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- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1013_en.txt +4 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1024_en.txt +2 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1048_en.txt +4 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1059_en.txt +11 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1065_en.txt +5 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1118_en.txt +6 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1122_en.txt +8 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1129_en.txt +3 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1143_en.txt +3 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1162_en.txt +6 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1179_en.txt +2 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1219_en.txt +3 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1224_en.txt +9 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1225_en.txt +6 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1234_en.txt +7 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1242_en.txt +4 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1249_en.txt +1 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1251_en.txt +3 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1275_en.txt +1 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1291_en.txt +1 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1304_en.txt +2 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1322_en.txt +5 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1332_en.txt +4 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1347_en.txt +5 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1378_en.txt +1 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1384_en.txt +9 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1397_en.txt +3 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1422_en.txt +2 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1426_en.txt +6 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1429_en.txt +2 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1441_en.txt +7 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1455_en.txt +6 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1464_en.txt +6 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1499_en.txt +4 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1520_en.txt +3 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1537_en.txt +2 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1540_en.txt +3 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1556_en.txt +4 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1591_en.txt +20 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1603_en.txt +6 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1628_en.txt +3 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1646_en.txt +3 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1651_en.txt +1 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1663_en.txt +2 -0
- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1670_en.txt +1 -0
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- data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1673_en.txt +2 -0
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1013_en.txt
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A 15 year old Caucasian female was transferred from a secondary care paediatric unit. She presented with a two-day history of progressive dyspnoea, cough and palpitations on a background of recent onset arthralgia, alopecia and oral ulceration. Clinical examination revealed hypertension (blood pressure 170/110 mmHg), pallor with a malar rash, symmetrical polyarthritis of the interphalangeal and metacarpophalangeal joints, alopecia and oral ulceration.
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Investigations revealed normocytic anaemia, haemoglobin 95 g/l (normal 120-160 g/l), lymphopaenia, lymphocytes 0.9 × 109/l (normal 1.2–5.2 × 109/l)), elevated inflammatory markers with an erythrocyte sedimentation rate (ESR) of 77 mm/hr. (normal 1-9 mm/hr) and c-reactive protein (CRP) of 38 mg/l (normal < 10 mg/l) and moderately impaired renal function with urea 14.4 mmol/l (normal 2.0–6.0 mmol/l), creatinine 154 μmol/l (normal 30-90 μmol/l). Coagulation screen showed a slightly prolonged prothrombin time (PT) of 13 s (normal 10.2–12.0 s) but was otherwise normal. Albumin was low (28 g/l, normal 36-50 g/l) and liver function tests were normal. Microscopic haematuria and proteinuria were present with an elevated urine albumin:creatinine ratio of 1217 mg/mmol (normal < 3.4 mg/mmol). Antinuclear antibody titres were strongly positive with a titre of 1:160, speckled pattern. Anti double-stranded DNA was positive with a titres of > 379 IU/ml (normal 0-10 IU/ml) and positive Crithidia assay >/= 1:160. Anti-Smith and anti-RNP antibodies were both positive with titres of > 480 U/ml (normal 0–5.0 U/ml) and > 240 U/ml (normal 0-5 U/ml) respectively. There was marked hypocomplementaemia with C3 0.44 g/l (normal 0.7–1.7 g/l), C4 0.06 g/l (normal 0.1–0.7 g/l) and absent CH100 classical and alternative pathway components. Antiphospholipid, anti-SSA and anti-SSB antibodies were all negative. Chest x-ray showed bilateral pleural effusions and cardiomegaly with a cardiothoracic ratio of 0.67. Initial echocardiography showed a large pericardial effusion with diastolic compression of the right atrium and ventricle suggestive of cardiac tamponade. The left ventricle was dilated with an ejection fraction of 25% and there was mild mitral, tricuspid and aortic valvular regurgitation. Treatment was commenced with high-dose intravenous methylprednisolone (30 mg/kg/dose, maximum dose of 1 g) and diuretics and immediate transfer to a tertiary paediatric intensive care unit was arranged.
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On admission to the intensive care unit she had developed periorbital oedema and ascites with worsening dyspnoea and reduced oxygen saturation. Echocardiography revealed a large pericardial effusion, oedematous myocardium and valvulitis with an ejection fraction of 13% with no evidence of tamponade (see Fig. ). Renal function deteriorated further with a creatinine increase to 270 μmol/l (normal range 30-90 μmol/l) and the patient became anuric. Intermittent positive pressure ventilation, inotropic support, plasma exchange and haemodialysis were required. High-dose intravenous methylprednisolone was continued for 3 days and then changed to oral prednisolone at 1 g/kg/day. Cyclophosphamide was commenced at a dose of 850 mg/m2 on day four of admission due to severe renal impairment and ongoing need for haemodialysis and multiorgan involvement.
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Follow-up echocardiography showed normalisation of function by day five of admission with a small pericardial effusion as the only persistent abnormality. Renal biopsy revealed grade 4 lupus nephritis. The patient was discharged from the intensive care unit on day seven of admission and subsequently discharged from the hospital on day fourteen. Treatment at discharge included a weaning dose of prednisolone, hydroxychloroquine, enalapril and carvedilol. Cyclophosphamide treatment was continued monthly for a total of six doses after which the patient was maintained on further immunosuppression. Remission has been maintained with mycophenolate mofetil and hydroxychloroquine over the past 2 years.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1024_en.txt
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A 51-year-old, gravida 1, para 1, Japanese female complained of abnormal genital bleeding for two months and presented to a clinic. An ovarian tumor was found during abdominal computed tomography (CT), and so the patient was referred to our hospital. The abnormal genital bleeding had stopped when she visited our hospital. An ultrasound scan of her right ovary revealed a swollen region of 7 cm in diameter, which contained multiple cysts, and the uterine endometrium was 9-mm-thick. Cervical cytology and an endometrial biopsy produced normal findings.
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On magnetic resonance imaging (MRI), an ovarian tumor, which measured 7 cm in diameter and contained multiple cysts, was detected, and a large part of the tumor exhibited high signal intensity on T1-weighted imaging and low signal intensity on T2-weighted imaging. No solid components were detected . We decided to perform a laparoscopic right salpingo-oophorectomy. The patient’s medical history included endometriosis from the age of 25 without specific therapy and subarachnoid hemorrhaging due to the rupturing of an aneurysm at the age of 43. The patient was diagnosed with hydrocephalus after she underwent surgery for the subarachnoid hemorrhaging, and an LP shunt was inserted. Her medical history also included kidney stones, schizophrenia, hypertension, and diabetes mellitus at the age of 50. We confirmed the route of the LP shunt on a CT scan, which had been conducted at another clinic. It revealed that the LP shunt had been placed from her left flank to Douglas’ pouch . Under general anesthesia, laparoscopic right adnexectomy was performed. A 12-mm trocar was inserted at the umbilicus, and three 5-mm trocars were inserted 3 cm inside the right and left upper anterior iliac crests and on the midline of the lower abdomen. The abdominal pressure was set at 8 mmHg. The ovarian tumor was located in Douglas’ pouch and had adhered to the back of the uterus. Also, the head of the shunt tube was located in Douglas’ pouch and was an obstacle to the operation. We temporarily shifted the head of the shunt tube from Douglas’ pouch to the vesicouterine pouch to prevent damage to the shunt and ensure that the operation could be conducted smoothly . The operation time was 2 h and 11 min, and the total volume of intraoperative blood loss was 50 ml. The patient’s postoperative course was uneventful, and she was discharged on postoperative day 3. The histological diagnosis was an endometriotic cyst. The patient was examined at 1 month after the surgery at our hospital’s outpatient clinic, and no adverse events were observed. She was followed-up at the outpatient clinic of a general practitioner.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1048_en.txt
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The patient is a 54-year-old gentleman, who presented with a few months of mid-epigastric pain, nausea and vomiting with associated weight loss in February 2012. CT and MRI scans revealed a 3.3 × 3.1 cm pancreatic head mass encasing superior mesenteric artery and vein with associated mesenteric periportal lymphadenopathy. He also had sub-centimeter lung nodules presumed to be metastatic deposits. He thus had a clinical stage 4 unresectable pancreatic cancer. Genomic analysis of tumor biopsies revealed the presence of KRAS mutation (G12D) and loss of CDKN2A/B.
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The patient was placed on a clinical trial with first-line treatment of Reolysin and gemcitabine, receiving cycle one day one on March 2012. Reolysin was administered at a dose of 1 × 1010 TCID50 IV on days 1, 2, 8, and 9 (immediately after gemcitabine on days 1 and 8) in combination with 800 mg/m2 IV gemcitabine on days 1 and 8, with 21-day cycles. The patient displayed a clinical response with improvement in cancer-related pain. The best radiographical response was documented as stable disease by Response Evaluation Criteria in Solid Tumors (RECIST) guidelines .
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With the patient on treatment, a biopsy of the pancreatic mass was performed after cycle 25 day 8 in February 2014. The biopsy features were consistent with the diagnosis of pancreatic adenocarcinoma, with confirmed KRAS mutation (G12D) and loss of CDKN2A/B. Immunohistochemistry (IHC) was performed on Reolysin-treated or untreated HCT116 colon cancer cells as a positive and negative control for reovirus staining, respectively . Viral replication was detected using antibodies against the reovirus protein, as the presence of viral RNA may not necessarily imply infectious virus particles. A polyclonal antibody, raised in goats, was derived from mature reovirus viral capsid proteins . Importantly, IHC analyses of biopsy specimens from a pancreatic cancer patient revealed strong positivity for reoviral protein and activated caspase 3 within the tumor . Biopsies from pancreatic cancer patients frequently contain benign fat, which may serve as an excellent internal negative control. Images of the stained fat cells were negative for reovirus and active caspase-3 and were from the same tissues that displayed positive staining for reovirus and active caspase-3 . Serial section analysis showed a very high concordance of reoviral protein and activated caspase-3, which is characteristic of a productive reovirus infection. In addition, co-expression analysis demonstrated that the reoviral protein and active caspase-3 were being expressed in many of the same cancer cells . Our preclinical studies with Reolysin identified induction of ER stress and NOXA to be key determinants for Reolysin-mediated apoptosis [, ]. In agreement with the induction of active caspase-3, we also noted a significant increase in the expression of GRP78/BIP, which is commonly induced following ER stress and NOXA in the biopsy sample following Reolysin and gemcitabine treatment .
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Toxicities were manageable and included grade 1 fever likely due to Reolysin and grade 3 thrombocytopenia and neutropenia due to gemcitabine. The patient also had a biliary obstruction, which required stenting in November 2013. He completed 27 cycles of treatment with the last one in April 2014. At this time, he presented with disease progression with ascites and jaundice.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1059_en.txt
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The subject of our study, a 56-year-old Caucasian Italian woman, presents with an occlusal open bite and a complete dental formula, with only the left superior second premolar missing, substituted by an implantoprosthetic rehabilitation . The patient, a medical doctor, has a normal blood pressure range, is not affected by any metabolic disease and is a non-cigarette smoker. For the evaluation of her occlusal muscle activity, a bilateral electromyography (EMG) of her masseter muscle was recorded using an evaluation system of mandibular movement (K6-I; Myotronics, Seattle, WA, USA) and Duo-trode surface Ag-AgCl electrodes (Duo-trode; interelectrode distance: 19.5mm, Myotronics). EMG data were recorded at a sampling rate of 240Hz and amplified at a time constant of 0.06 seconds. For the evaluation of her muscle activity, voluntary dental clenching was executed and recorded during swallowing. In accordance with the dental diagnostic protocol , a preliminary evaluation of the patient’s myoelectric activity in dental occlusion was performed through muscle EMG in order to assess their functional balance. Registered values showed a remarkable functional asymmetry of masseter muscles, 23mV for her left masseter and 103mV for her right masseter . According to the expressed electromyographic values, muscular activity was symmetrized by applying a 15 minutes transcutaneous stimulation of trigeminal motor branches at low frequency for elevator occlusal muscles and at medium frequency for submandibular antagonist muscles. This method allowed detection of the functional trajectory of occlusal elevator muscles and to record a symmetric craniomandibular relation, positioning a self-hardening material between the dental arches. The same material was used to make a cusp bite modeled on the inferior dental arch named orthotic-syntropic bite for its peculiar use of electrostimulation. When the orthotic was applied, electromyographic control was repeated to verify occlusal myoelectric balance. Registrations have documented substantially equal values: 57mV for left masseter muscle and 61mV for right masseter . Immediately after, the patient was submitted to pupillometric and hemodynamic examinations in habitual occlusion first and with the orthotic soon after.
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For pupillary diameter measurement, we used a computerized corneal topographer MODI02 software 2005 LITE (CSO, Florence, Italy), made of a survey section by Placido disk 24 loops, camera sensor charge-coupled device (CCD) 1/3 inch and a claim support. The instrument presents, during the pupillar acquisition phases, a constant lighting of the disk and a 56mm distance of work. The points measured during data acquisition are 6.144, with a model elaboration higher than 100.000 points. Registered pupillometric analysis showed a remarkable right and left baseline asymmetry, respectively 4.98mm and 4.40mm , whereas in the occlusal rebalance condition an equivalent pupil diameter was registered, 4.13mm right pupil and 4.10mm left pupil . Indeed, pupillometric data analysis registered in occlusal rebalance shows a more suitable reduction of the basal diameter, with clear right side decrease, relating to higher occlusal myoelectric values.
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For blood flow computerized examination, a GE HealthCare echograph, Voluson E8 Expert model, was used, with a 3D-4D-color-power Doppler volumetric probe. The duplex color scanner investigations were executed with an interval of 60 minutes, in habitual occlusion first, and with the orthotic after . The following evaluations were performed (see Table ).
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systolic pulsatility and average flow velocity: (P.I. Index);
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systolic and diastolic relationship-flow: (R.I. Index);
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systolic peak in cm/second: (P.S. Index);
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diastasis cordis in cm/second: (E.D. Index);
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systole-diastole relationship: (S-D Index);
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Carotid artery: C.a.;
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Vertebral artery: V.a.
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The registrations reveal that the patient’s left V.a. hemodynamic is more influenced by trigeminal proprioception. In fact, the orthotic application reduces on the left the S-D index of 70.94 and equilibrates the values of both vertebral arteries, 3.40 (left) and 3.21 (right), respectively. Whereas, in the ED index, diastolic flow increase of 12.06 cm/second of the left V.a. makes the values of both arteries equal, 12.70 (left) and 12.16 (right) respectively. Moreover, in the PI index it is possible to observe that the different average flow between the right (1.0) and left (2.88) vertebral arteries is totally cancelled in occlusal rebalance, with perfectly equal values (1.23). Also the PS Index confirms the previous results because a general reduction of hemodynamic values is registered both in carotid and vertebral arteries after orthotic application. In fact, the systolic hematic peak, expressed in cm/second, shows decreases of 2.05 on the right and of 7.69 on the left in the carotid arteries, while in vertebral arteries the decreases are of 7.42 on the right and of 4.37 on the left. The RI index does not seem to be influenced by occlusal proprioception.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1065_en.txt
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We describe the case of a 25-year-old black Cameroonian woman of Bakossi origin with basic primary education, gravida 3 para 1 (G3P1010), who lost a child in 2012 following complications of neonatal infection and later had an abortion in early 2015. She presented to a district hospital in the South-West Region of Cameroon for her first antenatal visit with a 21-week pregnancy. Her blood pressure was 107/66 mmHg and she had a uterine fundal height of 26 cm.
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She was requested to do some paraclinical examinations including blood group, hemoglobin level, glycemia, human immunodeficiency virus (HIV), syphilis, toxoplasma, rubella serology, stool analysis, urine analysis, and a fetal ultrasound. Most of these tests were done and were found to be normal. However, toxoplasma and rubella immunoglobulin G (IgG) serologic tests were both reactive; analysis was done with the aid of ImmunoComb® IgG and ImmunoComb® II IgG serologic tests, respectively. She also had a proteinuria of 100 mg/dl; her blood group is AB rhesus positive. She did not benefit from a morphologic fetal ultrasound partly because there was none in the hospital and because of the financial constraints she presented, which limited her movement to the nearest regional referral hospital located approximately 100 km from the site of her antenatal clinic via a poorly accessible road. She was, however, put on daily 65 mg of elemental iron and 5 mg of folic acid supplement, and she received anti-tetanus vaccine, intermittent preventive treatment against malaria, and a long-acting insecticide-treated bed net. She was encouraged to consult a gynecologist-obstetrician at the nearest referral hospital.
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By her next antenatal visit 4 weeks later, she had not consulted the specialist physician and was still unable to attend the paraclinical examination requested earlier. Emphasis was placed on the risk of her baby sustaining life-threatening malformations and she was advised to continue with the supplements and follow-up visits. She was again encouraged to undergo a fetal ultrasound and to consult a gynecologist-obstetrician. Adding to the challenges faced by this expectant mother, the district hospital did not have an ambulance that could have helped the health care provider to overcome the road accessibility and financial challenges she faced.
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During her 34th week of pregnancy she returned to the hospital in labor pains with a blood pressure of 110/68 mmHg, uterine fundal height of 40 cm, and was at 8 cm cervical dilation with bulging membranes. After placing her on a 5% glucose infusion, the membranes were ruptured, and a turbid amniotic fluid of approximately 2000 ml oozed out. This was followed by the delivery of an anencephalic recently dead baby boy weighing 1600 g. Active management of third stage of labor was done (Additional file ).
