyond the upper limit of normal, which could have been outside the normal range simply due to the UTI. During this admission, the same labs as appeared in Table were performed and no findings revealed a change in her degree of UCTD.
+Upon arriving to rehabilitation, her exam demonstrated a C7 left, T3 right ASIA Impairment Scale A, with a zone of sensory preservation to T8 bilaterally and complete absence of sensory and motor function from T9-S5. Her first month of rehabilitation was marked by expected neurogenic bowel and bladder, moderate thoracic non-radiating back pain, and mild spasticity below T9. She also had a band-like tightness in the T4-5 dermatomes in the absence of imaging findings there. The pain continued to intensify during subsequent weeks in rehabilitation, progressively taking on more neuropathic features with relentless mid-back and chest tightness.
+She was discharged home after 8 wk but continued to experience unrelenting truncal pain between the T3-T8 dermatomes, above and at the level of the infarct, estimated to be located at T8. Several additional acute care and rehabilitation admissions for pain and urinary tract infections ensued during the subsequent two months. Her exam in this time now showed T3 complete SCI with partial preservation to T8.
+Table gives additional studies undertaken in the diagnostic workup, including the presence of viruses other than SARS-CoV-2 (enterovirus, Varicella zoster, Herpes simplex, and West Nile), and markers of inflammatory, autoimmune, and neoplastic disorders. Specifically, there was no evidence of Neuromyelitis Optica, based on absent aquaporin-4, and no evidence of myelin oligodendrocyte glycoprotein antibody, which is characterized by immune mediated demyelination of the spinal cord and other regions of the central nervous system. Moreover, immunoglobulin G synthesis of the cerebral spinal fluid (CSF) index was also negative, suggesting other inflammatory processes were not present. No oligoclonal bands were detected in CSF, a finding commonly seen in multiple sclerosis (MS) and in neoplastic processes such as multiple myeloma. Myelin basic protein was elevated but is a nonspecific finding, present in autoimmune disorders such as MS and ischemic conditions. including stroke. Lumbar puncture on presentation had serum and cerebrospinal fluid studies that were entirely unremarkable.
+Her managing team at the acute care hospital did not have access to her outpatient records about her rheumatologic condition from her community physicians. They did perform a comprehensive serologic workup during her acute COVID admission, but the specimens were sent to an outside lab. Her results were not finalized prior to acute hospital discharge and thus were never added to her inpatient record, nor subsequently forwarded to the rehabilitation team.
+Several weeks into her first inpatient rehabilitation stay, partial rheumatologic history and the labs drawn while admitted for COVID-19 were eventually obtained from her outpatient physician’s office. This individual’s initial diagnosis of UCTD occurred in 1993, prior to acute COVID-19, and was classified as non-antinuclear antibody UCTD. Her condition was based on the presence of CREST syndrome, the pneumonic of which represents calcinosis, Raynaud’s syndrome, esophageal dysmotility, sclerodactyly, and telangiectasias. This information was from her first available outpatient record dating back to 2004, nearly 20 years preceding this publication. In 1993, her predominant features were Raynaud’s affecting fingers and sclerodactyly. She began on disease-modifying medication hydroxychloroquine and a plan was made to arrange for oral prednisone as needed for any exacerbations. Outpatient records from 2004-2020 indicate patient reported feeling well, with a “stable UCTD presentation”, without changes in lab indices, recorded hospitalizations, or flares. Documents did note an exacerbation of symptoms of neck and shoulder pain in 2016 that was managed as an outpatient with a combination of hydroxychloroquine and nifedipine, a calcium-channel blocker. At that time a core panel of rheumatologic markers was drawn, identical to the panel drawn in December 2020 given in Table . No specific rheumatologic markers were concerning, with the exception of an elevated erythrocyte sedimentation rate that resolved using the above medications. Between 2016-2020, she continued with annual visits to rheumatology without a documented flare or change in medications. Although normal values vary from one lab to another, the purpose of each test and the ratio of positive to negative values is similar between institutions. The labs were selected by the referring facility where the acute care team made the decisions in diagnostic workup.
+Initial workup included magnetic resonance imaging (MRI) of the cervical, thoracic, and lumbar spine, which showed acute cord ischemia T9 to the conus medullaris. Thoracic cord expansion and increased intramedullary signal extending many vertebral segments were compatible with a spinal cord infarct, particularly in light of the CSF findings and her acute onset of weakness. The above helped to differentiate an infarct from transverse myelitis. The brain MRI was negative for optic neuritis or lesions suggestive of MS, features needed to diagnose those conditions.
+Figure demonstrates a lengthy region of T2 hyperintensity from T9 to the conus, yet absent imaging findings above T9, despite observed sensory abnormalities for many segments rostral to T9. She was diagnosed with a T8 spinal cord thrombotic stroke. Her infarct occurred approximately 7 d after acute infection with COVID-19, consistent with the timing reported by Zhang et al in relation to COVID cytokine storm.

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+A 67-year-old man was referred for uncontrolled increased IOP in his left eye despite maximal tolerated medical therapy. He had previously been diagnosed with left secondary glaucoma related to idiopathic uveitis, which was diagnosed based on negative results in all systemic work-ups including serologic, radiologic test. His previous ocular history included laser iridotomy (LI) and trabeculectomy, which were performed three years prior to SLT procedure, as well as phacoemulsification with in-the-bag posterior chamber lens implantation which performed two years ago. His past medical history was unremarkable. Best corrected visual acuity was 20/20 in his right eye and 6/20 in his left eye. IOP measured by Goldmann applanation tonometry was 15 mmHg in his right eye and 28 mmHg in his left eye, with the latter being treated with a fixed combination of dorzolamide and timolol (Cosopt, MSD, Switzerland) twice daily, brimonidine 0.2% (Alphagan, Allergan, USA) twice daily and latanoprost 0.005% (Xalatan, Pfizer, Belgium) once nightly. Slit lamp examination showed deep anterior chambers in both eyes, as well as showing a shallow bleb, a patent LI hole at the 11 o’clock position of the iris, and an iridectomy site at the 12 o’clock position of the iris in the left eye. Gonioscopic examination of the left eye revealed peripheral anterior synechiae around the iridectomy site at the 12 o’clock position and hyperpigmented tissue within the trabecular meshwork in all quadrants . The patient was prescribed oral acetazolamide (Acetazol tab. 250 mg, Hanlim Pharm., Korea) twice daily for 1 week, reducing the IOP in his left eye to 17 mmHg as measured by Goldmann tonometry. Owing to drowsiness, however, the oral drug had to be discontinued. One week after discontinuing oral acetazolamide, the IOP returned to 30 mmHg. Therefore, it was decided to perform SLT while maintaining twice daily dosing of oral acetazolamide. SLT, rather than additional glaucoma surgery, was selected to reduce IOP because of following findings suggesting advanced glaucoma in the left eye , (1) a pale disc on fundus examination, (2) diffuse retinal nerve fiber layer (RNFL) loss on optical coherence tomography (OCT), and (3) severe field constriction on Humphrey visual field test .
+Proparacaine topical anesthetic solution was applied to the left eye, and hydroxypropyl methylcellulose (Hycell solution 2%, Samil Pharm Co., Ltd., Korea) was used with the gonioscopy lens. SLT was performed with 107 shots treating 360° of the trabecular meshwork with 1.1 mJ, which falls within the typical power range of 0.4–1.4 mJ . Thirty minutes after the treatment, the IOP in the left eye was 17 mmHg. The patient was instructed to apply fluorometholone acetate 0.1% (Flarex, Novartis Pharm., Switzerland) drops four times per day for 3 days and to return in a week for follow-up.
+One week after the procedure, the IOP in the left eye was 7 mmHg and there were no other symptoms other than foreign body sensation in the eye. Significant anterior chamber shallowing and inflammation were also not observed. Considering that the IOP decreased sufficiently, oral acetazolamide was discontinued and the patient followed-up 2 weeks later. At that visit, the patient reported ocular pain in the left eye when touched. The best corrected visual acuity and IOP of the left eye were 3/20 and 4 mmHg, respectively. Slit lamp examination showed a deep anterior chamber without evidence of marked inflammation. Fundus examination and B-scan ultrasonography revealed hypotonic maculopathy and choroidal detachment in the left eye .
+All anti-glaucomatous drugs were discontinued and the patient was started on oral prednisolone acetate (Solondo tab, Yuhanmedica, Korea) 30 mg per day. One week later, the IOP in the left eye was 4 mmHg, and the choroidal detachment did not improve. The patient was therefore started on additional atropine 1% (Isopto atropine, Alcon, USA) twice daily and prednisolone acetate suspension (Pred Forte 1%, Allergan, USA) four times daily. The IOP in his left eye was 7 mmHg 3 days later and 23 mmHg 10 days later, and the choroidal detachment had improved . One week after discontinuation of oral prednisolone acetate, atropine eye drops, and prednisolone acetate suspension, the IOP in his left eye was stable at 8 mmHg. Three months after SLT, the IOP in that eye was well maintained at 10 mmHg, with the patient being treated with only one anti-glaucomatous drug, brimonidine.

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+A 57-year old man with uremia on hemodialysis complicated by severe renal anemia, hypertension and heart failure, presented with a two-week history of recurrent fever and cough with purulent sputum. Chest pain, nausea, vomiting, abdominal pain, diarrhea and night sweat was denied. He had been diagnosed with end-stage renal disease (ESRD) nearly 2 months ago, and the etiology was primary glomerulonephritis. Hemodialysis with the central venous catheter started at that time. Two weeks before admission, he suffered from recurrent epileptic seizures, characterized by convulsions of the whole body, unconsciousness and fecal incontinence in other hospital. Shortly afterwards, fever and cough with yellow phlegm gradually appeared. His labs were notable for white blood cell count (WBC) of 11.6 × 10 9 /L with 87% neutrophils, hemoglobin (Hb) 61 g/L, and C-reactive protein (CRP) 74.06 mg/L. Blood and sputum cultures were negative. Computed tomography (CT) scan of the chest revealed pneumonia. Intravenous vancomycin (0.5 g three times a week) and meropenem (0.5 g Q8H) was administered empirically for suspected aspiration (given his lethargy after epileptic seizure). Then the symptoms improved gradually and indicators of infection dropped to normal during 1 week. Unexpectedly, the patient had fever again on the day of admission, with a temperature of 38.8 °C, accompanied by deteriorating general status. Therefore, he was transferred to our hospital for further treatment.
+Physical examination was significant for appearance of severe anemia, a temperature of 38.8 °C, decreased breath sounds at the lung bases bilaterally, a diffuse moist rale on respiratory exam and a slight exudation around the right jugular hemodialysis catheter. Initial laboratory investigations revealed WBC of 7.0 × 10 9 /L with 74.2% neutrophils, Hb 55 g/L, CRP 25.29 mg/L, procalcitonin (PCT) 3.02 ng/ml, Scr 557.1umol/L and B-type natriuretic peptide (BNP) greater than 5000 pg/ml. Chest CT demonstrated multiple exudation of both lungs, bilateral pleural effusion and atelectasis of both lower lobes . No valvular vegetation was found in echocardiography, and left ventricular ejection fraction (LVEF) was 43%. Initial diagnosis of admission was ESRD with hemodialysis, sever renal anemia, community acquired pneumonia, heart failure and suspected catheter-related infection. Treatment with intravenous piperacillin / tazobactam (2.25 g Q12H) for pneumonia and correction of heart failure and anemia were commenced. The dialysis catheter and urinary catheter were removed and peripheral blood cultures were collected. But his fever with a maximum temperature of 40 °C still persisted. Three consecutive blood, sputum culture and catheter cultures were negative. Additionally, thoracentesis and drainage were performed and hydrothorax culture was also negative. Laboratory detection of tuberculosis and fungi was all negative. Antibiotics were switched successively to cefoperazone sodium / sulbactam sodium (1.5 g Q12H) + moxifloxacin (0.4 g/day) + fluconazole (0.2 g/day), and vancomycin (0.5 g three times a week) + meropenem (0.5 g Q8H), according to consultation results of respiratory department. However, no apparent improvement was noted, and his general condition deteriorated progressively. Response of temperature and indicators of infection to antibiotic therapy was shown in Fig. and Fig. . A repeated chest CT showed increased multiple exudation of both lungs . Finally, fourth blood culture became positive for E. faecium at>105 CFU/ml (vanA genotype) on hospital day 13. At that point, antibiotic therapy was switched to intravenous linezolid (600 mg Q12H) based on the sensitivity pattern of isolates that were vancomycin, moxifloxacin, gentamicin, penicillin, rythromycin and ampicillin resistant, and linezolid, teicoplaninand and tegafycline sensitive. In the following days, the fever subsided gradually . And the CRP and PCT levels decreased steadily . The patient completed a four-week course of linezolid with complete resolution of chest CT abnormalities .