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The devastated mother and her partner received psychosocial care for 3 days; she was discharged from hospital and scheduled for routine psychosocial follow-up. She was further counseled on the need to consult a gynecologist-obstetrician before her next pregnancy.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1118_en.txt
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The patient is a 69-year-old female who underwent a right radical nephrectomy 10 years ago, in 2011 for a pT3b N1 M0 grade 3 clear cell carcinoma of the right kidney. Adjuvant sunitinib therapy was initiated and then discontinued after 2 months due to myelosuppression and rash. In February 2013, the patient was found to have recurrence in the right lung upon follow-up CT imaging. The patient was started on sunitinib and then switched to pazopanib February 2014 due to progression. Pazopanib was held briefly during radical radiotherapy to oligometastatic disease.
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The patient developed hypertension a couple of months after starting pazopanib. This was effectively treated with amlodipine. After persistently stable disease, she made a joint decision with her oncologist to discontinue her pazopanib June 2019. She did not experience any other side effects while on pazopanib except for some moderate gastric reflux. Her past medical history is only significant for hypothyroidism and hiatal hernia. She has family history of a father who died in his 60s of a myocardial infarction and sisters with hypertension. She has a substance history of a remote 3 pack year smoking history and occasional alcohol use. Her most recent BMI was calculated to be 24.4.
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In July 2020, CT imaging showed recurrence with enlargement of a left apical pulmonary nodule. She received radical intent radiotherapy with a dose of 60 Gray in 30 fractions, then she was started back on pazopanib. Due to severe reflux symptoms and the development of atrial fibrillation, pazopanib was briefly held January 2021 and restarted February 22, 2021. She was also placed on bisoprolol and warfarin by her cardiologist during this period. CT of her chest, abdomen, and pelvis on February 10, 2021 did not reveal any signs of disease progression and demonstrated normal splenic artery anatomy .
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On March 5, 2021 at 10 pm, the patient suddenly developed excruciating, sharp left upper quadrant pain that radiated to her entire abdomen. She had associated nausea and loose bowel movements but no vomiting, fever, lightheadedness, rashes or petechiae. She activated emergency medical services and was brought to her local emergency department in Northern Ontario. Her pain improved with IV opioid analgesics, but her abdomen became continually distended and her hemoglobin dropped into the low 70s. A CT of her abdomen and pelvis was performed to reveal free fluid within the peritoneal cavity and contrast pooling noted adjacent the splenic hilum, related to the splenic artery . The splenic artery measured 1.5 cm representing either a ruptured aneurysm or pseudoaneurysm. The patient ultimately received Vitamin K, 6 units of red blood cells and was transferred to a tertiary center elsewhere in Ontario for definitive treatment of her ruptured splenic artery aneurysm.
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She had coil embolization of the splenic artery by intervention radiology . Her recovery was complicated by a post-operative hematoma and elevated troponin, no intervention was required.
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After an extended stay in hospital, the patient was discharged home and pazopanib was discontinued. In a follow-up appointment, the patient does not disclose any complaints and states her home blood pressure has been stable. The patient remains in good health at the time of writing this case report.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1122_en.txt
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A 40-year-old female patient visited the emergency department (ED) with a 3 d history of fever, minor headache, and abdominal pain.
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The patient had been living in a postpartum care center after giving birth by cesarean section 3 wk prior to her ED visit. Eleven days prior, the front of her neck was swollen, and a needle aspiration was performed at a private surgical hospital; however, her thyroid gland showed no specific findings.
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| 3 |
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The patient had no relevant medical history, apart from a cesarean section performed 3 wk before presentation.
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The patient denied any family history of malignant tumors.
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| 5 |
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During physical examination in the ED, the patient’s vital signs were measured: Body temperature (40.6 ℃), blood pressure (100/48 mmHg), heart rate (100 bpm), and respiratory rate (18 breaths/min). No specific findings were observed in the thyroid gland. Moreover, no notable clinical findings such as neck stiffness, tonsil hypertrophy, abdominal tenderness, abnormal breath sounds, or costal spine angle tenderness were observed. Additionally, the patient exhibited no signs of infection at the site of abdominal surgery (cesarean section) or thyroid fine-needle aspiration. Colposcopy was performed to preclude endometritis; however, no specific findings were observed.
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The patient’s laboratory test results revealed bicytopenia (hemoglobin: 14.0 g/dL; platelets: 133000/μL; absolute neutrophil count: 2512/μL). However, other laboratory tests including total bilirubin level measurement (0.3 mg/dL), liver enzyme level measurement [aspartate transaminase (AST): 65 U/L; alanine transaminase (ALT): 35 U/L], thyroid function test (T3: 65.1 ng/dL; free T4: 0.88 ng/dL), and urinalysis (one white blood cell/high-powered field), showed no significant abnormalities. The C-reactive protein (CRP) level was elevated at 4.46 mg/dL.
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| 7 |
+
The patient’s chest radiograph was normal. Abdominal computed tomography (CT) was performed due to elevated CRP levels and intermittent post-delivery abdominal pain. However, a prominent infectious focus was not observed.
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After administration of an antipyretic drug, the patient’s fever subsided, and vital signs remained stable during long-term follow-up in the ED. Four days later, the patient was discharged with a prescription for broad-spectrum antibiotics and a referral to the infectious disease outpatient department to evaluate her fever of unknown etiology. However, 4 d after discharge, the patient returned to the ED with a fever of 38 ℃ and decreased blood pressure of 60/30 mmHg. Laboratory test results revealed thrombocytopenia (platelets: 94000/μL), and other test results [total bilirubin level: 3.1 mg/dL; liver enzyme levels (AST: 202 U/L; ALT: 444 U/L)] and renal function indicators (blood urea nitrogen: 42.1 mg/dL; creatinine: 3.35 mg/dL) indicated multiorgan failure. The patient’s ferritin and triglyceride levels were 3429.0 μg/L (normal range: 13.0-150.0 μg/L) and 957 mg/dL (normal range: 10.0-150.0 mg/dL), respectively.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1129_en.txt
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A 40-year-old woman and her husband had recently travelled from the United States to Bogota, Colombia for 7 days. They spent time outdoors in both urban and rural areas. She recollects having had mosquito bites and had three bite marks on her leg. She was asymptomatic during her stay.
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| 2 |
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On day 3 after returning to the USA, she developed itching of her scalp. On day 4, she felt fatigued and developed low-grade fever and back pain. On day 5, she presented to the outpatient infectious diseases clinic for evaluation after her scalp became erythematous and she started developing a pruritic, maculopapular rash on her face and trunk that rapidly spread over her entire body. Her wrist and ankle joints became very painful and swollen. She also developed a pressure-like sensation behind her eyes with conjunctival redness.
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She had received yellow fever vaccine previously. She lived in an area of Florida with no local transmission of CHIKV or DENV. There had been no other recent travel. Her husband who travelled with her was asymptomatic and was not tested.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1143_en.txt
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A 27-year-old Japanese man was brought to the emergency room with coma. He was diagnosed as having schizophrenia at the age of 13 and as having autism spectrum disorder at the age of 18. The medication at that time was 50 mg/day of atomoxetine, 5 mg/day of risperidone and 3 mg/day of guanfacine, although risperidone was decreased from 9 to 5 mg and guanfacine was increased from 2 to 3 mg 35 days before. He had been drinking over 4 L of water for the last few weeks. His impaired consciousness level was 3 points (E1V1M1) of the Glasgow coma scale (GCS). His vital signs were as follows: temperature, 39.1°C; blood pressure, 174/98 mmHg; heart rate, 95 beats/min; oxygen saturation, 92% (under 9 L of O2 supply). shows laboratory data in emergency room. He suffered from abnormal balance of electrolytes. As shown in , he had significant hyponatremia and hypochloremia with normal potassium concentration, and reduction of blood osmotic pressure. His inflammation markers were markedly elevated. In addition, he suffered from rhabdomyolysis. Indeed, his creatine kinase, myoglobin and urinary myoglobin levels were significantly high. As shown in , his head computed tomography (CT) revealed severe cerebral edema. In addition, significant fluid retention was observed throughout the body, namely, pleural effusion, pulmonary and intestinal edema . We evaluated the causes of hyponatremia in this patient. Since antidiuretic hormone (ADH) level was elevated to 0.8 pg/ml when sodium level was 109 mmol/L, we diagnosed him with syndrome of inappropriate secretion of ADH (SIADH). Based on these findings, we thought that he probably suffered from severe cerebral edema which was induced by hyponatremia associated with NMS and SIADH. In addition, rhabdomyolysis and NMS was diagnosed necessitating comprehensive therapy in intensive care unit (ICU).
|
| 2 |
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On admission to ICU, he required mechanical ventilation and administration of 0.9% NaCl. Moreover, we started immediately administering 10% glyceol (600 ml/once a day, 5 days + 400 ml/once a day, 2 days + 200 ml/once a day, 2 days) for cerebral edema and continuous furosemide (3 days) for diuresis. In addition, he was treated with methylprednisolone (1,000 mg/once a day, 3 days) for cerebral edema and suspection of autoimmune encephalitis, and with dantrolene (40 mg/once a day, 1 day + 100 mg/once a day, 4 days + 60 mg/once a day, 2 days) for NMS. Eye openings and spontaneous limb movements were observed several times at day 2 (his sodium level, 115 mmol/L). His impaired consciousness was improved and he was able to speak sometimes at day 3 (his sodium level, 130 mmol/L). The patient was extubated at day 3 and his head CT revealed the improvement of severe cerebral edema at day 4 . Finally, we successfully treated severe cerebral edema and hyponatremia, which was induced and complicated with NMS, water intoxication, SIADH and rhabdomyolysis. shows a time course of his cerebral edema and shows his clinical time course in ICU. His adrenal and thyroid function was normal (adrenocorticotropic hormone, 61.7 pg/ml; cortisol, 13.0 μg/dl; thyroid stimulating hormone, 3.208 μIU/ml; free triiodothyronine, 2.89 pg/ml; free thyroxine, 1.03 ng/dl; respectively) after correction of hyponatremia. He was transferred from ICU to general ward at day 9 and was discharged 29 days after admission.
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| 3 |
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After discharge, he was followed-up by the psychosomatic center of another hospital. He continued to receive the same psychosomatic treatment and did not have recurrence of malignant syndromes or water intoxication.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1162_en.txt
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A 20-year-old Greek man presented to our hospital in late May of 2010 because of high fever (up to 40°C, unresponsive to anti-inflammatory drugs), appetite loss, nausea and vomiting, persistent headache and a feeling of significant malaise for 5 days. He was diagnosed at a provincial hospital with an atypical infection and had received azithromycin for 3 days, without any improvement.
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| 2 |
+
He had not travelled recently either within the country or abroad. He denied intravenous drug use, new sexual partners or tattoos. He had no animal exposure. He did not use tobacco products or alcohol and had not taken any medication. He was previously healthy. According to his medical history, he reported allergic rhinitis and conjunctivitis for his first 5 years of life, chickenpox at the age of 5 years, a streptococcal pneumonia at the age of 6 years, several episodes of tonsillitis until the age of 12 years and a tonsillar abscess at the age of 11 years. He reported no drug allergies. No contacts with similar symptoms were identified. He had no antecedents of Asian origin. The family history was non-contributory and no family members had rheumatic diseases.
|
| 3 |
+
On admission, his temperature was 38.3°C, blood pressure at 80/50mmHg, pulse was measured at 100 beats per minute and blood oxygen saturation at 92%. A physical examination revealed bilateral conjunctival chemosis, strawberry lips and tongue, dry mucus membranes, a mild skin rash of his trunk, erythema of his thenar and opisthenar regions of both palms, an oedema of palms and soles and tachycardia with S3 and S4 gallop. Results of examinations of his lungs, abdomen, neurological and musculoskeletal systems were normal.
|
| 4 |
+
Laboratory findings revealed leucocytosis (13.2×103 per cubic millimetre) with neutrophilia (91%) and left shift with segmented neutrophils, anaemia (haematocrit 33%) and normal platelets upon admission, which were later elevated . Acute phase reactants were elevated: erythrocyte sedimentation rate (ESR), 127mm 1st hour; CRP, 30mg/dL and fibrinogen 761 seconds. Serum creatinine levels and serum glutamic oxaloacetic transaminase rates were normal, serum glutamic-pyruvic transaminase at 80IU/L, alkaline phosphatase at 147IU/L, gamma-glutamyl transpeptidase at 67IU/L, lactate dehydrogenase at 263IU/L, creatine kinase at 254IU/L, bilirubin was normal, albumin at 3.1g/dL and sodium at 132mmol/L. Urine analysis was normal. Results of blood and urine bacterial cultures and serological tests for bacteria and viruses were negative. Alpha 2 and gamma immunoglobulin levels were elevated. All blood tests for autoimmune diseases were negative. Immunophenotype examination revealed reduced cardinal number of CD3+CD8+ T lymphocytes. The results of a chest X-ray, an electrocardiogram and a transthoracic echocardiogram were normal.
|
| 5 |
+
The patient did not respond to broad-spectrum antibiotic treatment. Desquamation of his fingers and toes began on the seventh day since the disease onset. Autoimmune diseases and juvenile idiopathic arthritis were excluded, as he did not fulfil diagnostic criteria for any of these diseases. Drug hypersensitivity reactions could explain his clinical appearance; however, he was previously healthy and there was no need for him to take medication. Immediately after the suspicion of KD (on the 10th day after the onset of symptoms), he was given IVIG at 2000mg/kg once and aspirin at 50mg/kg orally for the first 3 days, and at 100mg per day for another 3 months. His treatment was based on the diagnostic criteria developed for KD in children because there had been no validated criteria for adult cases of KD. Antibiotic treatment was discontinued at this time.
|
| 6 |
+
Immunoglobulin and aspirin had a striking result, since the patient was afebrile and in better condition on the very next day after the initiation of treatment. During the following days, all clinico-laboratory findings gradually improved and only a reactive thrombocytosis remained. In total, he remained hospitalised for 10 days. A computed tomography coronary angiography performed 1 month later showed no coronary aneurysms. Today, about 5 years later, our patient remains healthy.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1179_en.txt
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| 1 |
+
A 65-year-old Japanese man was diagnosed in April 2010 with stage IV lung adenocarcinoma, manifesting multiple metastases in the lung, adrenal gland and brain. He received 31 Gy of basicranial radiation for the brain metastases. Given that he was found to harbor an epidermal growth factor receptor (EGFR) mutation, he was also treated with the EGFR-specific tyrosine kinase inhibitor (TKI) gefitinib (250 mg/day). As a result of the development of adverse effects including fatigue, dermatitis, and liver dysfunction, however, the dose of gefitinib was initially reduced by half and treatment with the drug was subsequently discontinued after a total of 2 months. Computed tomography and magnetic resonance imaging revealed that the size of the original lesion and the number of brain metastases had increased. Treatment with the combination of cisplatin (125 mg) and pemetrexed (0.75 mg) was initiated. After 8 weeks, this regimen was switched to vinorelbine (32 mg) and docetaxel (80 mg) because of the development of adverse effects. This latter treatment was also not tolerated well, and so administration of the EGFR-TKI erlotinib (150 mg/day) was initiated. The patient again experienced general adverse effects including dermal exanthema. At this time, he developed a foreign body sensation in both eyes and visited his local ophthalmologist, who referred him to the corneal service at Yamaguchi University Hospital for the treatment of corneal epithelial disorders with corneal thinning.
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| 2 |
+
Slitlamp microscopy revealed bilateral superficial punctate keratopathy and conjunctival epithelial disorders. Corneal ulceration on his right eye was also observed, but no signs of infection or inflammation were apparent. His visual acuity was 20/25 OD and 20/25 OS. Schirmer's test detected bilateral mild hypolacrimation (5 mm), and his corneal and conjunctival epithelial disorders were thus attributed to aqueous-deficient dry eye. We treated him by insertion of punctal plugs in both lower lacrimal puncta. Three weeks after plug insertion, his corneal and conjunctival epithelial disorders had apparently improved. However, 2 months after his first visit to our clinic, he was referred to us again for the treatment of bilateral corneal ulcers, which were confirmed by slitlamp microscopy . Slight stromal edema, ulceration with an opaque epithelium, and a shallow anterior chamber were also observed in the right eye. The next day, the anterior chamber of the right eye was flat, and so we treated this eye with a bandage soft contact lens. The right anterior chamber remained flat, however, and the patient was diagnosed with noninfectious corneal perforation of unknown cause and was prepared for tectonic keratoplasty. The oral administration of erlotinib was interrupted in preparation for general anesthesia, and the patient was treated with gatifloxacin eyedrops only. Two days later, the anterior chamber of his right eye had spontaneously reformed and the epithelial defects of both eyes had healed . The keratoplasty was therefore canceled and we monitored the patient carefully, but his corneal condition remained stable. Treatment with erlotinib at half the original dose was reinitiated and both eyes were maintained by the administration of artificial tears, with the punctal plugs remaining in place. Corneal ulceration or other corneal disorders did not recur.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1219_en.txt
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A 25-year-old woman was referred to our outpatient clinic with complaints of chronic headache and irregular menses. Hormone profile showed only moderate increase in Prolactin (96 ng/ml). Sellar magnetic resonance imaging (MRI) showed a pituitary mass. The patient had total pituitary adenectomy using an endoscopic endonasal transsphenoidal approach. After tumor resection, diaphragmatic opening was seen with intra-operative evidence of CSF leak. Sellar floor reconstruction was performed by mucosal graft and Glubran®2 glue filling the surgical cavity. Early post-operative period was uneventful and clinical and histopathologic finding were consistent with a non-functional pituitary adenoma.