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+The patient was a 79-year-old man with a history of methicillin-resistant Staphylococcus aureus infection (acquired during brain surgery), mitral regurgitation (MR), chronic atrial fibrillation for 9 years, and decreased left ventricular contractility.
+He had eight long-term hospitalizations during which he underwent multiple operations. Metal allergies to nickel (Ni) and cobalt (Co) were detected 8 years prior. The MR gradually worsened and became more severe. Dyspnoea on exertion appeared approximately 2 years prior and gradually worsened.
+One year prior, he was hospitalized for heart failure. Soon after discharge, he gained weight and experienced dyspnoea on exertion, accompanied by lower-leg oedema. Echocardiography showed severe MR, reduced ejection fraction (EF, 50%), and deterioration of pulmonary hypertension (pulmonary pressure: 37/16/25 mmHg).
+Because of recurrent heart failure, an elective surgery was planned after the previous hospital admission, following the successful management of heart failure. Preoperative echocardiography showed the following: left ventricular internal end-diastolic (LVEDD) and end-systolic diameters (LVESD) of 68 and 48 mm, respectively—EF of 45%, severe MR with central jet (tenting height, 12 mm) ( and ), moderate tricuspid regurgitation (TR) (tenting height, 8 mm) , a left atrial diameter of 66 mm, and progressive MR with increased diuretics. Using coronary angiogram and technetium-99m, cardiologists ruled out ischaemia and amyloidosis as the cause of LV dysfunction. Although the LV size was large, the LVEF was over 40% and the wall thickness was approximately 13 mm. Therefore, it was not a typical dilated cardiomyopathy (DCM); yet DCM could not be excluded as the cause of LV dysfunction.
+Prosthetic valves, rings, and TEER containing Ni and Co were contraindicated. Additionally, the sternal closure required a Ni- and Co-free sternal wire. We selected Ni- and Co-free rings for mitral and tricuspid annuloplasty. We used titanium wire for sternal closure as stainless steel can contain traces of nickel. Cardiopulmonary bypass was established through median sternotomy using standard aortic and bicaval cannulation. Antegrade blood cardioplegia was administered, and the left atrium was accessed via a transseptal approach.
+No chord rupture was observed. Left atrial ablation was performed using a modified maze procedure with cryoablation. The left atrial appendage was then resected. A 28-mm Ni- and Co-free Séguin Ring (Séguin Semi-Rigid Annuloplasty Ring; Abbot Medical, Austin, TX, USA) was chosen for mitral valve repair. After the annular mattress sutures were tied, they were passed around the annuloplasty ring again, taking additional bites of atrial tissue and tied again (the double-suture technique). The tricuspid valve was examined after the closure of the interatrial septum. The diameter of the annulus was 55 mm. In addition to annulus enlargement, tethering was also contributing to regurgitation.
+Subsequently, a pledgeted CV4 suture (GORE-TEX® Suture; W. L. Gore & Associates Inc., Newark, DE, USA) was placed at the base of the anterior papillary muscle (PM) and continuously sutured clockwise to the base of the secondary and then inferior PM. The CV4 suture crossed the interventricular septum and externalized the septal ring of the right atrium. After tricuspid annuloplasty using a 27-mm Ni- and Co-free ring (Duran Flexible Partial Ring; Medtronic Inc., Minneapolis, MN, USA) the CV4 suture was passed through the ring. Suture length adjustments were performed under a water test, and the sutures were tied (spiral suspension technique).
+Next, a pledgeted CV4 suture was passed through the head of the anterior and posterior PM via an aortotomy. It was passed from the left ventricular cavity through the mid-septal fibrous annulus and exteriorized through the aortic wall beneath the commissure between the non-coronary and left coronary aortic cusps (PM repositioning) ( and ). Aortotomy was closed with two layers of continuous sutures, and the sternum was closed with a pure titanium wire (Yokozuna wire; USCI Holdings, Tokyo, Japan). Transoesophageal echocardiography confirmed that the MR and TR had disappeared. Postoperative transthoracic echography revealed a trivial MR (tenting height, 8 mm) and disappearance of TR.
+After undergoing treatment for heart failure in the cardiology department, the patient was discharged from the hospital on the 26th postoperative day without dialysis intervention. Two years after surgery, MR and TR had not worsened on echocardiography .

data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1419_en.txt

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+A 62-year-old male presented to an outpatient ophthalmologist with a 5-day history of progressive binocular diplopia and was referred to our institution. On presentation, neurologic and ophthalmologic examination showed a right pupil-involving partial third nerve palsy with no other abnormal findings. Routine brain magnetic resonance imaging (MRI) and time-of-flight MR angiography (MRA) demonstrated an AVM located in the right frontal operculum extending to the anterior insula with venous drainage into the right basal vein of Rosenthal. There was no subarachnoid or intraparenchymal hemorrhage to suggest AVM rupture. A diagnostic cerebral angiogram was performed next and demonstrated a 1.9 cm × 2.2 cm AVM fed by the right middle and accessory meningeal and sphenopalatine arteries and opercular branches of the middle cerebral artery (MCA). The venous drainage followed a deep pattern into a dilated and tortuous right basal vein of Rosenthal to the vein of Galen and ultimately into the straight sinus . The patient underwent staged embolizations of the feeding pedicles using Onyx-18 embolic material (Medtronic, Minneapolis, USA) to facilitate planned surgical resection. In the first stage, superselective catheterization of the right middle meningeal, accessory meningeal, and sphenopalatine arteries was performed using a Marathon microcatheter (Medtronic, Minneapolis, USA) and a Synchro 10 microwire (Stryker, Kalamazoo, USA) . In the second stage, the next day, the feeding branches of the opercular segment of the MCA were accessed with a Scepter balloon-guided microcatheter (MicroVention Inc., Tustin, USA) and a Synchro 2 microwire . On the following day, the patient underwent a right pterional craniotomy for resection of the AVM. An intraoperative control angiogram confirmed complete obliteration of the AVM [ and ]. The pathologic tissue examination was consistent with AVM.
+At the 4-week follow-up, the patient reported complete resolution of the diplopia. Neurologic examination demonstrated no deficits and isocoric pupils with intact extraocular movements bilaterally. There was no recurrence of the diplopia 6 months after surgery.

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+She was 3 years old at the time of her first visit and presented on 16 September 2020 due to language delay. She is 5 years old now.
+Since age 6 mo, she had had obvious slow growth in height and weight. Language development was delayed. Her response to name calling was normal but there was no communication with people. Her eyes could not be met and there was no social smile. There was no autonomous language, However, the child had rich gesture language and body language, she could understand instructions, had a short temper, and when she wants to achieve something, she starts crying or shouting. She was thin, with a weight of 9 kg and height of 83 cm.
+There was no obvious abnormality at birth, weight 3 kg, height 50 cm. She raised her head at 3 mo, crawled at 7 mo, and walked at 15 mo. She had a history of febrile convulsions twice, each lasting about 2 min, which resolved spontaneously, and a 1-year history of ulcerative colitis.
+Both parents were healthy.
+Body temperature was 36.2 °C, heart rate 96 beats/min, breathing 24 beats/min, blood pressure 100/60 mmHg, height 83.0 cm and weight 9 kg. There was no special sick face, and cardiopulmonary and abdominal examinations showed no obvious abnormalities. Bilateral muscle strength and muscle tone were symmetrical and slightly decreased. Physiological reflexes were present but pathological reflexes were not elicited.
+Routine blood and urine examinations, myocardial enzymes, lactic acid, liver function, renal function, electrolytes, blood glucose, thyroid function, and hematuria showed no obvious abnormalities. The peak growth hormone challenge test was 5.77 ng/mL.
+Video electroencephalography showed no abnormalities. Magnetic resonance imaging (MRI) of the brain showed mild atrophy.

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+A 31-year-old black Congolese female patient, P3G3, who had a pregnancy of 38 weeks and four days, was transferred from a district hospital to a tertiary facility in Kinshasa, Democratic Republic of Congo, for severe preeclampsia with acute on chronic fetal distress. Her past medical history was notable for eclampsia during her first pregnancy in 2011 and preeclampsia in 2013 during her second pregnancy. She had had two cesarean sections for her pregnancies, and she had her antenatal care for her third pregnancy at a referral hospital. She was diagnosed with preeclampsia during her third pregnancy for which she received 250 mg alpha-methyl-dopa twice a day. ​​During the 30th week of gestation, the patient’s systolic blood pressure became labile, oscillating between 140 and 150 mmHg, despite her antihypertension medication. The patient consulted at a district hospital where she underwent a fetal wellbeing ultrasound which did not find anomalies.
+The patient was the 7th of 9 children, and her father was hypertensive. She weighed 72 kg for 155 cm, and upon arrival at the authors’ hospital, her blood pressure was 217/152 mmHg. Her heart rate was 101 bpm, her respiratory rate was 24 cpm, and SpO2 was 96% free air. The patient was in pain, she was lucid and coherent, her palpebral conjunctivae were colored, and she had bilateral pitting edema. The fundus height was at 30 cm, the presentation was cephalic, the fetus was bradycardic at 88 bpm, and there were no signs of genital bleeding. The cervix was median, soft, 80% effaced with a 2 cm dilation. Urine deep stick revealed 3+ proteinuria. She had 1.5 mg/dL of creatinine (normal: 0.5–1.5 mg/dL), 22 mg/dL of urea (normal: 10–50 mg/dL), 15,000 white blood cells/ml, 213,000 platelets/ml and 14 g/dL hemoglobin. Based on these findings, we indicated an emergency cesarean section for acute fetal distress, which resulted in the extraction of a dead infant.
+Postoperative suites were marked on day two by decompensated anemia (hemoglobin at 7.8 mg/dL) for which the patient was transfused two units of packed red blood cells. On postoperative day three, the patient presented an abdominal effusion, exacerbation of the bilateral pitting edema, blood pressure increase, hematemesis, melena, petechiae, hematuria, and oliguria. Her blood pressure was 215/120 mmHg and she had signs of renal failure (creatinine = 6.9 mg/dL (normal: 0.84–1.21 mg/dL); urea 132.5 mg/dL (normal: 5–20 mg/dL); hyperkalemia at 6.4 mmol/L (normal: 3.5–5 mmol/L); hyponatremia 109 mmol/L (normal: 136–145 mmol/L); hypocalcemia 0.88 mmol/L (normal: 1.12–1.32 mmol/L)), and signs of hepatic failure (AST 135 IU/L, normal: < 33 IU/L; ALT 325 IU/L, normal: < 33 IU/L; prothrombin ratio 100% (normal: 80–110%). PTT was 39 s (normal: 24–35 s), LDH was 1398 IU/L (normal: 120–280 IU/L), and total bilirubin was 0.35 mg/dL (normal: 0-1 mg/dL)). She equally had neutrophilic leukocytosis at 22,180 cells/mm3 and low platelets at 44,000 cells/mm3. Additionally, schistocytes were identified in the peripheral thin smear.
+The team excluded TTP and HELLP syndrome as possible causes of the postpartum microangiopathic hemolytic anemia (MAHA). This decision was based on the history, clinical presentation, and laboratory findings. Atypical hemolytic uremic syndrome was retained as the final diagnosis, and in the absence of anti-complement therapy, the patient underwent four sessions of hemodialysis. Hypertension was treated with Nicardipine, 5 mg/hr. IV with a 2.5 mg/hr. increase every 15 min without exceeding 15 mg/hr., and the goal was to lower the systolic blood pressure below 160 mmHg. Hyperkalemia was corrected with insulin and glucose (10 units of insulin dose with 25 g of glucose per each 1 mmol/L of potassium above the normal). A favorable clinical and biologic evolution was observed, and the patient was released for outpatient follow-up on postoperative day 18 .
+Laboratory tests could not be obtained more frequently due to their financial burden to the patient and her immediate family. The patient had a normal kidney function at postoperative day 160 (urea 24.2 g/dL, creatinine 0.8 mg/dL) and postoperative day 202 (urea 16.9 g/dL, creatinine 0.8 mg/dL). She did not present new episodes of microangiopathic hemolytic anemia.