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| 2 |
+
After 2 months of surgery, the patient complained of headache, facial pain and greenish foul-smelling nasal discharge with solid particles. Patient was diagnosed with rhinosinusitis and treated with multiple courses of nasal decongestants and antibiotics for 4 months but without improvement. Brain MRI showed inflammation and thickening of the sphenoidal and para-sphenoidal mucosa .
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| 3 |
+
Surgery with endoscopic endonasal approach was decided. Intra-operatively, the sellar floor was seen intact with no CSF leak nor discharge. A solid glass-like patches (acrylic glue) was seen in the inferior and lateral areas of the sphenoid sinus and was surrounded with inflamed infected mucosa and abundant pussy discharge . Efforts were made to erupt and de-crust the solid mass until total resection was achieved. Early post-operative period was uneventful, and a course of antibiotics was continued until total regression of the discharge. Endoscopic follow-up was performed in the 1st, 2nd and 3rd post-operative months, and showed no signs of rhinosinusitis with well-healed nasal mucosa.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1224_en.txt
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A 35-day-old girl was admitted to Kunming Children’s Hospital in October 2019 due to a lesion in the right frontotemporal region.
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| 2 |
+
The lesion was found at birth, as a subcutaneous mass with granular and papillary surface. The patient was firstly diagnosed with “cavernous hemangioma”, without treatment. The skin lesion easily bled upon touch, and showed repeated ulceration, erosion, and scab formation. There was no obvious enlargement of the lesion and subcutaneous mass from birth until now.
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| 3 |
+
The patient was born at 38 wk of pregnancy, with a birth weight of 3.1 kg and no perinatal infection or suffocation.
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| 4 |
+
The patient had no specific personal and family history.
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| 5 |
+
Physical examination revealed good general condition. The vital signs were stable, and no other abnormality was found. Dermatological examination showed a red lesion in the right frontotemporal region, with thick brown scab on the surface. After cleaning the scab, the surface of the skin lesion was bright red, appearing like granulation tissue. The lesion was granular and papillary and easily bled upon touch, with about 1.5 cm × 4 cm in size. A small amount of pale yellow thin secretion was observed on the lesion surface. There was a pedicle at the base of the skin lesion. A subcutaneous mass was felt at the base of the lesion, with slightly hard texture and a clear boundary. The mass expanded beyond the red area, with a size of about 3 cm × 5 cm. The surrounding skin had no redness or swelling, and the mass showed no tenderness .
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| 6 |
+
Blood routine test showed lymphocyte count at 4.51 × 109/L (1.0-3.0 × 109/L), lymphocyte percentage at 60.60% (20%-40%), neutrophil percentage at 30.80% (50%-70%), platelet count at 528 × 109/L (100-300 × 109/L), platelet hematocrit at 0.52% (0.108%-0.282%), and platelet distribution width at 10.0 fL (15.5-18.1 fL). The remaining indicators were unremarkable. Surface secretions were cultured for 48 h, and three plasma coagulase tests were negative; meanwhile, mixed growth of Staphylococcus was detected, with no Haemophilus isolated. Stool routine, urine routine, liver function, and kidney function tests were normal. These laboratory findings did not point to any specific diagnosis.
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| 7 |
+
Skull plain computed tomography (CT) and enhanced scans showed slightly thickened subcutaneous soft tissue of the right temporal region, and the stripes showed a high-density shadow, with a CT value of about 31 HU. Enhanced CT showed enhancement, with a CT value of about 61 HU. No obvious signs of damage were seen in the adjacent skull. There were no lesions with definite abnormal density in the brain parenchyma (no obvious abnormal enhancement). There was no enlargement, stenosis, or occlusion in the ventricular system; no widening of subarachnoid space of each ventricle or displacement of the midline structure was found.
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| 8 |
+
Dermatoscopy showed that the skin lesion was lobular and crumby. The lesion center was reddish or white, while the edges were white or yellowish band-like. There were polymorphic vascular structures and white radial streaks in the lesion, with some vascular clusters scattered .
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| 9 |
+
Pathological examination showed papilloma-like hyperplasia of the epidermis, with the epidermis partly sinking into the dermis to form several cystic depressions, lined with stratified squamous epithelium. Glandular cavity-like structures were seen in the dermis, with some opened into the epidermis. A large number of lymphocytes, neutrophils, and plasma cells infiltrated in the interstitial area was observed, as well as splinter hemorrhage. The cavity wall and villous epidermis of the glandular cavity were composed of two layers of epithelial cells; the inner layer included columnar cells, with oval and eosinophilic nuclei and abundant cytoplasm; apocrine secretion was observed .
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1225_en.txt
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On April 26th, 2020, a 68-year-old man presented to the emergency department with symptoms of acute progressive symmetric ascending flaccid tetraparesis. Patient medical history included dyslipidemia, benign prostatic hypertrophy, hypertension, and abdominal aortic aneurysm in follow-up. Ten days before admission, dry cough associated with fever, dysgeusia, and hyposmia appeared. Neurological manifestations started 5 days later with progressive acute weakness of distal lower extremities.
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| 2 |
+
On admission, oxygen saturation was 96% on room air, with a respiratory rate of 17 breaths/min, and the body temperature was 37.2 °C. Chest computed tomography highlighted a bilateral basilar ground glass opacity, with oropharyngeal swab positive for SARS-CoV-2 on reverse transcriptase-polymerase chain reaction (RT-PCR) assay. No pathological findings were auscultated on pulmonary objective examination.
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| 3 |
+
The patient was then isolated and antiviral drugs have been started. Neurological examination showed bifacial nerve palsy (House-Brackmann grade 3) and muscular weakness, with a Medical Research Council scale of 1/5 in proximal and 2/5 in distal of the lower limbs. The osteo-tendon reflexes were hypoactive with bilateral areflexia to the Achilles tendons. No sensory deficit was recorded. Upper motor neuron disorder or meningeal irritation signs have not been found.
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| 4 |
+
Baseline laboratoristic analysis showed thrombocytopenia (101 × 109/L, reference value: 125–300 × 109/L) and lymphocytopenia (0.48 × 109/L, reference value: 1.1–3.2 × 109/L). Cerebrospinal fluid assessment showed an albuminocytologic dissociation with increased protein level (98 mg/dL, reference value: 8–43 mg/dL) and normal cell count (2 × 106/L, reference value: 0–8 × 106/L). Additional serological tests (i.e., ANA, anti-DNA, c-ANCA, p-ANCA, Campylobacter jejuni, Mycoplasma pneumoniae, Salmonella enterica, Cytomegalovirus, Epstein-Barr virus, herpes simplex virus 1 and 2, Varicella-Zoster virus, influenza virus A and B, human immunodeficiency virus) were negative. Normal serum vitamin B12 level and serum protein electrophoresis were found.
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| 5 |
+
Four days after neurological symptoms and signs onset, motor nerve conduction studies showed delayed distal latencies and absent F waves in early course, supporting demyelinating pattern in accordance with GBS diagnostic criteria . Sensory nerve conduction showed nerve action potentials; the recorded values were all in range, in line with the patient clinic.
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| 6 |
+
A diagnosis of Guillain-Barré syndrome was then made. Intravenous immunoglobulin was administered at a dose of 0.4 g/kg for 5 days. Thrombocytopenia and lymphocytopenia progressively returned in the following days, with complete resolution of the admission radiological pulmonary findings. The improvement of the respiratory and laboratory clinic was followed by a progressive recovery of limb strength and a return to osteo-tendon normoreflexia. Thirty days after hospitalization, following the negative result of the oropharyngeal swab for SARS-CoV-2, the patient was discharged to continue the rehabilitation program at home.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1234_en.txt
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+
A 63-year-old Caucasian woman presented to the outpatient cardiology office with dyspnea on exertion and weakness.
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| 2 |
+
Patient presented with recent onset dyspnea on exertion and weakness for 1-2 wk. Review of systems was positive for palpitations, fatigue and weight gain, but negative for chest pain, syncope, fever and cough.
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| 3 |
+
Past medical history included hypertension, hypothyroidism, right breast ductal cell carcinoma treated with mastectomy and breast implant, platelet granule disorder, asthma requiring chronic intermittent prednisone use.
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| 4 |
+
Physical examination revealed a regular pulse of 72/min, blood pressure 138/95 mmHg and body mass index 26.7 kg/m2. Cardiac examination revealed normal heart sounds without murmur or gallop. Her lungs were clear to auscultation. Bilateral trace pitting edema was noted at her ankles.
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| 5 |
+
Electrocardiogram (EKG) showed normal sinus rhythm with right bundle branch block (RBBB), unchanged from prior EKG. Thirty-day event monitoring showed 3 episodes of isolated supraventricular ectopics which represented < 0.1% of the total beat count. During hospitalization for community-acquired pneumonia, the patient developed symptomatic paroxysmal atrial fibrillation (AF) .
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| 6 |
+
Transthoracic echocardiogram showed a right ventricular (RV) mass, preserved RV function and a preserved ejection fraction of 60%-65%. A biopsy was not pursued given the high risk of bleeding due to platelet granule disorder. Cardiac MRI showed LHIS as well as well-defined capsular mass along the epicardial surface of RV free wall diffusely infiltrating the myocardium and mediastinal lipomatosis . No early or late enhancement of mass with gadolinium contrast was seen, suggesting a benign cardiac lesion. The characteristic features of the lesions in RV and IAS on fat suppression of the imaging provided a diagnosis of cardiac lipoma and LHIS respectively.
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| 7 |
+
Genetic testing for arrhythmogenic right ventricular dysplasia (ARVD) and 24-h urine cortisol test was negative.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1242_en.txt
ADDED
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| 1 |
+
A 61-year-old German woman presented to our orthopedic clinic after Felix IV fracture in revision total knee arthroplasty. Two years ago, the patient had undergone revision TKA with a rotating hinge prosthesis complicated by an intraoperative fracture of the tibial tubercle. Screw fixation had been performed, but 3 months later nonunion of the fragment had persisted, resulting in plate osteosynthesis with a one-third tubular plate. After another dislocation of the tibial tubercle, the patient presented to our clinic with anterior knee pain, loss of extension strength, and a feeling of rotational instability. On clinical examination, pressure pain of the proximal tibia, decreased extension strength to Janda 3/5, and inability to raise the extended knee were noticed. This maintained extensor function is the result of an intact medial and lateral retinaculum. The knee’s range of motion was 0–110° of flexion with preserved mediolateral and anterior/posterior stability. X-ray showed the rotation hinge prosthesis without loosening signs, the one-third tubular plate, and the dislocated tibial tubercle fragment indicating persistent Felix IV C fracture .
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| 2 |
+
Reconstruction of the knee joint’s extension system was planned. After preparation of the subcutaneous tissue, the dislocated tibial tubercle appeared surrounded by extensive metallosis presumably induced by the contact between the one-third tubular plate and the tibial prosthesis. Following the removal of the plate, the fragment proved to be necrotic requiring a total extirpation instead of mobilization and refixation. Subsequently, the ventral surface of the tibial prosthesis was exposed . Reconstruction of the extension system should be performed by the implantation of MUTARS attachment tube made of polyethylene terephthalate. Since the tibial prosthesis did not offer any connecting points for the synthetic graft, cement was used as an extender to simultaneously serve as fixing point and to preserve the prosthesis from loosening. Afterwards, the tube was doubled into a laminar sheet and fixed with two cancellous bone screws in the ventral tibia . ORTHOCORD sutures were used to attach the tube to the articular capsule still beyond the patella . Extensive jet lavage was performed before wound closure. Check of patellar tracking was promising; likewise, postoperative X-ray showed regular patella position .
|
| 3 |
+
To support the integration of the tube in the surrounding subcutaneous tissue, knee flexion was at first limited to 30° and then escalated to 60° and 90° every 2 weeks with full weight-bearing.
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| 4 |
+
Follow-up was performed after 3 and 10 months. On clinical examination , the patient showed irritant-free skin and soft tissue conditions; no redness or overheating; extension/flexion 0–0–110°; straight-leg raise completely possible; and force level 4/5 on side comparison of the knee stretchers. Active knee stretching with a flexed knee joint was possible without any problems. There was a centered patella run and no subluxation of the patella. Peripheral circulation, motor skills, and sensitivity were intact. X-ray confirmed correct implant position and central patella tracking . The patient was highly pleased by the restored extension function and significantly reduced knee pain.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1249_en.txt
ADDED
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A 15-year-old male presented to the emergency department with a 4-hour history of substernal chest pain and reported an episode of syncope lasting a few minutes. He also reported homicidal ideation and audiovisual hallucinations. The patient reported using “Spice”, a synthetic cannabinoid, repeatedly over the last few hours in order to maintain his euphoric mood. He used a vaporizer for consuming “Spice”. The patient was agitated and experienced audiovisual hallucinations instructing him to harm himself and others. He had no prior psychiatric or medical history. He denied drug allergies. Surgical and family history was unremarkable. Social history revealed that the patient was an emancipated minor, smoking a pack of cigarettes per day, drinking 3-5 beers per month, and a regular user of marijuana and synthetic cannabinoids. He also reported smoking crack cocaine once at age of 13. Physical examination revealed normal cranial nerve examination, tachycardia, hyperventilation, and an erythematous lesion resembling a canker sore in the lateral tongue with surrounding erythema. Blood pressure was 137/83 mmHg, temperature was 37.3 ºC, pulse rate was 75 beats per minute, and respiratory rate was 12 breaths per minute. Laboratory testing revealed no electrolyte abnormalities. Electrocardiography (ECG) showed ST segment elevation in leads V1, V2, V3, and V4, non-specific ST, T-wave changes, and T-wave inversion. Erythrocyte sedimentation rate (ESR) was mildly elevated. Cardiac enzymes were 3.2 ng/ml. Echocardiography revealed hypokinetic systolic dysfunction of the left side of the heart. Liver function tests were within normal limits. Aspirin was immediately administered to the patient and he was admitted to the cardiac catheterization lab, where no blockages in the coronary vasculature were seen. He was given a diagnosis of Takotsubo cardiomyopathy, after that catecholamine levels were seen to be elevated and urine drug screen was negative.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1251_en.txt
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A 67-year-old man with a history of intrinsic asthma, but who otherwise had very good health condition, was admitted to our intensive care unit with an acute asthma attack. Peripheral oxygenation saturation had been 80–89% without oxygen, and he then received supplemental oxygen, combined with inhalative salbutamol, as well as intravenous prednisolone, dimetindene, and ranitidine by an emergency physician at his home.
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On admission to the intensive care unit, the patient was still awake, but severely tachy- and orthopnoic. Oxygen, 4 l min−1, resulted in 95% SpO2, but blood gas analysis showed a respiratory acidosis (pH 7.29, pCO2 55 mmHg, pO2 84 mmHg, HCO3−26.4, BE −1.6). Chest X-ray was normal, but severe expiratory wheezing could be heard on both lungs. The patient was on theophylline and formoterole/budesonide. Other relevant comorbidities were diabetes type 2 treated with metformin and coronary heart disease (1-vessel disease). He repeatedly inhaled salbutamol, ipatropiumbromide, and budesonide and received intravenous prednisolone, reproterole (bolus plus continuous), and magnesium. The patient was directly put on non-invasive ventilation (NIV; EVITA-4, Draeger®), facilitated with a cumulative dose of 4 mg morphine. While at first sight, the therapeutic regimen seemed to work and an ongoing deterioration with increasing pCO2-levels and signs of respiratory exhaustion were recognized. The patient’s vigilance became more and more impaired, and respiratory acidosis was later accompanied by a slight metabolic acidosis (blood gas analysis before ECCO2R: pH 7.24, pCO2 61 mmHg, pO2 289 mmHg, HCO3−26.1, BE −3.0). Meanwhile, other possible contributing causes, like pneumonia, lung embolism, and cardiac attack, were ruled out.