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+A 31-year-old Egyptian male with American Society of Anesthesiologists (ASA) I physical status, with history of polytrauma since 1 week, had a left arm and right leg fracture. A complete trauma survey was done at the time of admission, with no other injury and acceptable laboratory and radiological investigations.The operation was done first to the fracture on left hand under general anesthesia with no complications. Then after 1 week, the patient was scheduled for an operation on the right leg. While sitting in the L3–L4 interspace, a 22-gauge needle with a Quincke tip was used to deliver spinal anesthesia to the patient. About 120 seconds after receiving an injection of 20 mg (4 ml) of hyperbaric bupivacaine 0.5%, the patient had significant back and gluteal discomfort, followed by myoclonic movements in the lower limbs and a generalized convulsion.
+The arterial blood pressure of the patient was elevated to 170/100 mmHg, and his heart rate increased to 120 beats per minute. Immediate intravenous sedation with midazolam (5 mg) and fentanyl (50 μg) was delivered with no response in seizure termination. Phenytoin (1000 mg) was given by intravenous infusion and we subsequently applied the airway, breathing, and circulation (ABC) protocol. General anesthesia was induced by a thiopental sodium (250 mg) and atracurium (50 mg) infusion, the trachea of the patient was intubated, and respiratory parameters on mechanical ventilation were as follows: tidal volume (TV) 500 m/minute, respiratory rate (RR) 16 cycles/minute, fraction of inspired oxygen (FIO2) 100%, positive end-expiratory pressure (PEEP) 0 mmHg.
+Maintenance of anesthesia was attained by isoflurane 1.2 minimum alveolar concentration (MAC) and atracurium 10 mg every 20 minutes, and subsequent doses of thiopental sodium (100 mg) to control seizures. Although with the above interventions, the patient developed focal seizures in the hand and leg. The attending anesthesiologist had suspicions regarding intrathecal administration of the incorrect medicine after discovering a used TXA ampoule (500 mg/5 ml) in the trash. So, cerebrospinal fluid (CSF) lavage was done by inserting two spinal 22-gauge Quincke tip needles on level L2–L3 (drainage) and the other on L4–L5. Intrathecal normal saline infusion (150 ml) was done in 1 hour by passive flow. During CSF lavage, vital signs were as follows: blood pressure (BP) 140/85 mmHg, pulse 140 beats/minute, and the patient was on mechanical ventilation (MV) with FIO2 100 and oxygen saturation (SO2) 98%. Arterial blood gases (ABG) were pH 7.42, PaCO2 37, PaO2 157, and HCO3 24 after CSF lavage. The patient was stabilized, and he was transferred to the intensive care unit (ICU).
+About 2.5 hours after the injection, the patient was transferred to the ICU and with volume-controlled ventilation mode, the MV was continued. The patient was put on MV, and thiopental sodium infusion was continued, with 100 mg/hour increased to 300 mg/hour, but the patient developed multiple generalized myoclonic seizures so atracurium was started by loading 50 mg then 5–10 μg/kg/hour as apart of complete general anesthesia. However, the seizures were not controlled so we put the patient on an anesthesia machine and continued MV with isoflurane 1.2 MAC, with thiopental sodium 300 mg/hour and 10 μg/kg/hour atracurium.
+A central venous catheter was inserted on the right subclavian vein. The initial postoperative ABG examination showed pH of 7.44, PaO2 of 170, PaCO2 of 47, and HCO3− of 27. The MV parameter was adjusted to produce hyperventilation to target PaCo2 of 35–40 mmHg with continuous monitoring with capnogram. A complete blood test indicated no evidence of hepatic, renal, or hematological malfunction. Six hours postoperatively, the patient suffered tonico–clonic seizures of the upper limbs and face, which were managed by a continuous infusion of sodium thiopental (3–5 mg/kg/hour), atracurium 10 μg/kg/hour, isoflurane 1.2 MAC, and 150 mg phenytoin every 8 hours.
+Cranial computed tomography revealed no abnormality and fundus examination revealed papilledema, so protective brain strategies continued with mannitol 20% 150 ml every 8 hours for 2 days and isoflurane 1.2 MAC and mild fluid restriction and lasix 20 mg every 12 hours. To avoid ventricular arrhythmia, amiodarone was administered prophylactically at a dose of 10 mg/kg/24 hours for 24 hours. The patient developed sinus tachycardia and his heart rate increased to 150 beats/minute, which was controlled by an amiodarone infusion. After 3 hours from admission to ICU, the patient’s blood pressure decreased, with mean arterial blood pressure below 50 mmHg, and investigations showed normal electrocardiogram (ECG) sinus rhythm. Central venous pressure (CVP) was 10 cm H2O, so norepinephrine infusion was started at 0.05 μg/kg/minute to maintain tissue and cerebral perfusion. The mean arterial blood pressure then improved with norepinephrine and maintained above 75 mmHg.
+On the second day postoperatively, the sedation began to decrease: first isoflurane to reach 0.6 MAC, then isoflurane was stopped, and thiopental sodium was decreased to 200 mg/hour. The patient developed one-time seizures on the face and upper extremities, so sedation was continued for another 24 hours with decreasing thiopental sodium to 200 mg/hour only. Also, the patient became feverish (39 °C) in the second day so, 1 gm intravenous acetaminophen was given every 6 hours.
+Norepinephrine was stopped after 24 hours as mean arterial blood pressure was maintained over 75 mmHg without support.
+On the third day after surgery, sedation was discontinued. As the patient’s degree of consciousness improved, he moved his head and upper extremities in response to painful stimuli and absence of deep tendon reflexes in the lower limbs. On the fourth day postoperatively, he opened his eyes in response to voice instructions, followed simple directions, and breathed on his own. The trachea was extubated, and all neurologic examinations were acceptable. The patient was discharged from the ICU on the sixth day and transferred to the ward after 48 hours from weaning from MV. The patient was discharged home with recommendation to follow-up with neurology and to be fully evaluated after 6 months. The patient was monitored at 6-month and 1-year intervals and found to be in excellent condition with no neurological symptoms.

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+The patient is a 33-year-old female patient with personal history of NF1 (without any family history in the two previous generations) characterized by multiple Café au lait macules and multiple neurofibroma nodules in distinct regions of the skin which involve the scalp, neck, back, abdomen, and all the extremities.
+The patient has a normal evolution of her disease with no incidents; she is an independent professional and refers no other symptomatology. Eventually, she complains of pain due to the mechanical compression of one of the neurofibromas. After considering the genetic counseling, the patient decides to get pregnant. During the second trimester of her pregnancy, she started to note gradual and progressive growth of one of the neurofibromas located in the anterolateral left portion of the neck, in the angle formed by the thyroid gland and the common carotid artery. Such growth gradually increased to the point where by the end of the pregnancy it had a diameter of approximately 10 cm × 15 cm, it made swallowing difficult, dysphonia, and generated local pain (nonneuropathic pain) . The consistency was smooth in the peripheral contours, but firm in the center, mobile, and no skin changes were noted. She has an uneventful full term pregnancy with a C-section delivery.
+After neuroimaging evaluation, a surgical approach is decided 3 months after the C-section using general anesthesia and microsurgical dissection. A tumor mass was identified, with a superficial wall, free from vascular or cervical major nerve structures, with a clear serous liquid content that after decompression, modifies the tumoral morphology immediately, allowing identification of the layers of the cystic lesion. The visceral portion of the capsule was found attached to the external plane of the thyroid gland and to the carotid artery adventitia, which was preserved. The postsurgical evolution was normal, without any complications. There were no alterations regarding phonation or deglutition, and there was a normal recovery of the external anatomy of the neck without any evidence of tumoral mass. The analysis of the fluid reported no cytological alterations and culture was negative for infection. The hematoxylin and eosin stain shows the presence of neoplastic cells, nuclear and diffuse cytoplasmic positivity to S-100 protein .

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+A 30-year-old Japanese man was referred to our clinic complaining of pain, tenderness, and swelling on the left side of his palate for the past several months. Our initial clinical examination found that his left palatine mucosa was significantly swollen compared with his right side. The swelling was diffuse, and its borders were unclear . The swelling was especially pronounced in the left molar region of his palate, and his pain was exacerbated with the application of direct pressure to the lesion. The swelling exhibited increased signal intensity on T2-weighted magnetic resonance images (MRI, Fig. ). All of his left maxillary teeth were healthy, and no specific abnormalities in his left maxilla and maxillary sinus were observed on panoramic X-ray and computed tomography (CT) images. His medical and familial histories were unremarkable, and he was not aware of any history of trauma or inflammation of his head or neck. We administered antibiotics orally (cefcapene pivoxil hydrochloride hydrate 100 mg tablet every 8 hours) and non-steroidal anti-inflammatory drugs (loxoprofen sodium hydrate 60 mg tablet every 8 hours) for 7 days because we suspected that his symptoms were due to inflammation secondary to an infection. However, his symptoms did not improve.
+Based on his clinical and radiographic examinations, our initial diagnosis was a soft tissue tumor. An incisional biopsy was performed and histopathologic examination of the lesion revealed haphazard nodes and inflammatory cells in a fibrous stroma . Immunohistochemical analysis revealed significant staining for the neural marker S-100 in the bundles within the node . Factor VIII staining was positive in the fibrous stroma, but not in the bundles . These findings led to the diagnosis of a traumatic neuroma. The patient underwent resection of the tumor with a 5-mm margin using an electric scalpel under general anesthesia. Although the border of the mass was unclear and diffuse, the extent of the tumor could be determined based on the MRI images. As the tumor was conglutinated with a part of his palatine bone, we saucerized the bone surface including the overlying mucosa and the periosteum. His left greater palatine nerve was resected as the possible origin of the tumor. The open surgical wound was covered with a collagen-based artificial dermis (Terudermis, Olympus Terumo Biomaterials Corp, Tokyo, Japan) and a surgical splint. The size of the specimen was approximately 6×3 cm . The pathologic findings of the surgical specimen were the same as those of the incisional biopsy specimen, and the patient’s greater palatine nerve exhibited no pathologic changes. The tumor was not entirely encapsulated and some tumor cells were observed within the surgical margins. We decided to continue strict clinical follow-up without additional surgery because the traumatic neuroma is not a true neoplasm, and his pain subsided immediately after the surgery. No clinical evidence of a recurrence has been observed in the 3 years since the surgery.

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+The patient was 76-year-old male, right-handed, living by himself, and fully able to walk independently. His chief complaint was right shoulder pain, limited range of motion (ROM) in the right shoulder. He fell on his right shoulder while walking and injured it. He visited another hospital 3 days after the injury where he was diagnosed with dislocation of the right shoulder and received manual reduction followed by immobilization with a sling. Due to persistent pain and limited ROM of the right shoulder, plain magnetic resonance imaging (MRI)was performed and revealed a massive rotator cuff tear. He was then referred to our hospital 2 months after the injury. Physical findings on initial examination were markedly limited ROM and decreased abductor/external rotator muscle strength were observed, with an active flexion angle of 10°, active abduction angle of 10°, active external rotation angle of 0°, and manual muscle test (MMT) for abductor and lateral rotator (at a hanging position) muscle strength of 2 . Visually discernible atrophy of the deltoid, supraspinatus and infraspinatus muscles and hypoesthesia (5/10) in the axillary nerve region were also observed. At this point, the patient was given an American shoulder and elbow surgeons (ASES) scoring system of 10/100, University of California at Los Angeles (UCLA) shoulder scaling system of 4/35, and Japanese Orthopaedic Association (JOA) scoring system of 37/100. The plain X-ray findings were irregular glenohumeral joint surface and subacromial osteophytes, diagnosed as Grade 3 on the Hamada classification , were observed. The plain MRI findings were massive tear of the supraspinatus and infraspinatus muscles, which were withdrawn back to the glenoid fossa, diagnosed as Stage4 atrophy of supraspinatus muscle and Stage3 atrophy of infraspinatus muscle on the Goutallier classification was observed. The subscapular muscle was completely torn with bone fragment formation and diagnosed as Grade 3 on the ide classification . Electromyography was performed at the neurology department of our hospital to evaluate the degree of axillary nerve palsy. A motor nerve conduction study of the axillary nerve showed a marked decrease in compound muscle action potential in the deltoid muscle. An electromyogram showed a denervation potential suggestive of neurogenic changes in muscles innervated by the axillary nerve, leading to a diagnosis of axillary nerve palsy, leading to a diagnosis of neuropraxia in axillary nerve. However, muscle contraction was maintained in the axillary nerve region, suggesting the possibility of restoration. Therefore, a treatment plan was developed to conduct an outpatient rehabilitation program to improve the ROM and enhance the muscle strength of the shoulder until the palsy is improved, and then perform the surgical treatment. Hypoesthesia improved to 7—/10 with a reduced affected area. Furthermore, noted was an improved ROM, with active flexion, abduction, and external rotation angles of 20°, 20°, and 40°, respectively, and gradual improvement in muscle strength, with an abductor and external rotator (at a hanging position) muscle strength of 2 and 3 by MMT, respectively ( and ). Given these findings, ASCR was performed 6 months after injury.
+The operation was started with the patient placed in a beach chair position under general anesthesia. Two portals were made in the posterior and lateral aspects of the shoulder, and the posterior portal was used to perform intra-articular locking. Arthroscopy revealed no injury in the tendon of the long head of the biceps brachii muscle, but its origin was detached along with the labrum. The rotator cuff was extensively torn, involving the tendons of the subscapular, supraspinatus, and infraspinatus muscles, with the stumps withdrawn back to the glenoid fossa. Osteoarthritic changes were observed in the joint surface but were mild in severity. Mild injury of the glenoid labrum was observed, but it was not associated with joint dislocation under anesthesia. The subscapular muscle tear was repaired as it was considered reparable. In contrast, the supra/infraspinatus muscle tear was considered irreparable; therefore, the contralateral fascia lata was collected, folded in half and used as a graft for ASCR. Although it was initially planned to repair the humeral head side of the graft using a bridging suture, it was difficult to place four anchors due to poor bone quality. Therefore, the graft was fixed using single-row interrupted sutures. Finally, to complete the operation, the graft was attached to the residual teres minor muscle by interrupted sutures . After surgery, the patient wore a shoulder abduction pillow for 3 weeks, followed by immobilization with a sling for 2 weeks. On the day after the operation, the patient started shoulder girdle relaxation, passive ROM, and periscapular muscle training. An ultrasonography performed 4 weeks after operation showed coverage of the torn portion by the graft. External fixation was removed 5 weeks after the operation, and active ROM training was started. Hypoesthesia in the axillary nerve region was almost completely resolvedat 3 months after operation, with no bilateral difference. Pain and deltoid muscle atrophy were resolved by 4.5 months after operation. During the first 2 years after operation, improvements were observed in both the ROM and muscle strength of the shoulder, with an ASES shoulder score of 96, UCLA shoulder rating scale of 34, and JOA score of 95. An MRI performed 2 years after operation also showed adequate coverage of the torn portion by the graft ( and ).

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+A 70-year-old man was diagnosed with lung adenocarcinoma (clinical T4N0M0) involving a right upper lobe mass of 4.0 cm in diameter and a metastatic nodule in the middle lobe. He underwent right upper and middle bilobectomy and systematic lymph node dissection through a posterolateral thoracotomy. On the second postoperative day, 1750 mL of white turbid fluid was drained through the chest tube and the effusion was diagnosed as chylothorax. During the first 24 h following implementation of a fat-free dietary regimen, the color of the discharge became transparent, but another 630 mL of discharge was observed. Although the amount of discharge reduced gradually, it was persistent. Chemical pleurodesis was performed on the sixth postoperative day for which 5 KE of OK-432 (Picibanil; Chugai Pharmaceutical, Tokyo, Japan) and 300 mg of minocycline were administered into the thoracic cavity. The discharge began to progressively diminish. Three days thereafter, the amount of discharge had decreased to 150 mL/day, and on the ninth postoperative day, the chest tube was removed. On the 14th postoperative day, the patient complained of dyspnea and dysphagia, and an upper mediastinal mass was detected on chest radiogram . Chest computed tomography revealed a large mediastinal fluid collection 6 cm in diameter surrounded by a thick capsule that was compressing the trachea and esophagus . The mass was suspected to be a mediastinal chyloma. Since the patient’s symptoms were gradually progressing, we performed surgery on the 15th postoperative day. Thirty minutes before the surgery, ice cream was given to the patient to help confirm the leakage point in the thoracic duct. Thoracoscopy revealed a small amount of chylous effusion in the thoracic cavity and an elastic mass in the upper mediastinum. When the thick capsule was incised, chyle began to spill out . Once the chyle had drained completely, we confirmed the point of leakage and repaired it using a Z-suture with 4–0 Prolene (Ethicon, Somerville, NJ) . The postoperative course was uneventful and the patient was free of any symptoms. He remained asymptomatic 12 months after discharge from the hospital.

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+A 68-year-old Peruvian man had been suffering from lumbar pain for several days. His CT scan revealed a mass compressing his right ureter and iliac vessels. He underwent exploratory laparotomy with radical resection of a retroperitoneal tumor (10 cm × 8.3 cm × 8 cm), as well as ileocecectomy and ileocecal anastomosis. Pathological analysis showed that the tumor was a DDL (T2 N0 M0, FNCLCC grade 2, stage IIIA, <50% necrosis, R0). This diagnosis was corroborated by immunohistochemistry markers (ie, the positivity of D33 and NSE and negativity of h-CD and S100). One month after the surgery (for details of the disease course, see ), his initial postoperative scan showed the absence of disease. However, 2 months later (3 months after the surgery), his new CT scan revealed a 1.6 cm × 2.3 cm mass anterior to the right iliac vessels (first recurrence). He received neoadjuvant chemotherapy with doxorubicin plus ifosfamide (6 cycles). Then he underwent resection of the retroperitoneal tumor (R0) and right ureterectomy. The patient further received 3 cycles of doxorubicin plus ifosfamide postoperatively. Eight months after chemotherapy (11 months after the second surgery), a control imaging revealed 2 anterior psoas masses measuring 1.5 cm × 1.5 cm and 1.3 cm × 1 cm (second recurrence). The biopsy of one of the lesions revealed a malignant spindle cell neoplasm compatible with DDL. Two months later, the CT scan showed that the masses had enlarged to 3.0 cm × 1.9 cm and 2.1 cm × 1.6 cm. However, CT scans and a chest x-ray revealed no evidence of metastatic disease. The patient underwent a third surgery wherein the 2 masses and a right pelvic mass were resected entirely (R0). At this point, the patient sought for different treatment options involving an integrative approach. Three months later, he came to the Centro Médico Antroposófico (CMA) and became our patient.
+The recommended treatment was subcutaneous injections of VAE obtained from the host tree ash (AbnobaVISCUM® Fraxini); the injections were given thrice per week in increasing doses. The application of VAE Fraxini in the periumbilical area started at 0.2 mg; after 6 months, the dose was increased to 2 mg, which was then maintained for 7 months. The subcutaneous VAE injections occasionally induced self-limited local erythema and swelling of the skin around the application site, which could be tolerated by the patient. Nine months after the VAE treatment was initiated (12 months after the third surgery), a retroperitoneal mass measuring 4.1 cm × 3.0 cm was noticed (third recurrence). After 5 more months, the dose of VAE was increased to 20 mg thrice per week. Three months later, the patient underwent resection (fourth surgery) of a right iliac fossa tumor (a mass measuring 4.7 cm × 3.5 cm with a moderate amount of surrounding fibroadipose tissue) and a right juxtarenal psoas tumor (a well-encapsulated, focal fibro-fatty soft tissue measuring 8.7 cm × 6.5 cm with central areas of probable necrosis). Both tumors were DDLs (FNCLCC grade 3, pT2b). The patient had a negative margin resection (R0) for the larger sarcoma, and the other exhibited focal involvement by the tumor. A cholecystectomy (mild chronic cholecystitis and cholelithiasis) and appendectomy were also performed, and both organs were negative for tumor. Additionally, he received 12 cycles of three-dimensional conformal radiotherapy post-surgery.
+As a result of the previous surgeries, which involved a partial right ureter resection with psoas bladder hitch, the patient developed obstructive renal failure as evidenced by the right ureteral obstruction and abnormal serum creatinine levels. The patient then underwent a right percutaneous nephrostomy with stent placement.
+Throughout this time, the patient continued to receive VAE Fraxini. Follow-up magnetic resonance imaging was performed periodically post-surgery. Three-month breaks without VAE Fraxini application were set twice per year after obtaining the first negative follow-up magnetic resonance imaging result. The frequency of subcutaneous VAE Fraxini application was reduced to twice per week from month 54 on. The patient reached a recurrence-free interval of 69 months; however, the magnetic resonance imaging performed on month 86 of VAE Fraxini treatment showed a mass in the right iliac fossa. The tumor measuring 8.1 cm × 4.8 cm (FNCLCC grade 3, pT2b) was resected. The tumor showed areas of well-differentiated liposarcoma, which were mixed with areas of intermediate to highly dedifferentiated myxoid fibrosarcoma and high-grade undifferentiated pleomorphic sarcoma. The tumor was relatively well-circumscribed and mostly surrounded by fibroconnective and fibroadipose tissues of variable thickness. However, the resection margins were involved by the sarcoma. One month after the surgery, the VAE treatment was resumed. The patient started receiving intravenous infusion of 100 mg VAE obtained from pine as host tree (Helixor® P); the injections were administered in 500 mL of standard saline solution over 2 hours thrice a week. The dose was increased by 100 mg per application until 400 mg was reached which was maintained until 12 applications were completed. Then, the patient was subjected again to subcutaneous injection with 20 mg VAE Fraxini thrice per week. Five months after the surgery, multiple abdominal and retroperitoneal nodular tumor implants were detected, and their number and size increased within the following 9 months. For 2 weeks, the patient received intravenous infusion of VAE (Helixor® P, maximum dose: 400 mg) followed by subcutaneous infusion of 20 mg VAE Fraxini. One of the implants caused urinary tract obstruction, and the patient developed renal and abdominal pain, which was treated with buprenorphine 20 mg/25 cm2 transdermal patches and with anthroposophic remedies (Wala® Solum Inject, Wala® Plexus coeliacus D15, Wala® Bryonia/Stannum, Weleda® Formica comp injections, thrice per week). Weleda® Equisetum sulfuratum tostum D3 was applied (thrice a day) to support the urinary function. When the pain was relieved and controlled, intravenous infusions of VAE were resumed. He also received 1 cycle of eribulin (1.65 mg IV infusion). In month 103 of the VAE treatment, the patient underwent pleurodesis due to pleural effusion; however, he died 2 weeks later. Altogether, the patient received a total of 103 months (8.6 years) of VAE treatment and achieved 10.5 years of survival.
+Within approximately 2 years during which the first 3 surgeries were performed, the patient’s weight decreased from 84 kg to 71 kg. Since the VAE treatment started, the patient’s quality of life progressively improved as seen in his increased appetite, resulting in weight gain (up to 77 kg) during the low-dose VAE treatment. After the fourth surgery, his weight was 70 kg to 74 kg. After the fifth surgery, his weight decreased to 66 kg and then increased again to 70 kg . The ideal body weight based on his height (172 cm), gender, and age is 54.7 kg to 74.0 kg.
+The patient was married and had 3 grown-up children. He had a history of tobacco use, but he quit after being diagnosed with DDL. He consumed alcoholic beverages occasionally. His medical history included diphtheria and hemorrhoidectomy. His father died of leukemia, and his paternal uncle had an unknown cancer of the lower extremity. Further medications included allopurinol tablets for high blood uric acid level and a combination preparation of hydrocodone 10 mg and bitartrate and acetaminophen 500 mg tablets for left lumbar region pain. The patient stopped taking these medications on month 18 of VAE treatment.

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+A 62-year-old man with no history of eye surgery underwent 25G+ pars plana vitrectomy for proliferative diabetic retinopathy. After retrobulbar anesthesia, a vision system was used to view the surgical field, and an inferotemporal sclerotomy was created using a 25G+ trocar. The trocar obliquely punctured the bulbar conjunctiva and sclera at an angle of 45° (sclerotomy), approximately 4 mm from the limbus and parallel to it. The trocar was twisted into the eyeball, and its orientation was gradually changed perpendicular to the limbus. After confirming that the cannula was inside the eye, we pulled out the trocar and inserted an infusion cannula into the port. Two more sclerotomies were created in the superotemporal and superonasal quadrants. However, when we pulled out the superonasal trocar, the collar of the cannula fell off and the cannula tube was missing . Therefore, a bulbar conjunctival incision was placed to search for the missing cannula. No cannula was found in the subconjunctival space. We used a scleral depressor to look for the missing cannula tube along the peripheral retina and found the broken cannula tip in the ciliary body corresponding to the superonasal sclerotomy site. We created a new sclerotomy 2 mm above the original incision and 4 mm from the limbus and subsequently performed vitrectomy around the broken cannula to mobilize it for extraction. The new scleral incision was extended to 3 mm parallel to the limbus and allowed entry of a foreign body forceps . The broken tip of the cannula was brought into view by indenting the sclera adjacent to the original sclerotomy. We used the foreign body forceps to clamp and pull the fractured cannula toward the central vitreous body . With the help of the light probe, the longitudinal length of the cannula was aligned with the foreign body forceps and retrieved through the enlarged incision . No leakage occurred from the original sutureless scleral incision. The extended scleral incision was sutured with 7-0 polyglactin 910 suture.