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After careful consideration, and with the consent of the patient and his family, a ECCO2R system was prepared. Under non-invasive ventilation conditions and local anesthesia, a 22 French double lumen cannula (Twinport®, Novalung, Heilbronn, Germany) was placed in the right upper jugular vein under sonographic guidance. The system was started with a blood flow of 1 l min−1 and a sweep gas flow of 1 l min−1 oxygen, (ILA-activve®, Xenios, Heilbronn, Germany). Due to the respiratory effort of the patient along with hypovolemia, blood flow initially fluctuated between 0.6 and 1.5 l min−1. Fluid repletion was therefore conducted with balanced crystalloids combined with albumin to achieve a better intravascular effect. With the circuit running, a rapid improvement in almost all former deranged qualities was noticed: breath rate decreased from 40 to 16 per minute, SpO2 rose to 100%, and pCO2 was intentionally lowered very slowly (with 2 l min−1 sweep gas flow). Due to the sudden relief, the patient fell asleep for a few hours and NIV was down-graded to nasal oxygen (4 l min−1). Three hours after starting the ECCO2R circuit, blood gas analysis was normal (pH 7.39, pCO2 44 mmHg, pO2 93 mmHg, SpO2 97%, BE 1.2). On day two, the patient was put on oral prednisolone (50 mg day−1). There was no more dyspnea or wheezing and both, nasal oxygen and sweep gas flow, could be reduced. Early mobilization and physiotherapy was started the very same day. Thirty-four hours after initiating the ECCO2R system, the patient was completely weaned, and the cannula could be removed without any complication. On day 4, the patient could be discharged from the ICU without need for supplemental oxygen and 6 days later, he left the hospital without any impairment.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1275_en.txt
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A 47-year-old woman was transferred to our hospital complaining of abdominal pain. The pain was severe and accompanied by a loss of consciousness. She was known with chronic kidney disease and was on regular hemodialysis. On arrival at the hospital, her blood pressure was 93/67 mmHg, pulse 78 beats per minute, body temperature 36.7 °C, and Glasgow Coma Scale score of 13/15 (E3V4M6), with loss of consciousness. She had severe tenderness over the entire abdomen without rebound or guarding. An arterial blood gas analysis on room air showed a pH of 7.535, pCO2 of 28.1 mmHg, pO2 of 107 mmHg, HCO3 of 23.6 mmHg, base excess of − 5.1, and lactate of 10 mg/dl. Blood tests showed a mildly elevated white blood cell count of 10,950/μl, urea of 27.9 mg/dl, and creatinine of 5.59 g/dl, which was high for a dialysis patient, creatine kinase of 67 U/L, and C-reactive protein of 0.38 which was almost normal. Computed tomography (CT) revealed extensive portal vein gas and intestinal emphysema in the ileum and ascending colon. . The patient was diagnosed with NOMI and underwent emergency surgery. There was no intestinal fluid contamination in the abdominal cavity, but there was a moderate accumulation of serous ascites. The serosa of the ascending colon to cecum [Fig. A(a)] and terminal ileum [Fig. B(a)] were red in areas, but there was no obvious necrosis. Intraoperative ICG imaging with 5 mg intravenous ICG administration showed a granular distribution of the fluorescent dye (fine granular pattern) in the ascending colon to cecum [Fig. A(b)] and a poorly fluorescent lesion except around blood vessels (perivascular pattern) in the terminal ileum [Fig. B(b)] . Because the serosal side of the intestine was not grossly necrotic, we decided to manage the patient conservatively and only perform a second-look surgery if there were clinical, blood, and CT findings suggestive of necrosis the next day, and so bowel resection was not performed. Postoperatively, prostaglandin E1 was injected intravenously at 0.05 ug/kg/min. A contrast-enhanced CT performed the day after the surgery showed good blood flow in the ascending colon and ileum, and abdominal findings and blood tests had not worsened; therefore, a second-look surgery was not performed. Intraoperatively, the intestinal emphysema disappeared and the serous membrane color tended to improve, so postoperative open abdomen management was not performed and the abdomen was closed by conventionally. The acute postoperative course was uneventful; however, the patient required prolonged hospitalization for diabetes control. On POD 24, the patient suddenly passed a large quantity of bloody stool. An emergency colonoscopy revealed a longitudinal ulcer in the ascending colon to cecum , and a deep ulcer, with exposed blood vessels, in the terminal ileum . However, since there was no active bleeding, we decided to treat the patient conservatively with red blood cell transfusion alone, without emergency endoscopic treatment or surgery. On POD25, a large amount of blood was again found in her stool, and she went into shock. She received a massive blood transfusion and underwent an emergency laparotomy. The patient was in a state of shock and required urgent treatment. Although intravenous radiology was a treatment option, hemostasis by laparotomy was chosen, because the CT and endoscopy of the previous day showed that the bleeding site was in the terminal ileum, hemostasis by surgery was easy, and the patient was ready for surgery quickly. A large amount of blood in the colon and small intestine was seen through the serous membrane, suggesting a severe bleed. The terminal ileum wall 25 cm from the ileocecal valve was firm and thickened, but there were no obvious changes on the serous surface of the rest of the small intestine [Fig. B (a)]. The thickened terminal ileum was the most likely site of bleeding, and the mesenteric vessels in the area were first ligated to stop bleeding. Next, an incision was made in the terminal ileum, and intraoperative endoscopy was performed . This confirmed the presence of a deep longitudinal ulcer in the terminal ileum, where the origin of the bleeding was expected to be located [Fig. B(b)]. The extent of intestinal resection was determined after confirming that ulceration was present only in the terminal ileum and ascending colon to the cecum, with no ulcerative lesions on the oral side from the deep longitudinal ulcer in the terminal ileum . Right hemicolectomy including the terminal ileum of the bleeding ulcer lesion was performed and an ileo-transverse colon anastomosis was performed by hand. The resected specimen showed extensive mucosal erosion of the ascending colon to cecum and a deep longitudinal ulcer with exposed vessels in the terminal ileum . Thirty cm of the terminal ileum and 20 cm of the ascending colon to cecum was resected . Her postoperative course after the second surgery was uneventful, and she was discharged on the 28th day after the second surgery. One year after the surgery, NOMI, and intestinal bleeding had not recurred.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1291_en.txt
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A 54-year-old Caucasian Greek man presented to the Accident and Emergency department of our hospital with a 20-day history of abdominal pain, vomiting and loss of appetite. He mentioned an eight kg weight loss over the last 20 days, as he had been drinking almost exclusively water due to his symptoms. He had not presented to any hospital facility earlier because he lived in a remote area in the mountains. On admission, he had the septic image of paleness, tachypnea, tachycardia (110 beats/minute) and a fever of 38.5°C, as well as a rigid abdomen. Abdominal and plain chest X-rays demonstrated free gas under both the hemidiaphragms. After initial resuscitation (placement of intravenous lines and nasogastric tube followed by adequate administration of fluids), our patient underwent an emergency exploratory laparotomy. Our patient's worsening clinical image and his deteriorating clinical signs (tachypnea and tachycardia), along with the presence of his acute abdomen led us to conclude that an emergency laparotomy constituted the treatment of choice. In the face of the emergency situation a computed tomography (CT) scan was not performed. Laparotomy revealed peritonitis due to a perforated ulcer on the anterior wall of the duodenum, which was sutured, while the suture line was reinforced with an omental patch . After a thorough lavage of the peritoneal cavity, further exploration of the intra-abdominal organs revealed a second posterior pre-pyloric ulcer on the lesser curvature of the stomach, perforated into the lesser sac . A wedge resection with staplers was carried out , while no further acid reduction procedures were undertaken due to sepsis. A Nissen fundoplication was performed as an anti-reflux measure. Our patient recovered uneventfully and was discharged home on the 13th post-operative day; at this time we administered an appropriate eradication therapy. More specifically, we followed the protocol of triple therapy: a proton pump inhibitor, amoxicillin and clarithromycin were administered. After discharge our patient was referred to gastrointestinal specialists. Our colleagues planned a surveillance endoscopy according to their protocol.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1304_en.txt
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A 20-year-old female underwent deformity correction and spinal fusion surgery for presumed adult idiopathic scoliosis with posterior spinal instrumentation comprising pedicle screws and hooks extending from T3-T12 . The pre-operative assessment including an ECG did not demonstrate any abnormalities and her past medical history was uneventful while she had a normal level of physical activities including sports. The anesthetic and scoliosis surgery was uncomplicated with the patient maintaining good O2 levels and blood pressure while the intraoperative neuromonitoring showed stable motor and sensory potentials throughout. Her initial post-operative course was without incident until post-operative day 2 when she had episodes of acute de-saturation which prompted USG Doppler for bilateral lower limbs and computed tomography pulmonary angiography (CTPA). While both the studies ruled out any evidence of pulmonary embolism, CTPA revealed right heart strain pattern and an enlarged right side of the heart. A subsequent 2D echocardiography revealed a large atrial septal defect (ASD) which had remained asymptomatic up to that point. In addition, the CTPA demonstrated a lateral breech at the left T10 pedicle screw level with the screw tip being in close proximity to the aorta. A multidisciplinary team meeting was held where it was decided to prioritize cardiac management for ASD and keep the malpositioned screw under observation with removal planned for a later date. An ASD repair procedure was performed and this was uneventful with the patient making a good recovery.
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After recovery from the cardiac procedure, a repeat computed tomography (CT) scan was performed to plan removal of the screw; the CT scan showed the position of the left T10 screw in close vicinity of the aorta . To determine the exact position of the screw tip in relation to the aorta, an angiogram and an intravascular ultrasound was done which showed no evidence of intra-luminal extension of the screw tip. In addition, a transesophageal ultrasound was performed and this ruled out any extra-luminal contact with the aorta. Two years following the primary scoliosis correction, it was decided to proceed with removal of the spinal instrumentation with the vascular surgeon and intervention radiologists being on standby. The midline longitudinal scar was reopened and the spine was exposed across the previously operated segments from T3-T12. A solid posterior spinal fusion was noted across the previously operated levels which allowed the spinal instrumentation to be removed without compromising the surgical outcome of scoliosis correction. Intraoperative neuro-monitoring was used and the procedure was uncomplicated. The fusion mass was re-grafted using allograft bone. The patient was followed in our clinic for an additional period of two years during which there was no clinical or radiographic evidence of scoliosis recurrence.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1322_en.txt
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A 48-year-old Asian woman presented to an ear, nose and throat (ENT) surgeon at our facility with complaints of headache and bleeding from the right nasal cavity for 15 days. She was known to be hypertensive and was taking amlodipine and enalapril.
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Anterior rhinoscopy revealed a mildly deviated nasal septum and a right nasal polyp. A physical examination did not reveal any other abnormalities. There was no hepatosplenomegaly or lymphadenopathy.
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The results of a computed tomography (CT) scan showed a low-density lesion with a few areas of soft tissue density completely filling the right maxillary sinus extending to the middle meatus and posterior nasal cavity, with a widened antrum. There was no bony lesion. The radiological diagnosis was antrochoanal polyp.
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The results of all laboratory tests were normal. Subsequently, endoscopic polypectomy and middle meatal antrostomy were performed. Multiple irregular grey to dark brown soft tissue fragments measuring up to 3 × 2 × 1.5cm were sent to our histopathology laboratory. The culture from the surgical specimen was negative for fungus. A histological examination revealed mature adipose tissue mixed with hemopoietic cells . Hemopoietic cells are made up of trilineage elements: myeloid, erythroid and megakaryocytic cells .
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Based on this histomorphology, a hematological investigation including bone marrow aspiration and trephine biopsy were performed to rule out any underlying hematological disorders. Bone marrow aspirate and trephine biopsy were normocellular without fibrosis. Based on these findings, extra-adrenal myelolipoma was diagnosed. Our patient had an uneventful post-operative course and has remained disease-free at 36-month follow-up.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1332_en.txt
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Following a right radical orchidectomy and four cycles of chemotherapy for a metastatic non-seminomatous germ cell tumor of the testis, our patient, a 21-year-old man of Caucasian origin, underwent RPLND for a residual mass. The procedure was prolonged and in order to achieve complete surgical excision, a right radical nephrectomy and excision of the inferior vena cava from the iliac veins to the level of the left renal vein was necessary due to tumor infiltration and encasement.
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Three days postoperatively, the patient developed bilateral leg pain, lower limb oedema and abdominal distension secondary to abdominal ascites . This continued to worsen and on day nine postoperatively, he developed a paralytic ileus, pleural effusions and respiratory failure, and was transferred to the intensive care unit for elective intubation, ventilatory support and chest tube drainage of the pleural effusions .
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With fears that our patient would develop intra-abdominal compartment syndrome and that the respiratory compromise would be worsened, a 12 Fr pigtail drainage catheter was inserted under ultrasound guidance on postoperative day 22 into the abdominal cavity, immediately producing 11 litres of chylous fluid. Shortly after a drain was inserted, the respiratory compromise improved and the patient was extubated. The drain continued to maintain an output of six liters per day for a further four days before settling to an average output of between two and three liters per 24 hours. Conservative management consisted of a parenteral diet of medium chain triglycerides, diuretic therapy and 20% albumin three times a day. Daily intraperitoneal infusion of 200 mls of the water-soluble contrast medium Conray 280 mg I/ml (Iothalamate meglumine) in order to promote peritoneal lymphatic fibrosis was attempted but produced no real improvement. Blockage of the intra-abdominal drain necessitated its replacement on two separate occasions.
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On day 41, the patient was discharged to the ward where he maintained this improvement. Total parenteral nutrition was commenced to supplement poor oral intake. The patient had also developed bilateral foot drop on day 22 postoperatively. This was felt to be due to pedal oedema compressing each peroneal nerve at the head of fibula. It improved gradually with resolving peripheral oedema and physiotherapy. He was discharged to a peripheral hospital for further care on day 53, with an average output of 1.5 liters. Histologically, all the resected retroperitoneal tissue was free from residual tumor and contained only lymphoid tissue with large areas of necrosis.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1347_en.txt
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A 53-year-old Japanese man visited our hospital for a scheduled follow-up examination for uveitis due to BD. His best corrected visual acuity (BCVA) was 20/16 in both eyes. Intraocular pressure was 15 and 11 mmHg in his right eye and left eye, respectively. Slit lamp biomicroscopy with Goldmann three-mirror examination did not reveal active uveitis in either eye. Vitreous haze was graded as trace . Anterior chamber flare was evaluated based on the aqueous flare value measured with the Kowa FM-600® laser flare meter (Kowa Medicals, Nagoya, Japan) in photon counts per millisecond. Aqueous flare values measured with laser flare meter (LFs) were 12.6 and 7.6 photon counts per millisecond in his right eye and left eye, respectively; both were expected to be within normal range. An ultra-widefield (UWF™) high-resolution digital image (optomap®) was obtained with a Daytona imager (Optos, Scotland); no active uveitis lesions or vitreous opacity were detected . Spectral domain optical coherence tomography (SDOCT; RS-3000, Nidek Co., Ltd, Aichi, Japan) was used to analyze the macular lesion; no macular edema was observed.
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He had been diagnosed as having incomplete-type BD 11 years before. He was adequately treated with systemic corticosteroid and colchicine accompanied by occasional topical corticosteroids and mydriatics. Because his right visual function was disturbed by a preretinal membrane combined with vitreous opacity and secondary cataract in his right eye as a consequence of repeated bouts of severe uveitis, he underwent vitrectomy with inner limiting membrane peeling and phacoemulsification with intraocular implantation 2 years and 4 years after the diagnosis, respectively. Three years after the diagnosis he was given a systemic infusion of 5 mg/kg infliximab (Remicade®; Mitsubishi Tanabe Pharma Corporation, Osaka, Japan) every 8 weeks with no recurrence of uveitis attacks. He received no other treatments for BD besides the infliximab. He stated that his left eye had once shown mild intermediate to posterior uveitis, but that he had been completely stable since the commencement of systemic infliximab treatment.
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Four days after the scheduled follow-up examination, he returned to our hospital to receive his regularly scheduled systemic infusion of infliximab. At the visit, he complained of blurred vision in his right eye. BCVA was 20/25 and 20/16 in his right eye and left eye, respectively. Intraocular pressure was 17 and 11 mmHg in his right eye and left eye, respectively. LF was 72.0 and 6.2 in his right eye and left eye, respectively. Slit lamp biomicroscopy with Goldmann three-mirror examination revealed severe AAU and deteriorated aqueous flare in the anterior chamber, with anterior vitreous opacity that was shown by the silhouette against the retina in his right eye . Vitreous haze was graded as 2+. We did not observe any abnormal changes in his left eye (data not shown). SDOCT resulted in a cloudy image due to marked vitreous opacity, but we did not detect macular edema .
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He stated that 2 days prior he had received botulinum toxin (BOTOX®, botulinum toxin type A; GlaxoSmithKline K.K., Tokyo, Japan) 50 unit intracutaneous injections on both sides to treat axillary hyperhidrosis. Three hours after the injections, he noted severely increasing floaters and pain in his right eye. After he received the scheduled infliximab injection, however, he stated that the floaters and ocular pain in his right eye improved within a day. The severe vitreous opacity had attenuated considerably 1 month after the infliximab injection . BCVA was 20/16 in both eyes. Intraocular pressure was 10 and 9 mmHg in his right eye and left eye, respectively. LF was 31.1 and 26.3 in his right eye and left eye, respectively. Vitreous haze was graded as trace. Finally, LF was 15.2 and 14.6 in his right eye and left eye 3 months after the infliximab injection, respectively.
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After this event, he explained he had once received botulinum toxin injections in the same way last year. He received the scheduled infliximab injection 2 weeks prior. He felt no abnormality in both eyes, and a scheduled follow-up examination did not reveal active uveitis on that occasion.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1378_en.txt
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A 73-year-old woman with past medical history of hypertension and rheumatoid arthritis stage 4 under regular anti-hypertension medication and long-term corticosteroid therapy, presented to us in August 2010 with the chief complaint of decline of visual acuity of her right eye and right periorbital pain for 2 months. At the beginning of the clinical course, she had brain computed tomography (CT) scan and orbit magnetic resonance imaging (MRI) done in June 2010, which disclosed a small enhancing lesion, about 1.2 cm × 1.1 cm × 1 cm in size, near the right side orbital apex and adjacent right side superior orbital fissure with mild encasement of the right optic nerve, and this lesion showed mild extension to the adjacent right side posterior ethmoid sinus [Figure , ]. She had pulse steroid therapy in ophthalmology service, but it was ineffective. On admission, her neurological examination showed that she had right eye blindness, right ptosis, right ophthmaloplegia, and tingle in the territory of ophthalmic branch of right trigeminal nerve. Repeated MRI of orbit after admission in August 2010 showed the progression of the lesion which enlarged up to 1.5 cm × 1.3 cm × 1.2 cm [Figure , ]. She underwent endoscopic endonasal transethmoid approach with the removal of the lesion on 19 August 2010 under general anesthesia. After the surgery, she recovered well and her right periorbital pain was much released. However, 5 days after surgery, she experienced a severe headache followed by loss of consciousness. After endotracheal tube intubation and resuscitation, brain CT was checked which showed diffuse high-density acute SAH in the basal cistern, pre-pontine cistern, ambient cistern, quadrigeminal cistern, cerebellomedullary cistern, and right sylvian fissure, with acute hydrocephalus . Emergent external ventricular drainage was done followed by performing CT angiography which showed several bleb-like wide base aneurysms over right supraclinoid internal carotid artery (ICA), and one aneurysm, about 4 mm in size and located at the medial side of the right supraclinoid internal carotid artery, showed extravasation of contrast medium. The dome of the ruptured aneurysm projected medially and superiorly . On the same day, the histology examination reported that the lesion was composed of many fungal septate hyphae demonstrated on both HE stain and periodic acid-Schiff (PAS) stain [Figure , ]. Fungal infection was diagnosed and the culture turned out to be Aspergillus fumigatus. Her intracranial aneurysms were probably fungal aneurysms, which are one of the sequels of central nervous system (CNS) fungal infection. Unfortunately, after the event, she remained in deep coma and finally she expired due to central failure.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1384_en.txt
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This is a two-year-four-month old female, born by a primigravida. The girl was delivered at 39 week of gestation by the Cesarean section due to placenta failure. The girl was delivered with a general good condition, her Apgar score at 1 min after birth was 9 and she displayed features of intrauterine growth restriction (IUGR). Her birth weight was 1850 g (<3 percentile), height 44.5 cm (<3 percentile), head circumference 31 cm (<3 percentile). From day 7 on, the baby was exclusively breastfed which resulted in gradual weight gain. At 16 day, the baby girl weighed 2018 g and was discharged from hospital with a general good condition.
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At the age of three months, the infant was treated at the Paediatric ENT Department for suspected hypoacusis. The Auditory Brainstem Response (ABR) test performed in sleep revealed bilateral severe hearing loss. At follow-up ABR test, sensorineural hearing loss was confirmed. At the age of 4 months, she had a hearing aid placed.
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In her infancy, physical developmental delay was diagnosed – her weight and height were substantially below 3 percentile. Her psychomotor development was normal. The girl was able to sit at the age of 8 months and simultaneously she started to stand up and crawl. When she was 14 months old, she began to walk. She started talking when she was a thirteen-month-old. No abnormality was found in the MRI of her central nervous system.
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Low weight and height gains, some dysmorphic features (triangular-shaped face, prominent forehead, ocular depression, lipodystrophy at the lumbar region and around elbows led to suspicion of SHORT syndrome.
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Our patient presents most common signs and symptoms of SHORT syndrome except Rieger anomaly,insulin intolerance, hyperextensibility of joints and clinodactyly.
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The comparison of features typical of SHORT syndrome, with our patient’s features presents Table .
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While preforming molecular genetic testing, we have found a novel mutation in PIK3R1 -variant c.1956dupT (p.Lys653*) in exon 15 of PIK3R1 which is responsible for the symptoms in the patient.
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The variant has been confirmed to be de novo mutation (not present in biological parents) that has never been reported in the literature.
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At present, the patient is 2 years 4 months old and requires multi-speciality care. Her height and weight remain considerably below 3 percentile, though her psychomotor development is correct.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1397_en.txt
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A 61-year-old man was injured when his penis slipped out of his wife's vagina during penovaginal intercourse with penetration from behind (“doggy style”). His physician treated the penile swelling with hemostatic agents, but his symptoms worsened. When he presented to our institution, 13 hours had passed. Physical examination showed a swollen penis with an “eggplant” deformity caused by a hematoma on the distal ventral surface of the penis; he also had gross hematuria visible at the external urethral orifice . His past medical history was significant for benign prostatic hyperplasia, for which he was taking tadalafil.
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We ordered an immediate MRI; T2-weighted imaging revealed an isolated tear of the ventral tunica albuginea of the CS . We diagnosed a rupture of the CS with urethral injury and proceeded to the operating room. A 5-cm transverse incision of the epidermis just above the subcutaneous hematoma allowed us to remove as much blood and clot as possible. A 2-cm longitudinal injury of the tunica albuginea of the CS was visible, and the anterior urethra was ruptured; a 14-Fr urethral catheter was visible through the defect in the urethra . We repaired the tunica albuginea of the CS and the urethral mucosa using interrupted 3–0 and 4–0 absorbable sutures, respectively.
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The patient's postoperative course was unremarkable. We removed the urinary catheter on postoperative day 8, and the patient was discharged home. On postoperative day 17, he returned for follow-up. There was no discoloration or swelling of the penile shaft, and his erectile function had returned to his pre-injury status. Cystoscopy showed no obvious urethral stenosis or injury except for residual edema .
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1422_en.txt
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A 50-year-old man was referred to our institution with several years of right heart failure symptoms, AF, and liver disease of unknown aetiology. He was a fisherman and had contact with contaminated water in the past. He had lower limb oedema, significant ascites, jugular vein distention, and 3/6 pansystolic murmur heard loudest at the left lower sternal edge suggestive of tricuspid regurgitation. The patient came from the northeastern region of Brazil, where there is high prevalence of schistosomiasis. Considering the local epidemiology and the presence of hepatosplenomegaly, schistosomiasis was suspected. Due to the symptoms of right heart failure mentioned, cardiac investigations were performed as a primary cause of the liver disease.
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The electrocardiogram showed AF rhythm and there was cardiomegaly noted on chest radiograph, with gross enlargement of the right atrial shadow. Blood tests showed thrombocytopenia of 75 000/mm3 [normal values (NV): 150 000–400 000], normal renal function and liver enzymes, and brain natriuretic peptide of 198 pg/mL (NV ≤ 35). The TTE showed a left ventricle of normal dimensions with a preserved left ventricular ejection fraction (LVEF) (, ). However, the RV cavity was small secondary to a large homogeneous hypoechoic mass with evidence of severe tricuspid insufficiency, secondary to dilatation of the annulus, and severe tethering of the valve leaflets. Besides, the TTE exhibited an intracavitary thrombus adhered to the roof of the right atrium (RA; ; , ). The cardiac magnetic resonance (CMR) imaging showed severe RA dilation. This examination confirmed that RV had small cavity with reduced indexed end-diastolic and end-systolic volumes (38 and 13 mL/m2, respectively), normal systolic function (EF 65%), and moderate pericardial effusion . The late gadolinium enhancement sequence showed diffuse and heterogeneous subendocardial fibrosis in the RV apex . The patient was diagnosed with EMF and schistosomiasis by positive IgG ELISA and treated with praziquantel, but declined endocardiectomy. His heart failure symptoms improved on diuretics (furosemide 120 mg/day, spironolactone 50 mg/day, and hydrochlorothiazide 50 mg/day). In addition, the patient was commenced on warfarin with adequate international normalized ratio control for the presence of AF and thrombus.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1426_en.txt
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This case report describes to a Brazilian woman, 42 years-old, who presented with a renal failure and was submitted to haemodialysis for five years, before a kidney transplant, which occurred in 2007. After transplantation, the therapeutic regimen of immunosuppression included prednisone (5 mg daily), tacrolimus (5 mg daily) and azathioprine (50 mg daily). Dosage of serum tacrolimus was 5.8 ng/mL.
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The donor’s B19 status for this recipient was unknown. In December 2010, the patient developed significant anemia, which was resistant to erythropoietin (1,119.0 mUI/mL) and, eventually, required blood transfusion. After transfusion, the patient’s hemoglobin was 6.8 g/dL and her hematocrit was 20.2%.
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In April 2011, she presented cutaneous mucosa paleness, fatigue after minimal effort, arthropathy and malaise. She presented at the Hospital Felício Rocho, Belo Horizonte, MG, Brazil. Levels of hemoglobin and hematocrit were 3.6 g/dL and 10.3%, respectively. She received a transfusion of 600 mL of erythrocytes. Reticulocyte count was 7,200/mm3, leukocytes 4,100/mm3 and platelet 220,000/mm3. Dosage of serum creatinine was 2.3 mg/dL, iron (152 mcg/dL), transferrin saturation (89.9%), folate level (20.0 ng/mL), ferritin (938.6 ng/mL) and vitamin B12 (238.0 pg/mL), which did not suggest a nutritional or iron deficient anemia. Other laboratory investigations revealed she was seropositive for anti-Epstein-Barr (high IgG levels – 477.0 U/mL) and Cytomegalovirus (IgG positive) and negative for anti-hepatitis B, anti-hepatitis C and anti-HIV antibodies.
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At this time point, a bone marrow aspirate revealed hypocellular for red and white cells and platelets. Besides, there were dysplasia and megaloblastosis in the erythrocytic series, which were attributed to azathioprine associated with tacrolimus toxicity.
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A bone marrow biopsy was also obtained and showed severe hypoplasia of elements of the erythroid lineage, presence of larger cells with clear nuclei chromatin and eosinophilic nuclear inclusions, suggesting inclusions caused by B19. Nonetheless this evidence has indicated B19 infection, IgM and IgG assays were negative. However, as the symptoms and bone marrow biopsy were suggestive of B19 infection, a qualitative PCR testing for parvovirus B19 was performed, revealing the presence of this virus.
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The woman received 5 doses of intravenous gammaglobulin, 400 mg/Kg body weight daily, which improved the symptoms. A new evaluation revealed an important increase in hemoglobin, from 3.6 to 12.6 g/dL.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1429_en.txt
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In November 2006, a 36 years old male presented with severe plaque type psoriasis, to our hospital clinic. He has had psoriasis for the last 13 years; first it was localized to the scalp and periodically spread to other small areas of his body so he could control his disease with topical therapy. However, for the last six years the disease spread and covered the majority of his integument. He denied prior history of psoriatic arthritis. He had a positive family history of psoriasis, which affected his father, sister and paternal grandmother, but they all had a milder disease. His past treatments included various topical agents and several years ago he had a course of UVB with significant improvement, however he could not resume phototherapy because he lost his health insurance. Otherwise his past medical history was unremarkable. He had no known drug allergies and did not smoke. His current medications included over the counter iron pills. He denied any other systemic medications.
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Examination revealed severely erythematous scaly, excoriated thick plaques involving approximately 80% of his body surface area, and pitting of his nails. The rest of his physical examination was unremarkable. After completion of the screening tests which were within normal limits except from mild normocytic anemia (HGB = 12.0 gr/d) and elevated platelets count (470 × 103/mc, normal range 180-400 × 103/mc) and receiving informed consent he was treated with efalizumab (Raptiva) 0.7 mg/kg SC once weekly and subsequently 1 mg/kg as per label. Under treatment his skin condition has gradually improved. However, after 3 months of treatment he had started to complain of arthralgia first involving his right ankle and latter on extending to 2 fingers in both hands and eventually to his left ankle. Treatment with Ibouprofen 600 mg twice daily did not relieve his pain. X-ray analysis confirmed the diagnosis of psoriatic arthritis therefore treatment with Efalizumab was interrupted after 9 months. In addition during the 9 months of efalizumab therapy his platelets count rose substantially . Then, etanercept (Enbrel) 50 mg twice weekly was started. After an initial flare of his skin condition, which was expected after cessation of efalizumab, a significant improvement of both his skin and joints ensued. Interestingly during the sixteen months of etanercept treatment his platelets count returned to normal. But unfortunately due to health insurance coverage problems he had to stop etanercept and consequently his skin conditioned dramatically deteriorated and resembled his baseline condition when he first reported to our clinic. Therefore cyclosporine (Neoral) 200 mg twice daily was introduced for approximately 2 months till he received his insurance approval for adalimumab (Humira) and again his skin and arthritis gradually improved. His platelets count rose while being off etanercept and even when he was treated with cyclosporine and his skin condition started to improve his platelets counts remained persistently high and only after adalimumab was started they returned to normal values.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1441_en.txt
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A 65-year-old male Caucasian patient was admitted with respiratory distress and suspected non-Hodgkin's lymphoma. His medical history revealed arterial hypertension, diabetes mellitus type 2 and cholecystolithiasis.
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On clinical examination our obese patient (body mass index 41.5) suffered from dyspnea at rest. He presented with enlarged cervical and axillary lymph nodes, hepatosplenomegaly and diminished breath sounds over his right lung. A blood count revealed a leukocytosis of 35,000 leukocytes/μL of blood, with 80% partially atypical small lymphocytes and Gumprecht's shadow cells. Hemoglobin concentration and thrombocytes were within normal range. Immunophenotyping revealed that 67% of leukocytes were CD19+ B-lymphocytes, with co-expression of CD5, CD20, CD23 and a clonal restriction for the lambda light chain. This established the diagnosis of CLL. Bone marrow puncture demonstrated a medium degree of infiltration, with monoclonal B-cells beginning to replace the normal hematopoiesis.
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A chest X-ray was performed and showed a right-sided complete opacity suggesting a pleural effusion . Thoracentesis produced a milky pleural fluid . The cellular content consisted of 80% lymphocytes, two thirds of which expressed the B-CLL phenotype. Further analysis of the pleural fluid revealed triglyceride levels over 700 mg/dL and cholesterol levels below 70 mg/dL, establishing the diagnosis of chylothorax. Our patient received a pleural drainage, which initially produced nearly 3 liters of chyle per 24 hours. A computed tomography (CT) scan depicted enlarged lymph nodes in the cervical, axillary and mediastinal region, and suspected splenic involvement with several hypodense lesions. Taking the findings into account, our patient was diagnosed with a right-sided chylothorax caused by a concomitantly diagnosed CLL, stage Binet B or Rai II.
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The chylothorax represented a major complication of the CLL, and so immunochemotherapy consisting of fludarabine (25 mg/m2 on days one to three), cyclophosphamide (250 mg/m2 on days one to three) and rituximab (375 mg/m2 on day one) was initiated. Our patient received four courses, repeated every four weeks. Since the therapeutic effect of reduced dietary intake on chylothorax had been described previously, our patient received total parenteral nutrition for two weeks, starting with the first cycle of the immunochemotherapy. The chylous effusion disappeared nearly completely, and the chest drain could be removed after 10 days. After two weeks an enteral low-fat diet enriched with medium-chain triglycerides was started, to continue therapy on an out-patient basis. Unfortunately the chylothorax relapsed and thoracentesis of a volume of 1 L to 1.5 L once to twice a week became necessary. Due to the low-fat intake the appearance of the pleural effusion had changed from milky-white to clear amber-colored .
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| 5 |
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Our patient received four cycles of immunochemotherapy and regular thoracentesis on an out-patient basis. Since patients with protracted chylothorax are at risk of malnutrition and immunosuppression, our patient received antifungal and antiviral prophylaxis in addition to vitamin supplementation. However, the chylothorax persisted, despite a good clinical response of the CLL, with normalized blood counts and complete regression of the lymphadenopathy .
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In light of this, percutaneous radiotherapy of his mediastinum and thoracic duct, with an overall dose of 24 Gy, was initiated. Radiation induces an inflammatory response which can result in an obliteration of the disrupted thoracic duct . However, up to eight weeks after completion of the radiotherapy the chylothorax still persisted with continued requirement for regular pleural tapping.
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Finally our patient agreed to a surgical intervention. A supradiaphragmal ligation of the thoracic duct via a right muscle sparing thoracotomy was carried out. In addition, a decortication of his right lung was necessary because, during his surgery, a pleural fibrosis was diagnosed. The pleural fibrosis was most likely caused by the long-term chylothorax with repetitive thoracenteses. Our patient quickly recovered and the pleural effusions ceased completely. The time from the first diagnosis of chylothorax until the final surgical intervention was six months. Our patient is still in complete remission after 24 months of follow-up.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1455_en.txt
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A 62-year-old woman came to our center with extremely severe hydronephrosis and multiple right renal calculi found by annual physical check. She reported no renal colic, nausea or fever and had no current use of any medications. Her temperature was 36.7 °C, pulse 89 bpm, respiratory rate 18 bpm, and non-invasive blood pressure 130/57 mmHg. Unenhanced CT scan demonstrated extremely severe hydronephrosis and multiple right renal calculi with the largest diameter of 2 cm . Urine routine was positive for nitrites and leukocyte esterase, and microscopical examination showed + + + for leucocyte.
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After thorough examination, we performed prone-position mini-percutaneous nephrolithotomy under spinal anaesthesia. A single tract was created under the guidance of ultrasound to directly reach the median calyceal group. After the insertion of a guidewire, the channel was dilated to 16Fr with a fascia dilator. During the operation, swollen mucosa could hardly be seen through turbid purulent urine. Multiple golden stones embedded in the renal pelvis were fragmented with holmium laser and flushed out, and a considerable number of the stones were removed. After 2 h’ lithotripsy, the operation finished after successful indwelling of a 6Fr double-J stent and a 16 F nephrostomy tube.
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+
Two hours postoperatively, the patient complained of chilly and shiver. Her blood pressure dropped to 85/60 mmHg, and blood tests showed C-reactive protein 31.4 mg/L, White blood cell 9.55 × 109/L, D-dimer 570.0 ng/ml. Symptoms were relieved after empirically intravenous infusion of 300 mg biapenem bid and micro-pump injection with dopamine.
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| 4 |
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Three days later during the CT scan, the patient abruptly developed respiratory distress and loss of consciousness. Her blood pressure dropped to 76/45 mmHg, and oxygen saturation decreased to 85% under nasal catheter inhalation of oxygen. Clinical findings indicated the possibility of PE with shock. Supported by multi-channel intravenous rehydration, micro-pump injection with norepinephrine and mask oxygen inhalation, her blood pressure fluctuated between 108–124 and 65–78 mmHg. However, the patient still complained of dyspnea and chest pain, and her blood oxygen saturation remained unstable at an average of 92% under mask oxygen inhalation. Emergency laboratory tests showed a D-dimer of more than 3300 ng/ml. Considering the rising level of D-dimer and the patient’s clinical manifestation, we decided that PE might be the most likely diagnosis. Thus, we administrated anticoagulant therapy with 4000 U low molecular weight heparin (LMWH) at once and offered emergency CTPA, which revealed multiple embolisms in her left pulmonary artery and its branches . Meanwhile, doppler echocardiography showed that the patient’s left ventricular ejection fraction (LVEF) was 52% with severe tricuspid regurgitation, and experienced sonographers estimated that pulmonary arterial systolic pressure was about 40 mmHg (mild pulmonary hypertension). Doppler ultrasonography of lower limbs revealed intermuscular venous thrombosis in her left leg.