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+A 64-year-old woman with increased lethargy, generalized weakness, and shortness of breath on exertion was found to have pancytopenia on a routine blood count; hemoglobin 80 g/L, white blood cells 3.2 × 109/L, platelets 98 × 109/L. After bone marrow examination a diagnosis of refractory anemia with excess blasts (RAEB) was made. The symptoms were attributed to anemia and she received 5 units of packed red cells.
+Approximately 2 months later, she developed a 4-day course of intermittent chills and sweating but was afebrile when she came to the local emergency department. The CBC at admission demonstrated 6.9 × 109/L white blood cells with left shift and 0.21 × 109/L blasts, 76 g/L hemoglobin and 65 × 109/L platelets. During her hospital stay the white blood cells increased to 16.9 × 109/L with increasing left shift; anemia and thrombocytopenia persisted. There was central bronchial wall thickening and interstitial prominence in the chest radiograph suggestive of an early viral infectious process. The cardiomediastinal silhouette was within normal limits . The electrocardiogram (ECG) showed normal sinus rhythm. The patient was started on oral levofloxacin.
+Four days later, the patient became febrile (38.8 degrees) and developed increasing shortness of breath and retrosternal chest pain that radiated to both arms. There were bilateral crepitations and decreased breath sounds. Repeat chest radiograph demonstrated bilateral pleural effusions, basal consolidation of the left lower lobe and left ventricular enlargement. There was no evidence of cardiac failure . Right bundle branch block (RBBB) with sinus tachycardia was identified on ECG. An echocardiographic study identified a moderate pericardial effusion with no cardiac tamponade; the left ventricular ejection fraction was 66% and there were no regional wall motion abnormalities. The next day, a repeat echocardiographic study identified a 33% ejection fraction with left ventricular global hypokinesia and a moderate sized pericardial effusion without tamponade. The patient was treated for pneumonia, hypotension, acute renal failure, and anemia but developed heart block and cardiorespiratory compromise. Her condition deteriorated rapidly and she died five days post-admission.
+Peripheral blood and bone marrow, ante-mortem : In the peripheral blood there was dysplasia in the leukocytes (pseudo Pelger-Huet cells and hypogranular neutrophils), platelets (hypogranular platelets and large platelets) and red cells (macrocytic red cells and dimorphic red cells) was associated with a left shift and circulating blasts. The bone marrow was hypercellular with trilineage dysplasia (pseudo Pelger-Huet cells, erythroid precursors with nuclear bridging, irregular nuclear contours, irregular hemoglobinization of the cytoplasm and mononuclear and multinucleated megakaryocytes). There was abnormal localization of immature precursors (ALIP) in the core biopsy. The bone marrow aspirate differential count showed increased blasts (18.2%) while the erythroid precursors were less than 50% of the nucleated cells.
+Post-mortem examination was limited to heart and lungs at the request of the family. The heart lay free in the pericardial sac, surrounded by 300 mL of straw-colored pericardial effusion. There was fibrinous pericarditis. The free wall of the left ventricle and the interventricular septum had soft and hemorrhagic areas scattered throughout, with no definite transmural focus. The major coronary arteries (right coronary, left anterior descending, and left circumflex arteries) were involved to only a minor degree by old eccentric atherosclerotic plaques (maximum stenosis of 25 to 30%) with no evidence of an acute event (thromboembolus, hemorrhage, rupture). There was bilateral pulmonary edema and left lower lobe congestion and consolidation.
+Microscopic examination of the heart revealed a diffuse interstitial infiltrate of immature dysplastic hemopoietic cells involving the myocardium, endocardium and the pericardium. Cells of myeloid, erythroid and megakaryocytic lineages were present. These infiltrates were associated with single fibre myocyte necrosis as well as larger foci of necrosis. A majority of these cells were immunopositive for myeloperoxidase consisted with myeloid lineage.
+Pancytopenia associated with peripheral blood features including dysplastic changes in the granulocytes, <1% blasts and < 1 × 109/L monocytes coupled with multilineage dysplasia and 18.2% blasts in the bone marrow was in keeping with the diagnosis of refractory anemia with excess blasts-2 (RAEB-2) . Clinical presentation and clinical course of RAEB is typically related to the symptoms of decreased counts of one or more cell lineages and blast count [,]. The symptoms of lethargy, shortness of breath, and generalized weakness in this patient may be attributed to both anemia and cardiac infiltration by malignant cells, although the former is much more common clinically . Her cardiac symptoms were not due to drugs sometimes used in patients with myelodysplasia, since the patient had not received cytotoxic, immunomodulatory, putative differentiating agent, or hemopoietic growth factor therapy [-].
+Although cardiac involvement in leukemic extramedullary spread is relatively common (ranging from 37–44%) [-], clinical signs are found in less than 1% of cases [-] and leukemic cardiac involvement antemortem is usually not suspected . The most likely reason for this is the subclinical nature of the symptoms and signs in cardiac leukemic infiltration . This is in keeping with the observation that gross infiltrative disease at the time of initial diagnosis in patients with acute leukemia is rare [,,]. In the patient reported here extramedullary (cardiac) infiltration by dysplastic hemopoietic precursors by itself is not a reason to upgrade the diagnosis to acute leukemia. Extramedullary infiltration at other sites has been reported in patients with myelodysplastic syndromes [,], more frequently in patients with chronic myelomonocytic leukemia compared to RAEB and refractory cytopenia with multilineage dysplasia [,]. Although it may herald transformation to acute leukemia , this transformation may not be observed for some time [,] and sometimes not at all during follow-up [,]. Granulocyte-macrophage colony stimulating factor overproduction may lead to autonomous colony formation in the bone marrow of patients with myelodysplastic syndrome ; this may partially explain proliferation of malignant hemopoietic cells in the heart infiltrated by malignant cells.
+Although cardiac infiltration is usually associated with high WBC count (mostly due to blasts) and advanced disease , the presence of a high circulating white blood cell count is not a necessity for developing cardiac infiltration as infiltration has been shown to be present in aleukemic leukemia as well as in patients with very low white cell counts . The development of cardiac infiltration in our patient with myelodysplasia and pancytopenia would be consistent with this observation keeping with this pheneomenon; the rising white late in the course of the disease was was predominantly due to neutrophilia and left shift and not due to a large blast population.
+The effects of hemopoietic cell infiltrate in the heart are varied. Leukemic deposits may form mass lesions or thrombi . Pericardial involvement may lead to pericardial effusion contributing to restrictive myocardial dysfunction [,]. Reports of heart block in extramedullary cardiac leukemic involvement are few [,,]. Heart block has been observed in patients with both very high and very low peripheral blood white cell counts and may be reversible after local radiotherapy to the heart despite persistence of leukemic infiltration . However, infiltration of the conduction system is a potentially serious complication that may be fatal . Leukemic infiltration is a rare cause of restrictive cardiomyopathy . An antemortem study of 18 patients with acute leukemia (6 ALL, 12 AML) demonstrated no significant difference from controls in LV systolic function parameters including LV ejection fraction, similar to what was observed in our patient at initial echocardiography . However, LV diastolic dysfunction has been observed in 38 percent of leukemic patients, independent of age and heart rate. It is likely that cardiac compromise in our patient was due to a combination of restrictive cardiomyopathy due to leukemic infiltration, concomitant anemia, cardiac dilatation, conduction blocks and myocardial necrosis. Myocardial necrosis was most likely due to a combination of, a) ischemic damage secondary to anemia and prolonged hypotension and b) extensive leukemic infiltration. Markedly rapid decrease in ejection fraction from 66% to 33% also suggests the role of ischemia, since leukemic infiltration is not expected to cause this degree of systolic dysfunction over a 24-hour period.
+Usual causes of death in patients with myelodysplasia are related to bone marrow failure and transformation to acute leukemia [,,], however, in this patient, death was attributed to cardiac failure. It is likely that the rising white blood cell count during second admission, although predominantly due to neutrophilia and left shift, was associated with early transformation- in view of increased peripheral blood blast percentage – the limited autopsy did not permit evaluation of the bone marrow.
+Cardiac involvement in by malignant hemopoietic cells is of more than just academic interest, since cardiac function has been shown to improve following therapy directed against malignant infiltrate [,]. Incorrect diagnosis during life and the fatal outcome highlight the clinical importance of considering myocardial infiltration in patients with myelodysplasia and cardiac symptoms.

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+A 22-year-old Sri Lankan man presented with acute onset diplopia, progressively worsening over one week. He had noted that his eyelids were drooping, especially towards end of the day. He did not experience dysphagia, dysarthria or limb weakness. He had been diagnosed with end stage renal failure (ESRF) due to obstructive uropathy one year ago. Although his serum creatinine had been 16.4 mg/dl (normal: 0.7 – 1.3) five months ago, he had not consented for renal replacement therapy.
+On examination, he had a fatigable bilateral asymmetrical partial ptosis (additional file 1) and a positive curtain sign (manually raising the more ptotic lid causes increased ptosis on the opposite side), but the Cogan’s lid twitch and peek signs were negative. There was a complex external ophthalmoplegia without nystagmus . The pupils were normal. Limb power was 5/5 (modified medical research council score) in all four limbs, no cerebellar signs were noted and the sensation to pin prick and joint position sense was intact. The rest of the examination were normal apart from severe pallor. The blood pressure was 130/80 mmHg. The bedside ice-pack test for ocular myasthenia gravis was negative.
+The biochemical parameters on admission are given in the Table .
+After correcting the hypocalcaemia, haemodialysis was commenced because of the severe acidosis and continued on an alternate day frequency.
+In the evaluation for the cause of the patient’s complex ophthalmoplegia and fatigable ptosis, the following investigations were done .
+Acetylcholine receptor antibodies were not tested due to resource constraints.
+The patient’s ophthalmoplegia improved completely by the end of the first week after initiating haemodialysis and the ptosis resolved by the end of the second week . The MRI of the brain repeated after two weeks demonstrated marked improvement in the previously noted brainstem abnormalities with residual mild T2W/FLAIR hyperintensities in the midbrain. T2W hyperintensities in the internal capsule and cerebellar peduncles had completely resolved .

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+A 5-year-old Asian boy presented with decreased visual acuity in his right eye . He was born with CL/P at 40 weeks of gestation. However, he had no family history of CL/P. His mother received a measles, mumps, and rubella vaccine during the first trimester of pregnancy. No relevant history of smoking, alcohol consumption, folate deficiency, exposure to ionizing radiation, or any severe infection during pregnancy was found. Prenatal fetal ultrasonography showed unilateral CL/P on the right side without brain lesions. Postnatal renal ultrasonography of the child revealed mild hydronephrosis in the right kidney without dysfunction. Follow-up examination at 4 years of age confirmed that both the kidneys were normal. He underwent several cardiological and endocrinological investigations for the evaluation of congenital rubella syndrome, which revealed no abnormal findings. Neurological examination revealed no midline defect of the vertebral bodies. At 9 months of age, he underwent successful surgical repair of his unilateral CL on the right side . He experienced two episodes of febrile seizures at the age of 2 years with no sequelae. Electroencephalography after the seizures revealed no remarkable findings. Although genetic analysis was recommended, his parents refused to undergo chromosomal evaluation. Magnetic resonance imaging showed no other midline defects or neurological anomalies. He did not have any intellectual or psychomotor developmental delays.
+At initial presentation, his best-corrected visual acuity (BCVA) was 20/60 in the right eye and 20/25 in the left eye. Slit lamp examination revealed iris coloboma in the inferonasal quadrant of the right eye . Fundus examination showed optic nerve and chorioretinal colobomas in the inferonasal quadrant of the right eye . Spectral domain optical coherence tomography showed preserved foveal anatomy without retinoschisis or neurosensory detachment in the right eye . No evidence of microphthalmia, scleromalacia, congenital cataract, or ocular motility disorder was found. The left eye had no remarkable findings. He was prescribed glasses based on his cycloplegic refractive errors (Right eye: − 2.00 Dsph − 2.00 Dcyl × Axis 180°; Left eye: + 1.50 Dsph − 1.00 Dcyl × Axis 180°). We recommended daily occlusion therapy in the left eye for 4 h. After 3 months, BCVA in the right eye improved to 20/30. In addition, the patient was referred to the otolaryngology department for otological and audiological assessments, which revealed no relevant abnormalities.

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+A 56-year-old female military officer was referred to the Colorectal Surgical Department for mid-rectal cancer 8 cm from the anal verge. The patient had no past medical history. Her physical examination and routine laboratory studies were unremarkable. Her carcinoembryonic antigen level was 5.93 ng/ml, and an abdomino-pelvic computed tomography (CT) scan showed no intra-abdominal metastasis. Pelvic magnetic resonance imaging showed a clinical T2N0 tumor. The patient underwent laparoscopic low anterior resection and diverting loop ileostomy. The operation time was 310 min. The pathologic results showed that the adenocarcinoma had infiltrated the proper muscle layer (T2) with no lymph node metastasis (0/17). On postoperative day 3, the patient complained of vomiting and abdominal pain, and a follow-up abdomino-pelvic CT scan showed an ileo-ileal type intussusception . Two days of surgical observation were unsuccessful, and her nausea and abdominal pain continued. The patient then underwent exploratory laparotomy. On exploration, intussusception was found 40 cm proximal to the loop ileostomy site. The proximal ileum (P, intussusceptum) had invaginated into the distal segment (D, intussuscipiens), and segmental resection of the ileum was carried out . There was no pathological leading point on the resected ileum . The patient recovered uneventfully and was discharged on postoperative day 14 after the second operation. The patient has remained in good health for two years.