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| 5 |
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It was a contradictory situation with both the urgent need for thrombolysis therapy and the high vulnerability of surgery field bleeding. In order to solve the life-threatening problem first, our multi-disciplinary team administrated 50 mg of Alteplase ivgtt which was completed within 2 h for thrombolysis, and then transferred the patient to intensive care unit (ICU) for further life-supporting therapy. In order to prevent venous thromboembolism (VTE), 0.4 ml LMWH was subcutaneously injected every 12 h in ICU. Routine re-examination of the lower limbs venous ultrasonography and echocardiography was ordered to monitor the patient’s condition. Sonographers reported the remission trend of tricuspid regurgitation and pulmonary hypertension. Intermuscular venous thrombosis in her left leg could no longer be detected 6 days after the thrombolysis treatment.
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| 6 |
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On the 6th postoperative day, the patient suddenly developed unconsciousness and anhelation in ICU, and her blood oxygen saturation progressively dropped to 85%. Urgent intubation, mechanical ventilation and blood transfusion were applied to correct the patient’s anemia. Gradually, her oxygen saturation rose to 98%, but crimson and opaque drainage fluid kept flowing through her nephrostomy tube without any sign to stop even after clamping the catheter for 30 min. Her hemoglobin (Hb) level was still decreasing progressively . All the above clues were indicative of post thrombolysis bleeding. Diffused contrast medium in the middle and lower part of the right kidney was seen during DSA . SRAE was then performed under general anesthesia. The patient reported no obvious discomfort and generally recovered after conventional symptomatic treatment and blood transfusion. Anticoagulant treatment method was gradually changed to oral application of Warfarin 3 mg qn, and the patient was approved to be discharged 26 days postoperatively. She returned to her daily activity and reported no obvious discomfort, and during re-examination, the echocardiography showed LVEF of 70% with no obvious abnormality.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1464_en.txt
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A 74-year-old lady presented to our emergency department following 3 days’ history of watery diarrhoea and feeling generally unwell. She had been ‘off legs’ for 3 days and was not improving hence called the GP for a home visit. She was referred to the hospital as a case of severe sepsis for medical admission and pre-alerted into Resus by paramedics. She denied any cough, cold, or urinary symptoms. She had a past medical history of hypertension and CKD and was on Ramipril and Atorvastatin. She was at reasonably normal baseline health and 3 days back started with watery diarrhoea. There was no history of recent travel and no vomiting or per rectal bleed. On examination, she looked unwell, still responding to verbal commands, hypotensive at 80/50 mmHg, and tachycardic at 110 beats per minute with a temperature of 38.5 °C. She was hypoxic on air, with saturations of 90% on high flow oxygen. She had evidence of peripheral cyanosis and delayed capillary refill time. Her chest was clear and abdomen was soft, with no guarding or rigidity. Her Glasgow coma scale was 14 (E3V5M6). Her venous blood gas revealed metabolic acidosis with a lactate of 14.
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With a working diagnosis of severe sepsis of unknown source, she was started on broad-spectrum intravenous antibiotics and fluids. As there was no improvement in her haemodynamic status, a referral to the intensive care team was made for inotropic support.
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While all of these were being done, she was noticed to have a tender bruise on her leg; however, she denied any trauma or fall. On examination, she had a large area of blackish discolouration and vesicle formation on the posteromedial aspect of the left thigh , which was tender on palpation. The area looked suspicious of necrotising fasciitis. Her antibiotics were changed as per the microbiology advice to Tazocin and Clindamycin. A urinary catheter was inserted to monitor her fluid balance. An urgent referral to the surgical and orthopaedic team was made for definitive management of surgical debridement. Her initial blood results showed a white cell count of 13.1 and neutrophilia at 11.7. She had a CRP of 439, CPK of 4187 and an AKI stage 3 with urea at 15.2, creatinine of 291 and e-GFR of 13. Serum electrolytes showed a sodium of 137, potassium of 3.4 and chloride of 101.
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She underwent debridement of necrosed tissue within few hours of arrival into the emergency department. She subsequently stayed in the intensive care unit and had a further debridement and above-knee amputation of the affected limb . On the second surgery, she was found to have necrotic tissue extending up to the pelvis. A subsequent pus culture report confirmed group A Beta haemolytic streptococci as the causative organism. The blood culture showed no growth, and faeces culture was negative and showed no evidence of Salmonella, Shigella, Camplylobacter or Escherichia coli. MRSA was not isolated and there was no evidence of C-difficile in the stool.
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She eventually died after about 48 h of hospital stay despite an early diagnosis and prompt surgical debridement.
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Although necrotising fasciitis is a rare condition, each one of us may still come across a case in our clinical practice. As a learning point from this case, we would like to highlight the importance of a thorough clinical examination of patients with sepsis with no obvious source. As in this patient, the presenting complaint was diarrhoea, which was actually a manifestation rather than a cause for sepsis and clearly had a hidden diagnosis, which could have been missed if the patient was not adequately exposed.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1499_en.txt
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We evaluated a 28-year-old African-American woman with a history of myoclonus and epilepsy. She was born at term from an uncomplicated vaginal delivery, with initial normal development. A teacher noticed “hand tremors” at the age of 4 years. She had normal socialization and a mild learning disability but was able to finish high school and start college. At the age of 13, she developed her first generalized myoclonic seizure, followed by multiple episodes of early morning focal onset seizure with secondary generalization and additional episodes of generalized myoclonic seizures. She was treated with zonisamide and then topiramate with good control of the seizures. A previous EEG showed diffuse excessive fast activity. Brain MRI showed mild cerebellar atrophy .
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The “hand tremor” was later identified as myoclonus and worsened during her high school years, with prominent involvement of her upper limbs. She was treated with clonazepam with moderate benefit. At her last evaluation, she displayed multifocal myoclonus at rest, mostly involving her face and distal upper limbs, mild action myoclonus at target, and no clear stimulus sensitivity. There were only very mild cerebellar signs (including mild saccadic pursuits, dysdiadochokinesia, and appendicular dysmetria) with no significant gait impairment . Patient’s cognitive profile was not formally assessed but she presented a decline over the years affecting her school career. Her parents were both from Antigua. There was no consanguinity in the family and no family history of seizures or other neurological conditions. Written authorization for the acquisition of the video for publication for scientific purposes was signed by the patient.
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Previous genetic testing, including 21 genes of progressive myoclonic epilepsy and Dentatorubro-Pallidoluysian Atrophy (DRPLA) expansion, were negative. Targeted gene testing of NUS1 revealed a novel missense mutation of the NUS1 gene, c.868C>T (p.Arg290Cys), initially classified as a variant of unknown significance (VUS). The variant was not found in large population datasets and was absent in her parents (de novo). Therefore, the p.Arg290Cys was re-classified as likely pathogenic (ACMG criteria: PM1, PM2, PM5, PM6, PP3). This variant affects the same residues reported in previous cases of CDG with recessive mode of inheritance (p.R290H). We hypothesize that the different aminoacidic change in our case (p.R290C) may have a more profound impact on an important domain of the NUS1 protein due to the biochemical differences between Arginine and Cysteine, compared to Arginine and Histidine.
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| 4 |
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To the best of authors’ knowledge and as per Genetic Testing Registry (GTR, ) there are no gene panels for the myoclonic epilepsy in the US that include NUS1.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1520_en.txt
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A 48-year-old woman with a non-tender firm mass in the right breast was admitted to an affiliated hospital of Shahid Beheshti University of Medical Sciences in September 2008. A palpable and immobile mass in the lower outer quarter of the right breast, approximately 3.0 cm in diameter, was revealed on examination. The mass was not attached to the skin and there was no lymph node enlargement, nipple inversion, or mass in the opposite breast. A 3.5 × 1.5 cm tumor in the lower outer part of the right breast was reported by ultrasound . So we suspected it was a breast tumor and it was surgically removed (Lumpectomy). She underwent Sentinel lymph node biopsy and stage II A invasive ductal carcinoma of the right breast with no lymph node metastasis was reported by pathological examination. Immunohistochemistry showed that the tumor was estrogen receptor positive, progesterone receptor positive, and human epidermal growth factor receptor negative.
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The patient received adjuvant treatment with 8 cycles of chemotherapy (4 cycles of adriamycin and cyclophosphamide, and 4 cycles of docetaxel), followed by 25 fractions of radiotherapy and because the patient’s mass was pathologically estrogen positive, the patient was eligible for adjuvant hormonal therapy. The patient was regularly monitored for breast cancer and had no problems. In March 2023, the patient’s routine laboratory test results were as follows: WBC = 22,000 (lymphocyte = 55%), hemoglobin = 13, platelet = 180,000, BUN = 15, creatinine = 1.0, ALT = 20, AST = 25, ALK = 160, and LDH = 420. The patient did not mention B symptoms (fever, weight loss, or night sweats) and the clinical examination was normal. Due to leukocytosis with a lymphocyte predominance, peripheral blood flow cytometry was performed on the patient, and the results were as follows: HLA-DR: 84.5%, CD3: 10%, CD4: 5%, CD5: 96%, CD19: 89.5%, CD20: 89.6%, CD23: 34.8%, CD45: 85%, Cd5/CD19: 89.
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The patient was diagnosed with chronic lymphocytic leukemia (B-CLL). Abdominal and pelvic ultrasound showed no pathological findings and based on the absence of B symptoms and disease symptoms as well as other routine laboratory tests, the patient was followed up. In July 2023, the patient had vague abdominal pain, so a comprehensive examination, tests and an abdominal and pelvic ultrasound were performed. The abdominal ultrasound detected a 3.5 cm lesion in the right kidney. To examine the lesion in more detail, we recommended computed tomography (CT) with and without contrast, and a 4 cm mass with enhancement and necrosis was reported . Based on the history of CLL, we recommended an ultrasound-guided core biopsy of the renal mass. The patient's pathology confirmed RCC . After consulting with the urology department, the patient underwent a partial nephrectomy. Postoperative pathology also confirmed clear cell RCC. The patient is being monitored periodically for renal tumors and CLL, and her general health condition is good.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1537_en.txt
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A 67-year-old male farmer presented to the Ophthalmology Unit of Obafemi Awolowo University Teaching Hospitals Complex in Ile-Ife, Nigeria, with a two-week history of pain, mucopurulent discharge and redness in the right eye. There was no history of foreign body entry into the right eye, nor was there ocular trauma or instillation of traditional eye medication. The patient had earlier used chloramphenicol eye drops which he obtained over the counter. His fasting blood sugar, complete blood count and electrolyte urea and creatinine were essentially normal for his age. The patient’s HIV status was negative on serology testing.
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| 2 |
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Further, ocular examination revealed a visual acuity of hand movement in the right eye, unaided and aided. Slit lamp biomicroscopic examination of the right eye showed a diffuse conjunctival hyperemia and a 5.5 x 4 mm corneal ulcer with raised and irregular margins which stained with fluorescein . Whitish stromal infiltrates were present in the ulcer bed and around the ulcer margins with associated stromal oedema and folds in the Descemet’s membrane. Anterior chamber examination revealed hypopyon of about one-eighth of the anterior chamber height. Pupil was round but sluggishly reactive to light and there was early lens opacity and no glow on fundoscopy in the right eye. Ocular findings in the left eye were essentially normal. A presumptive diagnosis of infective keratitis was made. During the slit lamp biomicroscopy, corneal scrapings were taken from the margins and the base of the ulcer and were sent to the microbiology and parasitology laboratory for bacterial and fungal tests. Direct lactophenol cotton blue mounts revealed septate fungal hyphae, while direct Gram stain showed cellular debris but no microorganisms. Culture on chocolate agar yielded scanty growth of cottony white colonies after 48 hours of incubation at 37°C. However, culture on Sabouraud dextrose agar at room temperature supported growth of woolly mould with reddish brown pigmentation on the agar after 48 hours . Lactophenol cotton blue staining of the mould under light microscope (x400 magnification) revealed conidiophores consisting of phialides, arranged in brush-like structures. Moreover, the phialides were cylindrical with small collarettes producing hyaline, smooth-walled conidia, which were arranged in masses. The macroconidia were septate, cylindrical with rounded apex and flat base . No bacteria were seen. The morphology of the mould identified was consistent with C. lichenicola.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1540_en.txt
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A 23-year-old Sri Lankan man, who had been working as a motor mechanic for approximately 5 years, presented to our hospital with a 2-month history of progressive, yellowish discoloration of the eyes; bilateral ankle swelling; and abdominal distention not associated with right hypochondrial pain, pruritus, or fever. His past medical history was unremarkable except for being prescribed furosemide by a general practitioner for edema. He denied intake of any other drugs, health supplements, or herbs. He had no history of smoking and only occasionally consumed alcohol in safe amounts (within Asian standard <14 U/week). His last alcohol consumption had been several months prior to the onset of symptoms. He had no family history of chronic liver disease. He had worked in a garage as a motor mechanic and used to remove gasoline from carburetors by sucking using his mouth when suction pumps were not available. He did not practice proper mouth washing and used to swallow petroleum compounds in substantial amounts during most of his working days. He had continued this malpractice for nearly 5 years until he developed symptoms.
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| 2 |
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His clinical examination revealed icterus and ankle edema with nontender hepatomegaly and moderate ascites. The results of the rest of his clinical examination were normal. His laboratory data were as follows: hemoglobin 12.2 g/dl, white blood cell count 8920/mm3, platelet count 204,000/mm3, erythrocyte sedimentation rate 16 mm at the end of the first hour, aspartate aminotransferase 190 U/L, alanine aminotransferase 45 U/L, alkaline phosphatase 465 U/L, γ-glutamyl transpeptidase 72 U/L, total bilirubin 26.4 mg/dl (direct bilirubin 12.8 mg/dl), total protein 58.4 g/L (albumin 23.2 g/L, globulin 35.2 g/L), prothrombin time 19.8 seconds (international normalized ratio 1.67), and serum creatinine 0.9 mg/dl. His laboratory results were negative for anti-hepatitis A virus (HAV) immunoglobulin M antibody, anti-HAV immunoglobulin G antibody, hepatitis B surface antigen, anti-hepatitis C virus antibody, human immunodeficiency virus (HIV) antibody and antigen, antinuclear antibody, anti-smooth muscle antibody, and antimitochondrial antibodies. His levels of serum ferritin, serum copper, and serum ceruloplasmin were within normal ranges. The result of slit-lamp biomicroscopy was normal. Abdominal ultrasonography revealed hepatomegaly with a coarse hepatic echotexture suggestive of cirrhosis, portal hypertension, and moderate ascites without focal liver lesions. Esophagogastroduodenoscopy revealed small esophageal varices with portal hypertensive gastropathy. His liver biopsy revealed evidence of cirrhosis with regenerating hepatocytes, but with no clue to the underlying etiology of his liver disease .
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The patient was managed conservatively with symptomatic treatment. His regular medications included ursodeoxycholic acid, spironolactone, furosemide, lactulose, and carvedilol. His symptoms and laboratory parameters gradually improved during his hospital stay and stabilized over several weeks . He was able continue his regular occupation with cautious handling of petroleum compounds. Given his advanced Child-Turcotte-Pugh (CTP) class C (CTP score 10/15) and high Model for End-Stage Liver Disease score (25), he is currently being worked up for a live-donor liver transplant.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1556_en.txt
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A 59-year-old woman born in Southern Italy was admitted to our ward in March 2020 after experiencing malaise, nausea, vomiting and fever lasting about a week. Chest x-ray showed bilateral basal interstitial pneumonia and SARS-CoV-2 RT-PCR in a oropharyngeal/nasal swab resulted positive. Since arterial pO2 was 57 mmHg, she was started on high-flow supplemental oxygen support. The patient reported chronic treatment with low dose prednisone for adult Still’s disease since 2010 and atenolol for hypertension.
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Treatment with hydroxychloroquine, lopinavir/ritonavir, and dexamethasone was started together with enoxaparin prophylaxis. On the 5th day of hospitalization due to severe hypoxia and worsening of respiratory performance, she underwent non-invasive mechanical ventilation with continuous positive airway pressure (CPAP), which was continued for a total of 11 days. On day 7th she was treated with two doses of tocilizumab 8 mg/kg 12 h apart. Dexamethasone treatment was given at the dose of 20 mg/day for 5 days, followed by 10 mg/day for other 6 days. During the hospitalization, she presented an episode of atrial fibrillation, which was successfully reverted by amiodarone, and hyperglycemia, for which she started insulin-based treatment, later switched to oral hypoglycemic agents. Overall her clinical condition gradually improved, and she completed oxygen weaning on day 27th of hospitalization.
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On day 25th her eosinophil absolute count (EAC) increased up to 5540 cell/µL and the patient reported abdominal pain and itching. Stool examination revealed the presence of rhabditiform larvae of S. stercoralis, while IFAT serology tested positive at a titre of 1:640. A 4-day oral treatment with ivermectin (200 mcg/kg) was administered, with a rapid decrease of eosinophil cell count and symptom improvement. She was discharged and a follow-up visit 1 month later was scheduled to check EAC, serology for S. stercoralis and stool examination.
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The patient did not develop fever or worsening clinical condition concomitant to EAC rising. She denied travelling to tropical or subtropical areas and revealed recent moving to Lombardia region from Calabria region (Southern Italy). She reported repeated episodes of diffuse itching in the last 10 years, treated with topical steroids with partial improvement.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1591_en.txt
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Our patient was a 20-year-old Arabic Middle Eastern woman. She was not known to have any medical illness. She had had two previous uneventful pregnancies with uncomplicated vaginal deliveries. Her only antenatal visit to our hospital was at 38 weeks of gestation, when she presented in early labor. Her general physical examination was unremarkable. An ultrasound (US) scan showed a cephalic, normally grown fetus with decreased amniotic fluid. The patient’s whole blood platelet count was 182 × 109/L, white blood cell count (WBC) was 11 × 109/L, and whole blood hemoglobin (Hb) was 116 g/L. Her blood group was AB positive.
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On vaginal examination, she was found to have a 3-cm dilated, 80% effaced cervix and intact membranes. She was augmented with artificial rupture of her membranes and syntocinon intravenous infusion. Six hours later, she had an uneventful vaginal delivery of a healthy male newborn weighing 3.06 kg. The baby’s Apgar scores at 1 and 5 minutes were 8 and 9, respectively.
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On the morning of her first postpartum day, the patient complained of a nonpruritic maculopapular skin rash over her upper limbs , abdomen , and back. It appeared suddenly as patchy lesions. It was not associated with pustules or vesicles. Her neck, face, and the palmar aspects of her hands and lower limbs were spared. There were no noticeable striae over her abdomen. She was not known to have any allergic reactions, and she did not receive any medications that could explain the findings. Twelve hours later, she was feeling very unwell and tired. She then developed generalized abdominal pain that increased in severity and was associated with nausea and occasional vomiting. Her vital signs were normal (blood pressure [BP] 120/70 mmHg, pulse rate 83 beats/minute, and oral temperature 37.1 °C). Her urine was yellow and turbid with 3+ proteinuria, and she had numerous WBC/high-power field (HPF) but no glycosuria. The same result was confirmed by testing a second urine sample that was obtained via a Foley catheter. A dermatologist’s review indicated nonspecific maculopapular skin rash, and the dermatologist advised only observation with no specific therapy but to investigate further. This advice alerted the medical staff to do further testing, which showed that her liver function, kidney function, whole blood count, serum glucose, serum lactate dehydrogenase (LDH), and coagulation profile were within normal limits.
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| 4 |
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Day 2 postpartum was marked by persistence of nausea and vomiting and a decrease in the intensity of skin rash. On day 3 postpartum, she had nausea, vomiting, and abdominal pain. Her skin rash showed a further decrease in intensity. She was very sick, pale, and jaundiced with epigastric and right upper quadrant abdominal tenderness. Her vital signs were stable. Investigations were repeated and showed thrombocytopenia (platelet count 54 × 109/L), hypoglycemia (serum glucose 2.11 mmol/L), renal impairment (serum creatinine 228.75 μmol/L), impaired liver function (serum alanine aminotransferase [ALT] 0.735 μkat/L, serum aspartate aminotransferase [AST] 1.15 μkat/L, serum LDH 19.8 μkat/L, serum total bilirubin 68.4 μmol/L, serum direct bilirubin 58.15 μmol/L), and coagulopathy (plasma prothrombin time [PT] 22 seconds, control 14 seconds, blood partial thromboplastin time [PTT] 36 seconds, control 26 seconds, international normalized ratio [INR] 1.85) with normal urinalysis and normal plasma d-dimer and fibrin degradation products.
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| 5 |
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Acute fatty liver was suspected, and the patient was admitted to the ICU in the evening. In the ICU, her blood Hb was 88 g/L (dropped from 105 g/L), and her blood platelet count was 51 × 109/L. Internist, hematologist, and anesthetist consultants were involved in her care. Septic workup was done, including urine and blood cultures, as well as high vaginal and endocervical swabs for culture and sensitivity. Because she was critically ill in the ICU with too many intravenous catheters and an indwelling urinary catheter, and because patients with AFLP are at risk of infection, a decision was taken by the multidisciplinary team to start her on a renal dose of imipenem/cilastatin. She was kept on intravenous fluid, normal saline (N/S) 100 ml/hour, and dextrose infusion. Five units of fresh frozen plasma (FFP), 5 U of cryoprecipitate, and 2 U of packed red blood cells (PRBCs) were given.
|
| 6 |
+
On the fourth day postpartum, the patient had persistent nausea, vomiting, and epigastric and right upper quadrant abdominal pain. Her vital signs were stable. She was jaundiced. Her skin rash had significantly decreased in distribution and intensity. She had a strict fluid input-output observation. Her urine output remained around 45–60 ml/hour. Her investigations showed anemia and thrombocytopenia (blood Hb 79 g/L and blood platelet count 44 × 109/L), acute renal impairment (serum creatinine 316.4 μmol/L), very high serum LDH (19.7 μkat/L), elevated serum ALT (0.77 μkat/L), and elevated serum AST (1.52 μkat/L) with elevated serum direct and total bilirubin. Her serum glucose was 3.38 mmol/L (on dextrose infusion), and her total serum bile acids level was normal (6 μmol/L). Blood film showed hypochromic microcytic anemia, few schistocytes and acanthocytes, neutrophilia with toxic granulation of neutrophils, a majority of neutrophils that were hypersegmented, and thrombocytopenia. She received 2 U of PRBCs, 2 U of FFP, and 4 U of cryoprecipitate and was started on dexamethasone 4 mg intravenously every 8 hours.
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| 7 |
+
In the afternoon, after transfusion of blood and blood products, her blood platelet count was 38 × 109/L, blood Hb 97 g/L, and blood WBC 14.9 × 109/L. Other tests revealed plasma PT 17.5 seconds, blood PTT 29.7 seconds, and INR 1.4 (corrected by the infusion of the blood and blood products).
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| 8 |
+
An abdominopelvic computed tomographic (CT) scan without contrast enhancement revealed only hyperdense free fluid (ascites). A chest x-ray (CXR) showed congestive pulmonary changes and blunted bilateral costophrenic angles. She was started on furosemide 20 mg intravenously every 4 hours, intravenous fluid dextrose 25% 50 ml/hour, and N/S 0.9% 50 ml/hour.
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| 9 |
+
On the fifth day postpartum (the third day in the ICU), the patient still felt unwell with epigastric and right upper quadrant abdominal pain and recurrent attacks of hypoglycemia. She had no skin rash at all. She had normal BP readings with mild epigastric and right upper quadrant tenderness. Her laboratory tests showed anemia, thrombocytopenia, hypoglycemia, leukocytosis, renal impairment, hyperbilirubinemia, and elevated serum LDH. Urinalysis showed 1+ proteinuria and hematuria. The result of a viral hepatitis screen was negative.
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| 10 |
+
An abdominal U/S scan showed a marked amount of free fluid in the abdomen, liver span 17 cm, spleen span 14 cm, and a normal hepatobiliary tree with no stones or dilatation. A CXR was normal. She was given 5 U of FFP and kept on the antibiotic because of the ascitic fluid.
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| 11 |
+
On the sixth day postpartum (fourth day in the ICU), the patient showed significant clinical improvement with stable vital signs (V/S). Her blood tests showed persistent anemia, thrombocytopenia, leukocytosis, elevated serum creatinine, elevated serum LDH, mild elevation of serum bilirubin, normal serum glucose, and normal liver enzymes and coagulation. A repeat blood film showed hypochromic microcytic anemia with mild anisocytosis, neutrophilic leukocytosis, few hypersegmented neutrophils and thrombocytopenia with large forms. She was prophylactically given 5 U of FFP as suggested by the multidisciplinary team.
|
| 12 |
+
On the seventh day postpartum (fifth day in the ICU), the patient started to show much clinical improvement (very mild nausea, occasional vomiting, and mild abdominal pain) with stable V/S. Blood tests showed Hb 98 g/L, blood platelet count 60 × 109/L, blood WBC 16 × 109/L (76% neutrophils and 16% lymphocytes), serum glucose 6.1 mmol/L, serum creatinine 251.6 μmol/L, serum urea nitrogen 52.1 mmol/L, and serum LDH 11.6 μkat/L with normal electrolytes and liver enzymes.
|
| 13 |
+
A CXR showed reticular shadowing bilaterally, a blunt left costophrenic angle, and a clear right costophrenic angle, which further supported the continuation of the antibiotic. She was given 4 U of FFP.
|
| 14 |
+
On the eighth day postpartum (the sixth day in the ICU), the patient was very well with no nausea, vomiting, or abdominal pain. Her dextrose infusion was disconnected. She was started on oral intake of fluids. She remained normoglycemic. She was prophylactically given 5 U of cryoprecipitate, 5 U of FFP, and 2 U of PRBCs for of her mild thrombocytopenia and anemia. In the evening, repeat blood test results were normal apart from mild elevation of serum creatinine. A decision was taken to discharge her from the ICU.
|
| 15 |
+
On the ninth day postpartum (the first day in the obstetric ward), the patient was very well with no complaints. She resumed breastfeeding in addition to artificial supplement. Her laboratory test results were normal. Her full septic workup result was negative. Imipenem/cilastatin was discontinued.
|
| 16 |
+
On the tenth day postpartum, the patient was very well and had no complaint. The results of her blood tests were normal apart from very mildly elevated serum creatinine.
|
| 17 |
+
The patient’s 11th postpartum day was unremarkable; she had no complaints and normal laboratory test results.
|
| 18 |
+
On the 12th day postpartum (4th day in the obstetric ward), the patient was very well with stable vital signs and no complaints. She had normal serum glucose, normal serum electrolytes, and normal liver enzymes and serum bilirubin (total and direct). Her serum LDH was 10.1 μkat/L, blood Hb 105 g/L, blood platelet count 584 × 109/L, blood WBC 11.6 × 106/L, and serum creatinine 1.43. In the afternoon, she was discharged to home receiving no medications.
|
| 19 |
+
The patient was seen in the clinic 1 week later. She was doing well with no complaints and was seeking contraception.
|
| 20 |
+
One month later, she and her baby were doing well with no complaints. In the clinic, she had an intrauterine contraceptive device inserted. The chronological order of her symptomatology and laboratory results are shown in Tables and , respectively.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1603_en.txt
ADDED
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A 57-year-old Caucasian woman reported a decrease in visual acuity for 2 weeks. Her best-corrected visual acuity for her right eye was 20/20 and for her left eye 20/100. A slit-lamp examination and intraocular pressure were unremarkable in both eyes. Fundus examination of her left eye revealed temporal intraretinal infiltrates and vitreous opacities . Her right eye was unremarkable.
|
| 2 |
+
Fluorescein angiography showed hyperfluorescence of her optic disc, leakage along the vessels, and chorioretinal hyperfluorescent infiltrates . The diagnosis of OT was based on the typical morphology of her ocular lesions and a positive serological testing for Toxoplasma gondii (immunoglobulin G concentration = 537IU/mL).
|
| 3 |
+
She was treated with clindamycin (Clindamycin® H) 4 × 300mg daily over 3 days without any significant improvement of visual acuity. On the fourth day of hospitalization, she received 100mg prednisolone-21-hydrogensuccinate (Solu-Decortin® H) intravenously in addition to her treatment with clindamycin (Clindamycin® H). Within 2 minutes she developed an acute erythema, particularly of her legs and abdomen , angioedema, hypotension (blood pressure 80/40mmHg), tachycardia (heart rate 140/minute), hyperthermia (38.8°C), and respiratory distress. Subsequently, she was transferred to the Intensive Care Unit to be monitored and treated with clemastine fumarate (Tavegil®), ranitidin (Ranitic®), and intravenous fluids. After 1 hour she recovered and after 12 hours she was transferred back to the ophthalmological ward. Her erythema and angioedema persisted for 32 hours. She had no history of previous steroid use. Subsequent allergy testing was conducted after 3 months in the Department of Dermatology in our hospital. The testing showed a positive skin-prick test for prednisolone and methylprednisolone in the form of a 5mm wheal, and negative results for dexamethasone and hydrocortisone , which confirmed her suspected allergy to prednisolone. Because of her allergic reaction to class A (prednisone-type) corticosteroids and possible complications due to cross-reactions to class D2 (prednicarbate-type) corticosteroids, we avoided any further treatment with systemic or intravitreal corticosteroids.
|
| 4 |
+
In addition, an oral exposure test with a step-by-step elevation of doses up to 2.0mg of dexamethasone (Fortecortin®) and 1.5mg betamethasone (Celestamine®) was conducted to find alternative corticosteroids for future treatments. For both substances, no local or systemic side effects were observed.
|
| 5 |
+
After 1 month of treatment with clindamycin (Clindamycin® H) monotherapy without any increase in visual acuity, the patient underwent a vitrectomy with balanced salt solution filling because of heavy vitreous opacities, and to obtain a sample of the vitreous body. The polymerase chain reaction (PCR) on the sample was positive for Toxoplasma gondii.
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| 6 |
+
The postoperative examination of her left eye revealed chorioretinal scars and infiltrates . Her right eye was still unremarkable. Fluorescein angiography of her left eye also revealed hyperfluorescent intraretinal infiltrates of the temporal hemisphere and a scar of the inferotemporal retinal vein branch . Her visual acuity recovered to right eye 20/20 and left eye 20/40.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1628_en.txt
ADDED
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A 20-year-old nulliparous woman presented to our gynecologic department because of intermittent abdominal pain and a 3-month history of dysmenorrhea. She had a history of 2 right ovarian teratomas that were managed surgically. At the age of 16 years, she experienced lower abdominal pain for 2 weeks. A subsequent pelvic sonography showed a complex, right ovarian cyst, of approximately 5.36 × 4.3 cm in size; her carbohydrate antigen (CA) 125 level was 23.4 U/mL (normal, 0–25 U/mL, at our hospital). We performed a laparoscopically assisted ovarian cystectomy, and the subsequent pathologic analysis revealed a mature cystic teratoma. During the laparoscopy, the left ovary was visually examined, and morbid findings were not noted. One month after the surgery, her symptoms had improved and no residual tumor was observed on pelvic sonography. The patient was subsequently lost to follow-up. After 1 year, she presented to our out-patient department with a 2-month history of prolonged menstrual periods; a right ovarian complex mass, approximately 3.7 × 4.3 cm, with a solid component, was noted during a pelvic ultrasound examination (Figure ). Her CA125 level was 11.9 U/mL. She, again, underwent laparoscopically assisted ovarian cystectomy in our hospital, and the pathological report revealed another mature cystic teratoma. However, no abnormal findings were noted for the left ovary.
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| 2 |
+
She received regular follow-up care every 6 months and had been well for the next 3 years. However, at the age of 20 years, she presented with intermittent abdominal pain as well as dysmenorrhea that had persisted for several months. A complex mass, that had an approximately 10% solid component, was detected on sonographic examination. In addition, her CA125 level was 103.1 U/mL. Based on the findings of serological tests, we suspected the presence of a malignancy. The patient underwent a contrast-enhanced abdominal and pelvic computed tomography (CT) scan, which revealed an 8.9 × 5.7-cm, complex, cystic tumor of the left adnexa, with compression and displacement of the urinary bladder. Moreover, a 5.1 × 3.9-cm, complex, cystic, partially solid tumor was noted on the right adnexa (Figure ).
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| 3 |
+
Due to the presence of bilateral adnexal lesions and the suspicion of malignancy, the patient underwent an exploratory laparotomy, bilateral ovarian cystectomy, and pelvic adhesiolysis. During the laparotomy, a capsulated, enlarged, 9 × 6 cm, left ovarian tumor was detected, with abundant sebaceous and hair-containing tissue. The right mass appeared to be a teratoma, 5 × 4 cm in size. Histopathological findings confirmed the presence of bilateral, mature cystic teratomas, composed of sebaceous and keratinous materials as well as hair shaft components. No evidence of malignancy was found. After discharge, the patient underwent follow-up at 1, 3, 9, and 15 months. She did not report abdominal pain or menstrual abnormalities, and a pelvic sonography did not demonstrate any signs of recurrence or residual tumor.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1646_en.txt
ADDED
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A 68-year-old man presented with acute-onset cognitive and memory disturbance 10 days before admission. He experienced disorientation and had a score of 12 points on the mini-mental state examination (MMSE). He had no headache, nausea, or visual disturbance, including a visual field defect. Endocrinological examinations revealed hyponatremia (119 mEq/L), serum hypo-osmolality (242 mOsm/L), urinal hyper-osmolality (475 mOsm/L), presence of serum antidiuretic hormone (1.6 pg/mL), continued renal excretion of sodium (93.6 meq/L), normal adrenocortical function, absence of clinical evidence of volume depletion, absence of other causes of hyponatremia, and correction of hyponatremia with fluid restriction, which met the criteria of SIADH. Computed tomography (CT) indicated a high-density mass located in the third ventricle that caused left unilateral hydrocephalus due to obstruction of the foramen Monroe . Intraventricular hemorrhage was not apparent. On magnetic resonance imaging (MRI), the tumor showed high intensity in both T1-weighted images (T1WIs) and T2-weighted images (T2WIs), low intensity in susceptibility-weighted images (SWIs), and a low intensity peripheral rim in T2WIs, suggesting subacute intralesional hemorrhage. The mass was not enhanced with gadolinium. Cerebral angiography revealed no mass stains.