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+A 52-year-old previously healthy woman with no family history of endocrine disease was admitted to our hospital with suspected PA based on high blood pressure (193/105 mmHg), spontaneous hypokalemia (potassium [K], 3.4 mmol/L), and a high aldosterone-to-renin ratio (ARR 71 ng/dL per ng/mL/h [plasma renin activity (PRA) 0.2 ng/mL/h and plasma aldosterone concentration (PAC) 14.2 ng/dL]). On admission, the patient showed no clinical features of Cushing syndrome, and no catecholamine excess symptoms other than hypertension, such as headache or excessive sweating. Before the initiation of antihypertensive drugs, PA was confirmed by the positive captopril challenge test (PRA: 0.2 ng/mL/h, PAC: 9.6 ng/dL, ARR: 48 [> 20]; Table ) according to the Japan Endocrine Society Clinical Practice Guidelines for PA and the Japanese Society of Hypertension Guidelines for the Management of Hypertension . Abdominal computed tomography (CT) revealed bilateral adrenal masses (right, 16 × 11 mm; left, 13 × 9 mm), with baseline CT attenuation values of 30–60 Hounsfield units (HU) on the left and 10 HU on the right , and contrast-enhanced CT showed a stronger contrast effect in the left adrenal mass than in the right adrenal mass . Although overnight 1mg dexamethasone suppression test (DST) showed mild autonomous cortisol secretion (2.25 µg/dL [< 1.8]; Table ), plasma level of ACTH in the early morning before DST was not suppressed (52.1 pg/mL [> 7.07]; Table ), and the diurnal variation of serum cortisol was preserved . Based on the Japanese Endocrine Society criteria , adrenal subclinical Cushing's syndrome was ruled out. The 24-h urinary catecholamines (epinephrine, 23.7 μg/day [< 41]; norepinephrine, 151.6 μg/day [< 160]; dopamine, 582.1 μg/day [< 1100]) were within normal limits, and the urinary fractionated metanephrines (metanephrine, 0.47 mg/day [< 0.19] and normetanephrine, 0.46 mg/day [< 0.33]) were slightly elevated but did not reach 3-fold of the upper limit of normal range . Adrenal vein sampling (AVS) was performed because she requested surgical treatment at that time and the results were interpreted according to previous guidelines . The findings confirmed that the right adrenal gland was responsible for aldosterone hypersecretion (post-cosyntropin stimulation lateralization ratio 24.67 [> 4], contralateral ratio 0.575 [< 1]; Table ). She refused right adrenalectomy at the last minute, and medical therapy with the mineralocorticoid receptor (MR) antagonist, eplerenone (50 mg) was initiated; however, she abruptly discontinued treatment and the follow-up visit. Five years after the first AVS, she visited a local clinic with complaints of headache and high blood pressure (208/109 mmHg) and was administered a calcium blocker (cilnidipine 10 mg). At this time, she requested surgery for PA and was readmitted to our hospital. On admission, her blood pressure was 127/96 mmHg, and she was taking oral cilnidipine 20 mg/day. No symptoms of catecholamine excess or Cushing's signs were observed. Repeated abdominal CT showed no significant change in the right adrenal mass (16 × 11 mm); however, the left adrenal mass was enlarged to 26 × 13 mm . At the surgeon's request, AVS was performed a second time to confirm PA localization. The second AVS confirmed the right unilateral hyperaldosteronism (post-cosyntropin stimulation lateralization ratio: 12.60; contralateral suppression index: 0.40) had not changed. . Repeated 1mg DST showed mild autonomous cortisol secretion, but the diurnal variation of cortisol was preserved (11:00 pm cortisol: 4.46 µg/dL). The 24-h urinary excretion assay revealed that norepinephrine (142.3 μg/day), epinephrine (26.5 μg/day), and dopamine (644.0 μg/day) levels were normal; however, metanephrine (0.81 mg/day) and normetanephrine (0.60 mg/day) concentrations were higher than those measured 5 years earlier . 123I-MIBG scintigraphy showed a tracer-avid left adrenal mass but no metastatic lesions . Based on these findings, a left pheochromocytoma was diagnosed preoperatively. After the temporary discharge, we had a conference with the department of urology of our institution, and we decided to perform partial adrenalectomy for the left pheochromocytoma and medical treatment for the right unilateral PA. The patient was started on α-blocker (doxazosin, 2 mg/day), a non-steroidal MR antagonist (esaxerenone, 5 mg/day), and continued cilnidipine 20 mg/day. Two months later, she was readmitted to our hospital. After preoperative administration of saline (1 L/day) for 7 days and an α-blocker (doxazosin, 2.0 mg/day) for 2 months, laparoscopic left partial adrenalectomy was performed. No intraoperative or postoperative hemodynamic instability occurred. Histologically, the tumor cells were arranged in diffuse sheets or nests and were large with prominent nucleoli . The pheochromocytoma of the adrenal gland scaled score was 0 indicating a low grade pheochromocytoma. Immunohistochemical examination of the tumor showed that chromogranin A and synaptophysin were positive , leading to the final diagnosis of left pheochromocytoma; Succinate dehydrogenase subunit B (SDHB) was positive ; cytochrome P450 (CYP) 11B2 was negative, Ki 67 was weakly positive , and ACTH was negative . The left adrenal gland tissue adjacent to the tumor was normal . Although we could not perform genetic analysis, as consent could not be obtained from the patient, the positive immunostaining for SDHB, suggested against SDH-related paraganglioma syndromes. Doxazosin was discontinued after surgery and esaxerenone (5 mg) and cilnidipine (20 mg) were continued. One month after surgery, the patient’s blood pressure was 126/84 mmHg, and her serum K (4.27 mmol/L), PAC (47.38 ng/dL), active renin concentration (ARC) (36.57 μU/mL), and random fractionated urinary metanephrines (metanephrine 152 ng/mg Cr [29–158], normetanephrine 363 ng/mg Cr [122–500]) were normalized. One year after surgery, blood pressure and serum K levels remained well controlled. No surgical treatment for the right adrenal mass has been performed, and pheochromocytoma has not recurred.

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+A 25-year-old African American female presented to the Emergency Department (ED) complaining of diffuse abdominal pain, non-bloody diarrhea, nausea, and non-bloody emesis.
+The patient’s symptoms started the day prior to arrival to the ED. She described the abdominal pain as sudden onset, sharp and stabbing in quality, 10 out of 10 in intensity, and located in the suprapubic region with radiation to the right and left flanks. She denied any rash (including malar erythema), aphthous ulcers, hematuria, pleuritic chest pain, shortness of breath, or fever. Of note, several months prior, the patient had developed left eyelid swelling non-specific arthralgias (without swelling) of her wrists, fingers, and ankles. Her workup, including autoimmune laboratory tests, was inconclusive at the time. No diagnosis was made. Her arthralgias resolved spontaneously after a few days. She denied any arthralgias at the time of examination. The rest of her review of systems was non-contributory.
+Her past medical history was significant for seasonal allergies. Her family history was significant for discoid lupus in her father, rheumatoid arthritis (RA) in one of her paternal cousins, and SLE in another paternal cousin.
+On presentation, the patient’s vital signs were normal: 36.7 °C, heart rate of 92 bpm, blood pressure of 110/70 mmHg, respiratory rate of 18, and oxygen saturation of 100% on room air. Her abdominal exam revealed normal bowel sounds, mild abdominal distention but no lesions, scars, or hernias. There was significant lower abdominal tenderness without guarding or rigidity.
+Initial laboratory testing included a complete blood count (CBC) and comprehensive metabolic panel (CMP) . The patient had leukopenia with a WBC count of 3.25 k/uL, lymphopenia with an absolute lymphocyte count of 740, and anemia with a hemoglobin level of 11.7 g/dL. The CMP revealed a low albumin of 3.1 but was otherwise normal.
+A contrast computed tomography of the abdomen and pelvis done in the emergency room revealed marked circumferential wall thickening and edema of the proximal and mid small bowel loops predominantly involving the submucosa .
+At this point, the main differential diagnoses were intestinal angioedema and mesenteric vein thrombosis given the radiographic findings. However, the mesenteric vessels were patent, and there was no evidence of thrombosis. Laboratory testing for hereditary angioedema showed a normal C1 Esterase inhibitor level, low C3 (48 mg/dL), and low C4 (4 mg/dL) . Autoimmune work-up revealed elevated ANA of 13.6, normal double stranded DNA antibody of 25 IU/mL (anti-dsDNA ab), high anti-Smith antibody (>8 AI), and high anti-ribonucleic protein of 6.9 AI (anti-RNP) antibody . A urinalysis to screen for concomitant lupus nephritis did not show hematuria or red blood cell casts, and a urine protein to creatinine ratio was negative (0.1).

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+A 33-year-old male presented to our institute with pain in the left elbow on extending the elbow. He had limited extension of 10–15 degrees. Patient had developed painful elbow on throwing the cricket ball from the periphery of the ground. This pain started to increase on repeated throws. He had conservative treatment for the same. Over the span of 18 months, he developed loss of terminal extension.
+On clinical examination, he had tenderness in the posterior aspect of elbow along with crepitus and extension lag of 15 degrees and painful passive and active terminal extension. He did not have any instability of the medial and lateral ulnar collateral ligament.
+Roentgenogram showed no radiological abnormality. Magnetic resonance imaging MRI revealed posterior fat pad hypertrophy withimpingement between olecranon and olecranon fossa whichwas the primary cause of pain and extension lag. After getting informed consent patient was posted for arthroscopic excision of posterior fat pad. Patient positioned in right lateral position and left elbow scrubbed, painted, and draped under aseptic precautions. Standard anterolateral portal was made and the anterior joint was visualized. Later on standard posterior and posterolateral portals were made revealing posterior fat pad hypertrophy locked and preventing complete olecranon extension.
+The fat pad was shaved off using 3.5 mm shaver and no impingement of soft-tissue was evident. An incidental finding of small foramen was found in the olecranon fossa. It was found that the rent in the olecranon fossa got the fat pad locked into it, causing impingement on elbow extension.
+Portals were closed and postoperatively dressings were changed and active complete elbow mobilization was started on post-operative day 1and 2,respectively. Patient was advised against heavy usage of elbow such as lifting heavy objects for 3 weeks. Patient was on regular follow-up and was symptom free. He got back to contact sports in 1 month duration. His last visit was 1year following surgery; he was comfortable with full range of movements.

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+Without significant previous medical history, a 67-year-old Caucasian man developed spinal symptoms with temporary hypesthesia and hypoalgesia in both legs. These symptoms spontaneously resolved without any specific diagnosis at that time. At the age of 73, our patient suffered from bilateral optic neuritis and he was diagnosed with MS at an outside hospital. His expanded disability status scale (EDSS) score was at that time 2.5. Magnetic resonance imaging (MRI) studies of the spinal cord revealed a diffuse cord swelling and longitudinally extensive T2 hypertensive lesions extending from C2 to T3 (see Figure depicting a T2-weighted MRI scan, which shows residual longitudinal myelitis with extensive cord atrophy). A cranial MRI scan displayed few periventricular and cerebellar lesions without contrast enhancement and without fulfilling the Barkhof criteria. Moreover, analysis of the cerebrospinal fluid (CSF) presented oligoclonal bands. At that time, anti-AQP-4 antibody testing was not performed. A therapy with interferon beta 1a was started for six months and was replaced by interferon beta 1b at the discretion of the treating outside neurologist. Our patient developed two further spinal relapses during the treatment with interferon beta preparations. They were treated with corticosteroid pulses without any success and his EDSS score worsened from 2.5 to 4.0. Although a subsequent therapy with natalizumab was initiated at an outside clinic, our patient continued to present another three relapses. The first relapse occurred four months after starting natalizumab, the second after six months and the third relapse after eight months. All relapses repeatedly affected both optic nerves and the spinal cord each with increasing visual and motor impairment. Thus, our patient developed a high-grade spastic tetraparesis as well as impaired visual acuity of both eyes and his EDSS score progressed from 4.0 to 8.0. At that point, NMO was discussed after referral to our hospital and natalizumab therapy was discontinued after nine courses. After repeated cycles of plasma exchange, the disease course stabilized and a therapy with rituxan was started. Although B cells were completely depleted, our patient experienced another severe myelitis relapse upon further follow-up three months later. Consequently, an additional immunosuppressive therapy with cyclophosphamide at a dosage of 600mg/m2 was initiated. In the meantime, we performed repetitive anti-AQP-4 antibody tests in an approved external laboratory employing an immunofluorescence assay (IFA) cell-based analysis. Negative anti-AQP-4 antibody tests were obtained via IFA analyses upon first admission and then in six-monthly intervals after first contact at our hospital. It was only after 18 months that anti-AQP-4 antibodies became positive after three negative results. At that time, the anti-AQP-4-immunoglobulin (Ig)G antibody titer was 1:1000 while IgM and IgA titers were negative. There were no other autoantibodies and no signs of other autoimmune diseases or malignancy.
+Under combination treatment with cyclophosphamide (13 cycles every six weeks, cumulative dosage of 8300mg/m2) followed by another cycle of rituxan, our patient developed no further relapses over an observation period of 2.5 years.

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+A previously healthy six-year-old girl was admitted with fever, dyspnea, abdominal pain, and pain in the right arm and shoulder. Four days before admission she had fallen from a tree while playing. Shortly after admission she was transferred to the ICU because she acutely developed signs of shock, anemia and progressive abdominal pain. Splenic rupture was suspected and confirmed by ultrasound showing sub-capsular spleen hematoma and free intra-abdominal fluid. During the ICU stay she developed an abscess on the right shoulder, for which antibiotic treatment was started. The culture of the aspirate, taken before start of antibiotics, from this abscess was positive for Staphylococcus aureus. After 1 month she was transferred to our center under the suspicion of pericarditis, because of persistent fever and cardiomegaly on the chest X-ray. Echocardiography revealed pericardial effusion, located mostly behind the left ventricular (LV) posterior wall (Additional file ), with a to and fro blood flow through a fistula between the left ventricular lumen and a cavity in the pericardial space, and echogenic densities suggestive for fibrin strands and clots (see Fig. ). Cardiac function was good with mild mitral valve regurgitation. Findings were suggestive for advanced purulent bacterial pericarditis complicated by covered left ventricular perforation (pseudo-aneurysm).
+High doses of intravenous cefotaxime and flucloxacillin, already started in the referring hospital, were continued. She developed arthritis of the left knee and right elbow which were both aspirated but with negative cultures. Two weeks after admission her clinical condition did not improve with persistent leukocytosis and high C-reactive protein levels. A pericardial abscess with ongoing bacteremia was suspected and surgical intervention was scheduled.
+A median sternotomy was performed, leaving the pleural space closed. The patient was placed on extracorporeal circulation using standard bicaval cannulation. The operation was performed on a beating heart. On opening of the pericardium multiple small abscesses and adhesions were identified and removed, as were thick vegetations on the left ventricular posterior wall. The fistula in the LV myocardium connecting the LV lumen with an abscess on the posterior-lateral wall of the LV was found and closed with prolene sutures with felt (see Fig. ). The pericardial space was irrigated multiple times with a solution of sodium-chloride and iodine. Cultures of the abscesses were negative. Post-operatively she had a quick recovery without fever episodes. She was discharged from the hospital in good condition 2 weeks after surgery. Antibiotics were continued for almost 4 months because of persistent osteomyelitis of the right upper arm and a septic arthritis of the right elbow. Echocardiograms during follow-up revealed no abnormalities.

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+A 4-year-old boy was admitted because of persistent lower limb pain and claudication in the left lower limb over the past 9 mo.
+The patient had mild persistent lower limb pain and claudication without any inducement. Claudication worsened in one day. The child had no fever, urinary frequency or urgency, numbness, fatigue, or lameness. For further assessment and treatment, he was admitted to our joint hand surgery department.
+The child had no history past illness.
+The child had no history of family illness, and his medical history was unremarkable.
+Pressing pain and local swelling were present in the left shank. The results of sensation and strengthening test, and tendon reflex test were normal in both lower limbs. No pathological signs were observed upon physical examination.
+Laboratory examinations were normal.
+Preoperative imaging examinations, including X-ray photography, computed tomography, and magnetic resonance imaging, showed erosion-like changes with bone expansion of the left middle and lower fibular segment . No invasion of circumferential soft tissue or pathological fracture of the lesion site was observed. Initial pathological examination revealed fibular fibrous dysplasia . Postoperative photography showed that an allograft bone was implanted into the fibular medullary cavity . Recurrent fibular fibrous dysplasia was observed at the age of 6 years .

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+A 40-year-old pregnant woman at 28th week of pregnancy was admitted to an obstetric emergency department in Isfahan, Iran, with chief complaints of epistaxis and gingival bleeding that were manifested about a week before admission.
+She had no previous family history of bleeding disorders. But in her past medical history, it is highly notable that she had several hours of bleeding after eyebrow tattooing about 5 years before admission and two episodes of abortion in the first pregnancy trimester, 4 and 2 years before the current pregnancy. Moreover, her first pregnancy was successful. There were no abnormal data pertaining to her first labor.
+Her medications were aspirin due to previous pregnancy losses, daily perinatal multivitamins, and iron supplements. She did not smoke or drink alcohol. Considering the patient’s condition, aspirin administration was discontinued and her symptoms reduced in intensity.
+On admission, her vital signs were blood pressure 120/70, pulse 82, temperature 37 degrees C, respiratory rate 17. A detailed physical examination was performed but all findings were normal and no evidence of bleeding was found.
+In her laboratory data, platelet count was in the normal range but prothrombin time (PT) and partial thromboplastin time (PTT) were both significantly elevated, so a mixing test was done. In the mixing test, both PT and PTT corrected instantly and after two hours of incubation at room temperature. Based on these results, the patient was suspected of having a deficiency of one or more coagulation factors. Thus, the activity level of coagulation factors were tested . Laboratory results showed that the activity level of factor V was decreased significantly and the patient was diagnosed with factor V deficiency. In accordance with the mixing test result, the congenital form of FVD was approved.
+The patient had a history of two unsuccessful pregnancies and some complications were possible due to significantly elevated PT and PTT. Thus, the patient was started on fresh frozen plasma (FFP) every three days -two units each time (15–20 ml/kg bodyweight)- from week 30 of pregnancy until the parturition and she responded well with increase in FV activity to the normal range. At 40 + 2 weeks gestation, the vaginal delivery was done successfully and the baby was born with 3820 gr weight and Apgar score of 9 and 10 in 1st and 5th minute respectively. The newborn was tested for bleeding disorders and diagnosed with congenital FVD. As the patient and her husband were cousins, the infant was a case of congenital FVD with parental consanguinity.

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+A 46-year-old man had been diagnosed with a clear cell carcinoma with rhabdoid differentiation (World Health Organization grade 4) of the left kidney in May 2018 through a renal biopsy. The tumor was locally invasive, associated with metastases to retroperitoneal lymph nodes, the liver and the lungs. Because of the widely metastatic disease, nephrectomy was not performed. At initial diagnosis, the thyroid function tests showed a discrete elevation of his thyroid-stimulating hormone (TSH) at 4.5 mU/L (reference range 0.27-4.2 mU/L), with normal levels of fT4 (16 pmol/L, reference range 12.0–22.0 pmol/L) and fT3 (4 pmol/L, reference range 3.1–6.8 pmol/L) . He was subsequently started on systemic therapy with the tyrosine kinase inhibitor sunitinib in May 2018, pending approval for immunotherapy with nivolumab and ipilimumab. Therapy with nivolumab was initiated in June, and ipilimumab was added in August. The therapy with sunitinib was definitely stopped in October after completion of the mutational analysis of the primary tumor (next-generation 400 gene sequencing panel), which showed mutations in the TERT promoter and the MET gene (exon 15: p.V1088A), and amplification of SETD2 (SET domain containing 2, histone-lysine N-methyltransferase) and MET. Moreover, the tumor showed significant expression of programmed death ligand 1 (80%).
+Shortly after the introduction of ipilimumab, he developed transient thyrotoxicosis secondary to immune checkpoint inhibitor-associated thyroiditis, with subsequent hypothyroidism (October 2018: TSH 26.3 mU/L, fT4 9 pmol/L, fT3 2.0 pmol/L). At this stage, levothyroxine substitution was introduced (100 µg/day, corresponding to about 1.3 µg/kg/day). However, the TSH levels further increased to 72.7 mU/L after 4 weeks of therapy. The situation remained unchanged in the following months; in January 2019, the TSH was 81.5 mU/L, the fT4 was decreased at 9 pmol/L, and the fT3 was particularly low at 1.5 pmol/L. On February 18, 2019, the levothyroxine dosage was increased to 300 µg/day (corresponding to 4.3 µg/kg/day). Despite that, the fT4 and fT3 levels remained at similar levels after 2 weeks with 10.4 and 1.1 pmol/L.
+The patient was hospitalized in March 2019 with a diffuse atopic eczema and was found to be severely anemic. He was hypotensive and tachycardic, and the dermatologic exam revealed dry skin and eczema eruptions with erythematous and squamous papules and plaques.
+At that time, endocrinology was consulted for the first time. The patient reported profound weakness, a weight loss of 14 kg during the last 8 months, constipation, and a generalized pruritic rash. He plausibly reported regular and appropriate intake of the levothyroxine. Of note, the patient did not present any symptoms of malabsorption. At that time, the patient intermittently took proton pump inhibitors but took no other medication known to interfere with thyroid hormone absorption or metabolism.
+Although he then took the levothyroxine under supervision during a week, the thyroid function tests did not improve: fT4 was 8.2 pmol/L, fT3 1.1 pmol/L, total T4 46 nmol/L (reference range 66–181 nmol/L), and total T3 0.5 nmol/L (reference range 1.3–3.1 nmol/L). Suspecting that the patient might have consumptive hypothyroidism, rT3 was ordered and immunohistochemistry of the tumor for D3 expression was planned. The rT3 level drawn 9 days prior to his passing but only available about a month later was found to be elevated at 0.79 nmol/L (reference range 0.14–0.54 nmol/L). Of note, the estimated increase of his tumor burden based on cross-sectional imaging studies was about 57% between June 2018 and March 2019 (557.01 cm3 to 878.73 cm3 based on RECIST (Response Evaluation Criteria in Solid Tumors) criteria).
+The patient and his family opted for palliative care and he left the hospital; he passed away shortly thereafter at home.

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+An 11-year-old girl was referred to our hospital with the chief complaint of a swollen left-sided neck mass. Two days prior, hoarseness began in the morning, followed by fever and sore throat in the afternoon. On the next day, neck discomfort with tenderness occurred. On admission, she had a fever of 38.2 °C, hoarseness, and an elastic soft mass with mild tenderness on the left anterior neck . Pharyngeal redness or swollen tonsils were not observed. Laboratory data indicated mild inflammation and thyrotoxicosis; increased white blood cell of 17,500/mm3 (neutrophils, 86.6% and lymphocytes, 8.6%) and C-reactive protein level of 3.4 mg/dL; increased free T4 of 1.98 ng/dL [reference 1.02~1.52 ng/dL], decreased free T3 and thyroid-stimulating hormone (TSH) level of 2.71 pg/mL [reference 2.78~4.90 pg/mL] and 0.009 μIU/mL [reference 0.62~3.36 μIU/mL] respectively; and an elevated thyroglobulin level of 308 ng/mL [reference 0~33.7 ng/mL]. Contrast-enhanced computed tomography (CT) of the cervical region revealed an abscess partially infiltrating the thyroid gland and an air pocket near the piriform sinus . Pharyngoscopy revealed swelling of the arytenoid region, with purulent retention . From the purulent discharge, Klebsiella oxytoca was isolated. The left vocal cord was swollen but not paralyzed. No evidence of airway narrowing was identified. Suspecting PSF infection, parenteral treatment with cefotaxime at 100 mg/kg/day and dexamethasone (DEX) at 0.16 mg/kg/day was initiated . On the day after admission, the hoarseness disappeared, and the fever resolved. On the third day of admission, pharyngoscopy revealed that the swelling had disappeared . DEX was tapered off within 5 days. On the seventh day of admission, a subsequent contrast-enhanced CT of the cervical region revealed a prominent reduction in the abscess. The patient was discharged on the eighth day of admission, and the antibiotic was switched to oral cefdinir 10 mg/kg/day.
+Three weeks after discharge, a barium esophagogram revealed residual contrast in the left pyriform sinus, and PSF was diagnosed . However, abscess was not detected by ultrasonography. At that time, thyroid function returned to the normal range (FT3, 4.19 pg/ml; FT4, 1.19 ng/dl; TSH level, 2.63 μIU/mL; and thyroglobulin level, 16.4 ng/mL). Chemocauterization was proposed to the patient’s family because this was the first episode of a neck abscess. However, the family did not opt for this method, and the patient is currently under observation without recurrence for a year.

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+An Italian 7-year-old girl with a TMAU-like phenotype has come to our attention after her mother reported the production of strong body odor. The child’s history revealed that she is the third child of healthy, unrelated parents. Her two brothers aged 16 and 10 years were both apparently healthy.
+All her hematological parameters and her biochemical indices for renal, thyroid and liver function were within the normal range.
+TMAU was suspected and it was suggested that the child’s DNA be examined for mutations in the FMO3 gene. The study was approved by our local ethics committee. Written informed consent was obtained from the patient’s parents.
+Molecular analysis of FMO3 gene in the index patient and family members was performed. Genomic DNA was extracted from heparinized peripheral blood of all family members using the salting out method . Upstream sequence, the non-coding exon 1 and each of the coding exons (exons 2 to 9) of the FMO3 gene were amplified from genomic DNA by polymerase chain reaction using the primer pairs shown in Table .
+PCR products were sequenced with the BigDye® Terminator sequencing kit version 1.1 on the 377 ABI PRISM® Sequencer Analyzer (Applied Biosystems).
+We also analyzed urine samples from the proband and all family members for the presence of TMA and TMAO. A first urine sample was collected for 24 hours under normal dietary conditions (a diet not containing TMA-rich foods) and a second was collected for 6 to 8 hours after a 300g marine fish meal.
+Urine samples were acidified to pH 3.0 with formic acid and stored at -20°C. Creatinine was measured by the Jaffe reaction on an autoanalyzer.
+Derivatization of TMA was carried out according to the method by Johnson using ethyl bromoacetate as a derivative reagent [,]. Each sample was analyzed in duplicate.
+Mutations analysis of nine exons of the FMO3 gene was performed on all family members.
+The proband was found heterozygous for the previously reported polymorphism c.472 G>A p. E158K (rs 2266782) in exon 4, and a G-to-A transition at codon 158 (GAG to AAG) resulting in a glutamic acid to lysine substitution (Glu158 to Lys158).
+E158K polymorphism reduces FMO3 catalytic activity that appears to vary depending on the substrate [-]. Previous in vitro expression studies showed that the K158 form of the protein is a poorer TMA N-oxygenator than the E158 form.
+In some populations, this variant was found in a high degree of linkage disequilibrium with the E308G variant. When present on the same allele, the E158K and E308G exhibit an even more pronounced effect on FMO3 function , even leading to mild or transient forms of TMAU .
+The proband was heterozygous also for two polymorphisms in intronic regions: c.627+10 C>G (IVS5+10G>C) (rs 2066534) and c.485-21 G>A (IVS4-22G>A) (rs 1920149).
+The first, a variant of uncertain functional relevance, was found in cis with E158K polymorphism while the second was an intronic A-to-G substitution at the -21 position from the acceptor splice site of exon [,]. The parents and the eldest of two brothers were heterozygous for the same variants while the younger brother did not show any variation.
+Since the latter was wild-type it is possible to deduce that he has inherited the wild-type allele from each parent and that c.472 G>A, c.485-21 G>A and c.627+10C>G polymorphisms occurred in cis configuration on one of the two FMO3 alleles of the father and mother.On the basis of this it is possible to infer that the proband and the elder of the two brothers, as well as the parents, were compound heterozygotes for the three polymorphisms . However, among them, only the proband showed a TMAU-like phenotype.
+Therefore, we wanted to analyze the upstream region of FMO3 gene in order to identify polymorphic variants that could affect the enzymatic activity. No variants were identified in any family members. Analysis of the urine samples collected for 24 hours from both parents and two brothers under normal dietary conditions (a diet not containing TMA-rich foods such as fish or eggs) showed the presence of relatively small amounts of TMA excreted. The N-oxidation metabolic ratio (TMA/TMAO ratio) for the four subjects ranged from 0.02 to 0.04.
+For the proband the TMA excretion accounted for only 29.0% of total TMA excretion. The N-oxidation metabolic ratio for the proband was 2.4, two orders of magnitude greater than those observed for the parents and two brothers (affected ratio TMA/TMAO >0.2).
+After oral TMA challenge, the amount of urinary TMA excreted as TMAO, in the parents and two brothers remained high and it was very similar to the values under normal dietary conditions. N-oxidation metabolic ratio ranged from 0.02 to 0.04.
+After oral TMA challenge, in the proband, TMAO excretion accounted for 19.4% of total TMA excreted .

data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1655_en.txt

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+A 35-year-old Caucasian male presented to the Maxillofacial Surgery service of Campo Limpo Hospital, in São Paulo, Brazil, with the main complaint of an intraoral swelling that had been growing for the last 8 years. The lesion was asymptomatic, and even though the patient had been aware of its constant growth, he decided to look for professional help only when its proportion began to cause him speaking impairment.
+The physical examination revealed a firm mushroom-like mass, with bony consistency covered by smooth regular mucosa spanning almost the entire right alveolar border of the mandible. The area was edentulous and, according to the patient’s report, had initiated its growth shortly after the extraction of a molar, which the patient could not specify. As it developed, the remaining teeth had been extruded until complete avulsion (teeth 28 through 32, in universal numbering system). No extraoral abnormalities were observed. The patient was in good health, with no history of previous diseases, smoking, or substance abuse. The diagnosis of Gardner syndrome was discarded due to the lack of any other symptoms, such as gastrointestinal implications or supernumerary teeth .
+Computed tomography revealed a well-defined pedunculated mass attached to the right body of the mandible with radiographic characteristics resembling the original bone, consisting of a central area of moderated radiopacity similar to medullary bone, surrounded by a denser, more radiopaque thin area, comparable to cortical bone. According to Rodriguez (2011), these particular growth characteristics make it easy to diagnose a peripheral osteoma clinically and radiographically .
+Since the tumor presented both clinical and radiographic features of a benign lesion, the patient underwent an excisional biopsy, with complete removal of the mass and an osteoplasty of the mandible. The access was intraoral, with an incision directly over the lesion, and divulsion of the mucoperiosteal tissues, preserving their integrity for suture later . After the complete exposure of the lesion, surgical drills were used to mark the limits of excision, and the mass was removed in two pieces, with the use of a chisel and hammer. An oval drill was used to perform an osteoplasty of the jaw, recovering its original shape and thickness . After surgical resection, the mucosa flaps had their wedges trimmed, to obtain straight margins that were sutured with 3–0 resorbable thread. The surgical piece was a white, oval, bony fragment, with a regular surface of approximately 4.2 × 4.8 × 2.5 cm . The postoperative course was uneventful, except for discrete dehiscence of the suture 5 days after the procedure, which was spontaneously healed with chlorhexidine mouthwash on clinical follow-up for the next 7 days . The radiographic aspect of the jaw, 14 days after surgery showing regular shape and dimensions .
+Histopathological analysis revealed mature adipose tissue, permeated by viable compact bone lamellae, consisting of medullary tissue, delimited by a thin and well-vascularized lamellar cortical bone. Thin and congested blood vessels were noted throughout the whole sample.

data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1658_en.txt

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+A 54-year-old male presented with numbness and edema in bilateral lower limbs in 2018 and then underwent positron emission tomography-computed tomography (PET-CT) at a hospital, indicating intense metabolic activity in multiple bones throughout the body. However, a definitive diagnosis wasn’t made. Subsequently, he experienced progressive numbness and edema as well as developed weakness in bilateral lower limbs for which he intermittently received Chinese medicine. Unfortunately, symptoms didn’t improve. In Sep 2022, he underwent a chest CT at another hospital, showing bilateral mild pleural effusion. For further diagnosis and treatment, he was admitted to the Rheumatology and Immunology Department of our hospital in Oct 2022. Since the disease’s onset, he has been frustrated and lethargic and has a normal diet and sleep, regular voiding, and no significant weight changes. Meanwhile, he denied a history of chronic diseases, tobacco and alcohol use, food and drug allergies, and genetic disorders.
+The patient’s vital signs were stable. He had no signs of jaundice, anemia, or cyanosis. His bilateral breasts were significantly protruded . Besides, fresh red hemangiomas were scattered throughout the anterior portion of his chest and back, with a maximum size of about 0.40 cm×0.50 cm . There were no apparent abnormalities in the cardiopulmonary and abdominal examination. However, pitting edema was noted in bilateral lower limbs . Neurological examination revealed normal cranial nerves and no cerebellar signs. However, there was diminished power in the bilateral lower limbs (4/5) by the Manual Muscle Test (MMT). Physiological reflexes were present and pathological reflexes were negative. Deep and shallow sensations were weakened below the bilateral ankle joints. The upper limb examination was unremarkable.
+His complete blood count, clotting test, and blood glucose were generally normal. IgA, IgG, IgM, and IgE were also within the normal range. His serum/urine PEP and IFE showed negative M-protein. The levels of serum-free light chains κ and λ were increased, while the ratio of κ/λ in serum was normal . The levels of serum VEGF were elevated. FT3 and FT4 were decreased, and TSH was increased. Sex hormone measurement revealed increased prolactin (PRL), follicular estrogen (FSH), estradiol (E2), and progestational hormone (P) but normal testosterone (T). ACTH was increased and cortisol (COR) at 8:00 AM was decreased. Rheumatism-related indicators, hepatitis B and C, syphilis, and AIDS serology tests were all negative. The detailed results are shown in Table .
+The thyroid ultrasound showed two small hypoechoic nodes in the lower pole of the right lobe of the thyroid gland, the larger being 0.47 cm×0.29 cm. Echocardiography revealed bilateral atrial enlargement and pericardial effusion (small amount). Abdominal ultrasound displayed splenomegaly with an intercostal thickness of about 5.70 cm and a length of 16.30 cm. Chest and abdominal CT revealed enlarged lymph nodes in the bilateral axilla and mediastinum (the largest with a diameter of approximately 1.10 cm), as well as small amounts of pleural effusion and pericardial effusion. Bone scintigraphy with [99mTc]-methylene-diphosphonate (MDP) single-photon emission computed tomography/computed tomography (SPECT/CT) exhibited a symmetrical bilateral skeleton and mixed sclerotic and lytic bone lesions in bilateral ilium, vertebral bodies, and ribs. .
+BM smears revealed that the proportion and morphology of red blood cells, granulocytes, and megakaryocytes were generally normal, and mature PCs constituted 2% of cells. Flow cytometry of BM specimens showed no significant evidence of monoclonal PCs and other abnormal cells (immunophenotypic abnormalities). Besides, the karyotype revealed normal male chromosomes. BM biopsy of the posterior superior iliac spine displayed no increase in the abundance of immature cells, lymphocytes, and PCs .
+He experienced a CT-guided coarse needle puncture of the posterior superior iliac spine. Pathological assessments indicated no increase in the number of PCs and lymphocytes. The results of immunohistochemistry indicated CK (-), LCA (+), langerin (-), CD68 (+), CD163 (+), CD1α (-), S100 (-), Ki-67 (80% +), CD138 (-), and CD56 (-) .
+The classic symptoms of MM are elevated calcium level, renal insufficiency, anemia, and lytic bone lesions, which were not found in our case. MM doesn’t generally present with peripheral neuropathy, organ enlargement, multiple endocrine gland abnormalities, skin-specific changes, sclerotic bone lesions, and increased VEGF levels, which all were present in our patient. In addition, the proportion of monoclonal PCs in the BM of MM should be at least 10%, while monoclonal PCs in the BM of our patient were not present.
+The CD is clinically divided into focal and multicenter types. The former is more common in young people. Multicentric Castleman disease (MCD) also presents with lymphadenopathy, hepatomegaly, splenomegaly, rash, and cavity effusion. However, it is usually not accompanied by peripheral neuropathy, sclerotic bone lesions, endocrinopathy, and increased VEGF levels, which were present in our patient. Patients with MCD are prone to infection and lymphoma. MCD usually has an aggressive course and poor overall survival (OS). However, the onset of this patient is insidious, and the course is chronic and stable, just like POEMS syndrome.
+Both GBS and POEMS syndrome can lead to motor neuron paralysis, but GBS is not accompanied by visceral enlargement, endocrinopathy, skin changes, bone lesions, and increased VEGF, which all were present in our patient.
+POEMS syndrome and CIDP affect the motor and sensory nerves, slowing nerve conduction. However, CIDP doesn’t present with organ enlargement, endocrinopathy, M-protein deposition, skin changes, bone lesions, or increased VEGF levels, most of which were present in our patient.
+Although the M-protein of the patient was undetectable, he had peripheral neuropathies in bilateral lower limbs. Additionally, he showed signs of male breast development and characteristic hemangiomas in the anterior chest and back. Hormonal tests revealed hypothyroidism, hyperprolactinemia, hypoadrenalism, and feminization. More importantly, he had an increased VEGF level, and SPECT/CT revealed sclerotic bone lesions. Ultrasound and CT showed enlargement of lymph nodes, splenomegaly, and extravascular volume overload. After excluding the disorders that are easily confused with POEMS syndrome, we proposed the diagnosis of POEMS syndrome with undetectable M-protein.
+Then the patient was treated with the RD regimen (25 mg/d of lenalidomide capsules on days 1–21, 20 mg/d of dexamethasone tablets on days 1–4 and 8–11, each cycle is 28 days). At the same time, he received levothyroxine sodium tablets (25 µg/d) to improve hypothyroidism and aspirin to prevent coagulation. Nearly 6 months after receiving the treatment, the numbness and edema of bilateral lower limbs significantly improved, and the color of skin hemangiomas altered from fresh red to dark red. Elevate serum VEGF and free light chains have returned to normal. All indicators were within the normal range on the thyroid, adrenal gland, and sex hormone tests. Imaging examinations exhibited normal volume of lymph nodes, normal size and morphology of the liver and spleen, and no signs of extravascular volume overload. Bone X-rays still indicated high-density shadows in multiple bone areas throughout the body. Thus, we will continue the follow-up.