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| 2 |
+
The mass was removed via a basal interhemispheric translamina terminalis approach . An old hematoma was suctioned after incision of the capsule. The mass adhered tightly to the left hypothalamus, which was supposed to the origin and was well circumscribed from the surroundings. We carefully separated the mass from the left hypothalamus and completely excised the mass. Histopathological examination indicated that the specimen was composed of variant vessels, hematomas, and hemosiderin according to hematoxylin-eosin staining . Elastica van Gieson staining showed thin blood vessel walls containing endothelium as well as a collagenous adventitia. CD34-immunoreactivity was identified in the endothelial-like cells. The histopathological diagnosis was CCM.
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| 3 |
+
Hyponatremia and serum hypo-osmolality improved (Na: 137 meq/L, serum osmolarity: 279 mOsm/L) without fluid restriction 7 days postoperatively. Diabetes insipidus did not appear. Postoperative T1WIs showed that the mass was completely excised and that the left unilateral hydrocephalus improved . However, disorientation and memory disturbance did not recover after the operation, and he was transferred to another hospital for rehabilitation of higher brain function. His MMSE score improved to 21 points, and he could perform indoor activities of daily living, however, he could not resume work at 1 year after the operation.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1651_en.txt
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An 83-year-old male patient had no family history of hypertension, chronic obstructive pulmonary disease, or malignancy. He smoked for 40 years and had a smoking index of 20 pack-years. He was admitted to the hospital for a physical examination, during which a chest computed tomography (CT) scan revealed a left hilar occupancy measuring approximately 5.9x3.6 cm, obstructive atelectasis in the left lung field, and a small pleural effusion. Further fiberoptic bronchoscopy revealed that the left main bronchus was blocked by new organisms, the surfaces of which oozed blood. This location was the site of the biopsy, which revealed lung squamous cell carcinoma . P40 (+), CK56 (-), ki-67 > 25%, TTF-1 (-) in immunohistochemistry. The patient ceased chemotherapy because he could not endure the adverse effects of nausea and vomiting after one cycle of perfusion chemotherapy (40 mg nedaplatin via bronchial artery infusion administration) and paclitaxel systemic intravenous treatment. After 7 months, the patient developed hemoptysis with a daily volume of about 10-20 mL, and chest CT scan revealed a left deviation of the mediastinum, left lung consolidation and atelectasis, a soft tissue mass in the left hilum with a size of about 8.1x4.6 cm, left main bronchial obstruction, and enlarged lymph nodes in the left cervical root and mediastinum. No obvious metastatic lesions had been found after head MRI, whole-body bone imaging, whole-abdomen enhancement CT. We took the disease’s progression into consideration (Clinical Stage, cT4N3M1a, stage IVA). Subsequently, the BRCA2 EXON15 G25085 mutation was detected by blood next-generation sequencing, and the tumor mutation load TMB was 5.98 mutations/Mb. Based on the sequencing test results, we immediately started aggressive treatment and decided to use the PARP inhibitor Olaparib (300mg twice a day) with the PD-1 inhibitor Cindilimab. After one week, the patient’s hemoptysis stopped. A repeat chest CT revealed that the left hilar mass was substantially smaller than before, with a long diameter of around 4.5 cm, and that the left lung was recruiting and the pleural effusion was absorbed after receiving Olaparib for two months and PD-1 inhibitor for two immunotherapy sessions. At this time, the patient appeared new symptoms, puffy eyelids, decreased urine volume, and generalized weakness. In further testing of common serological indicators, we found that blood creatinine increased from normal value at the beginning of the disease to 163.90μmol/L. Meanwhile, urine precipitation microscopy showed urine protein (+) without a tubular pattern. Routine blood, liver function, inflammation indicators, tumor indicators were normal, and autoantibodies were negative. Following the multidisciplinary team’s discussion, we took into account the kidney damage caused by immune checkpoint inhibitors, which was graded as 2, and stopped using the PD-1 inhibitor in accordance with the Chinese Society of Clinical Oncology (CSCO) 2022 recommendation. One month after quitting the PD-1 inhibitor, the serum creatinine level was back to normal. Six months after starting Olaparib monotherapy, the patient was more advanced. The therapy options, disease response, and PFS for each treatment line are summarized in .
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1663_en.txt
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A 23-year-old man presented with nausea, imbalance, occasional urinary and fecal incontinence and a severe headache for 1 month. The patient was a farmer with an unremarkable past experience for his relatives. Neurological examination was completely normal. Magnetic resonance imaging (MRI) demonstrated a left cerebellar mass lesion of 3×2×1.5 cm in size with marked peripheral contrast enhancement . Computed tomography (CT) examination of the chest and abdomen were performed for a primary origin. Multiple calcified mass lesions with lobulated contours were shown in the right upper lobe of lung, right liver and another solid tumor between right kidney and liver. Suboccipital craniotomy was performed and a left intracerebellar pale yellow mass was excised grossly as total. The tumor was almost avascular and it was easily dissected from the surrounding cerebellar tissues. Postoperative course was unremarkable without any neurological deficit. Histopathological examination revealed PAS (+) cuticular membrane with wide areas of necrosis and inflammation which were typical for EM . Serological tests at the postoperative period confirmed the presence of EM with indirect hemagglutination test.
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| 2 |
+
Albendazole (800 mg, bid, 3 cure, 28-day cycle followed by a 14-day albendazole-free interval) and cephotaxime (4 g, bid) were prescribed for postoperative treatment. A further operation was performed to resect the lesion in the lung a month after intracranial surgery. Postoperative early CT examination and MRI performed 6 months after surgery showed no recurrence.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1670_en.txt
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A 64-year-old woman with a past history of type 2 diabetes mellitus (under medical control by sitagliptin 100 mg per day for 5 years) experienced progressive voiding difficulty without fever for 2 mo. She had not undergone any previous urological or gynecological surgery. Urinary analysis showed pyuria, and she was admitted to our ward for further treatment. Bladder ultrasonography revealed urinary retention and a pelvic cystic lesion with a mass effect on the bladder . During admission, she also complained of perineal pain when she started to sit on a chair. Therefore, we arranged a pelvic computed tomography and the report showed a cystic lesion (9.1 cm) in the right lower pelvic region . Urologists were consulted and urodynamic studies were arranged. Uroflowmetry revealed an interrupted flow pattern with elevated post-void residual urine. Video urodynamics showed fair cystometric capacity and detrusor contraction, but the sphincter did not open during the examination. The results of the examinations all supported a diagnosis of bladder outlet obstruction due to a pelvic anatomical lesion. We consulted a gynecological expert, and a mass bulging from the right vaginal wall was found during pelvic examination. Transvaginal ultrasound revealed a pelvic cystic lesion originated from the vaginal wall. A vaginal abscess causing voiding dysfunction was diagnosed.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1671_en.txt
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A 45-year-old man presented to the outpatient clinic at our hospital with abnormal electrocardiogram (ECG) findings.
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The patient underwent ECG as part of a regular health check, and had no cardiac symptoms such as chest pain or shortness of breath.
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He had no specific comorbidities and no history of trauma.
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The patient had a smoking history of 20 pack-years and an alcohol consumption history of 3–4 bottles of soju per week. His younger brother was diagnosed with a myocardial bridge, and there was no other family history of cardiovascular disease.
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The patient had a height of 176 cm and weight of 73 kg, and his vital signs were stable, with a blood pressure of 121/74 mmHg and pulse of 100 beats/min. There were no other significant findings on physical examination.
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Blood tests revealed no abnormalities, and cardiac markers were normal. The ECG showed T wave inversion in the anterior lead, and chest radiography findings were unremarkable.
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Echocardiography revealed that the LV was divided into two compartments by myocardial muscle fibers, along with tears in the apical lateral and inferior segments . There were no other significant abnormalities. Based on these findings, LV aneurysm dissection or LV pseudoaneurysm secondary to myocardial infarction (MI) were suspected.
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Coronary angiography was performed to assess for coronary artery disease (CAD) such as MI. However, no significant luminal narrowing was observed. Although the findings regarding CAD did not appear, treatment was discussed with a thoracic surgeon in light of the possibility of aneurysmal dissection. After consulting with the surgeon, it was decided to prioritize a definitive diagnosis because surgical treatment in cases of asymptomatic aneurysm dissection is not urgent.
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CCTA was performed for a more detailed evaluation of the anatomy and myocardial condition. On CCTA, it was shown that the LV was divided into two. A separated accessory chamber (AC) was connected to the LV by a narrow slit-like communication in the LV apical-mid posterolateral wall . No other abnormal findings, such as coronary artery anomaly, were seen, and no findings were suggestive of myocardial ischemia. Together, these findings indicated DCLV as a more likely diagnosis than LV pseudoaneurysm or aneurysm.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1672_en.txt
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Patient is a 90-year-old Caucasian female with a past medical history of gastroesophageal reflux disease symptomatically managed with pantoprazole 40 mg daily, hypothyroidism, depression, anxiety, and peripheral neuropath; who presented to the emergency department (ED) with nausea, vomiting and abdominal pain. She also had a fever of 101.5 F and was complaining of chills. She initially went to a local ED where laboratory evaluation revealed a urinary tract infection. She was found to have elevated serum amylase (890 U/L) and lipase (3500 U/L) levels as well. Her white blood cell count was 11,000/mcL. Total bilirubin, alanine aminotransferase and aspartate aminotransferase levels were normal. Her blood cultures grew Gram-negative rods and Gram-positive cocci for which she was started on vancomycin [1250 mg every 12 h] and Zosyn® [3.375 gm every 6 h].
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A computed tomography (CT) scan of the abdomen and pelvis without intravenous contrast was performed which showed a very large hiatal hernia compressing and deforming the heart amongst other structures. The majority of the stomach along with the body and tail of the pancreas were herniated into the mediastinum. There was a large amount of free fluid in the mediastinum. There was dependent cholelithiasis and a distended gallbladder with signs of acute cholecystitis. A right upper quadrant ultrasound (RUQ US) showed intra and extra-hepatic biliary ductal dilation with possible echogenic material within the common bile duct. There was gallbladder wall thickening and peri-cholecystic fluid, these findings were thought to represent either acute cholecystitis or secondary to pancreatitis. The patient underwent an echocardiogram which showed left ventricular ejection fraction of 74%. There were no regional wall motion abnormalities.
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Based on the findings of RUQ US, an endoscopic retrograde cholangiopancreatogram (ERCP) was performed which showed a normal esophagus, large hiatal hernia with most of the stomach above the diaphragm and a duodenal diverticulum. The major papilla was located entirely within the diverticulum. The entire main bile duct was dilated. Choledocholithiasis was found.
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A repeat CT scan of the chest, abdomen and pelvis with intravenous contrast was performed. The body and tail of the pancreas was found to be herniating into the mediastinum .
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The patient was continued on vancomycin and Zosyn®. The bacteria were found to be ampicillin-sensitive Enterococcus durans and a pan-sensitive E. coli. She was switched to ampicillin [2 g every 6 h] for the next 2 days and finally to oral amoxicillin PO [500 mg every 8 h]. Given the findings of large hiatal hernia, General Surgery was consulted. Given the chronicity of the patient’s symptoms, her age and relatively good symptom control with proton pump inhibitors, a conservative approach to therapy was recommended with no surgical consideration for hiatal hernia repair. An elective cholecystectomy was offered to the patient and she elected to discuss this at a clinic visit in the upcoming weeks. On the day of discharge, the patient was tolerating a diet, had no pain or nausea, and was feeling well.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1673_en.txt
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Three years ago, a 59-year-old male Moroccan presented to the hospital with a dyspnea, dry cough, and a chest pain that had started 6 months before. He had smoked about 30 cigarette packs a year. He was diagnosed non-insulin dependent diabetes 1 year before and was under oral anti-diabetics. He had undergone a successfully surgical intervention for priapism 4 years before the current episode of sickness. His sister is known to have a breast adenocarcinoma. Physical examination at admission revealed a patient with performance status according to World Health Organization (WHO) quote one, and dyspnea type II according to NYHA (New York Heart Association). The pulmonary examination was poor. Head and neck examination found a right thyroid nodule without clinical signs of hypothyroidism or hyperthyroidism. Chest and neck computed tomography (CT) scan were performed and revealed a tumor in the left upper lobe of the lung, in contact with the pulmonary artery . The pulmonary tumor measured 5.5 × 6 cm without mediastinal lymph nodes . The neck CT-scan showed one nodule in the right lobe of the thyroid plunging into the superior mediastinum measuring 8 × 4 cm with homolateral cervical lymph nodes . The level of the thyroid stimulating hormone (TSH) was normal. For the pulmonary tumor, we performed transbronchial biopsies. Pathological examination of the biopsy revealed an adenocarcinoma of the lung, positive thyroid transcription factor (TTF-1).
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Other explorations conducted such as brain CT and bone scan and abdominal ultrasound were normal. We concluded a diagnosis of pulmonary adenocarcinoma classified T4N0M0 with a suspected nodule of the thyroid right lobe. We performed a repeated fine needle aspiration biopsy (FNAB) of the thyroid right lobe but the anatomopathologic results were negatives. We decided to performed a total thyroidectomy and lymph node dissection after extemporaneous anatomopathologic exam, confirming the malignancy of the thyroid right lobe nodule. The pathologic examination revealed a moderately differentiated tubulopapillary adenocarcinoma and three lymph nodes with extracapsular effraction. The immunohistochemistry showed positive tumor cells with TTF1 and cytokeratin (CK) 7 but negative tumor cells with thyroglobulin and CK20 . Thus, the pulmonary tumor was classified stage IV (T4N0M1) according to the 2009 UICC (Union for International Cancer Control) staging. The multidisciplinary team found that lung tumor was inoperable because it was in contact with the pulmonary artery. The decision to administrate chemotherapy followed by the chemoradiation was retained because there was lack of places on the linear accelerator. A chemotherapy based on the combination of cisplatin and etoposide was administrated along with supportive care. The chemotherapy consisted of the combination of cisplatin and etoposide that were administered according to the following schema: for every cycle, cisplatin 75 mg/m2 on day 1 and etoposide 100 mg/m2 on day 1–3. The length of time between the treatments was 21 days. In total, two cycles of this chemotherapy were performed. We didn’t report any side effect regarding this chemotherapy. After the two cycles, the patient presented dizziness and headaches. A brain magnetic resonance imaging (MRI) was performed and showed multiples brain metastases. The cranial palliative radiotherapy 10 × 3 grays including five fractions per week was realized with best supportive care. This radiation therapy was well tolerated. Particularly, there was no deleterious effect on cognition. After the radiation therapy, we decided to go on with the chemotherapy administration. But the performance status of the patient was poor. Unfortunately, despite reanimation measures and best supportive care, the patient died 2 months later after brain radiotherapy.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_1685_en.txt
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A 5-year old, previously healthy female was admitted to the hospital in December 2020 with a 2-week history of periorbital swelling, with progressive involvement of abdominal and ankle swelling. Prior to admission, the child had developed isolated left eye swelling which was not associated with any other symptoms or vision changes. A week later, evaluation at her primary care physician (PCP)‘s office was notable for 4+ protein on urinalysis. The child was then referred to pediatric nephrology for further evaluation and management. In the renal clinic, on examination she was noted to have moderate abdominal swelling with ascites and pretibial edema. She had further gained 2 kg of weight since her visit to the pediatrician’s office 1 week prior. The child’s mother denied any recent illnesses such as fevers, chills, cough, rhinorrhea, congestion, nausea, vomiting, sore throat, gross hematuria, or diarrhea, and there were no known sick contacts. There was no known family history of kidney diseases.
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Urine analysis revealed 3+ proteinuria with no blood . Spot urine protein was greater than 2 g/dL and urine protein-to-creatinine ratio greater than 12 mg/mg, which suggested the presence of nephrotic-range proteinuria. The patient had mild hyponatremia with serum sodium of 133 mmol/L. Serum creatinine was 0.27, and BUN was 20. Serum albumin was 2 g/dL, total cholesterol elevated at 307 mg/dL, elevated triglycerides at 644 mg/dL, with normal complements C3 and C4 at 87 mg/dL and 21 mg/dL, respectively. Our patient’s blood work was also notable for elevated D-dimer 2.49 (normal < 0.4 Ug/mL) and partial thromboplastin time (PTT) 39.1 (25.6–32.4) seconds. She had a mildly elevated TSH (5.6 IU/mL) with a normal free T4 (0.9 ng/dL), a low 25-hydroxy vitamin D level, and a low ferritin of 29. Of note, the surveillance COVID-19 testing (RT-PCR, performed via nasopharyngeal swab), which was performed as part of the general hospital admission process during the time of this case report, returned positive for SARS-CoV-2, and further immunoglobulin (Ig) testing was positive for both IgM and IgG antibodies. The SARS-CoV-2 RT-PCR nasopharyngeal swab test was performed using the Hologic Aptima SARS-CoV-2 Assay (approved for emergency use authorization by the US FDA), and the SARS-CoV-2 immunoglobulin testing was performed on the Abbott Architect i1000 platform (approved for emergency use authorization by the FDA).
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The patient received intravenous 25% albumin and furosemide for diuresis, with excellent response. In addition to a fluid and sodium restriction, she started on oral vitamin D supplements and following a negative purified protein derivative (PPD) skin test, she started corticosteroid therapy at 2 mg/kg per day. Throughout her four-day hospital stay, patient remained asymptomatic from COVID-19 perspective. Her vital signs were stable throughout admission (temperature: 36.1–36.9 C, pulse: 79–107 beats per minute, respiratory rate: 14–22 breaths per minute, SpO2: 97–100% on room air). Although our patient was at an increased risk for hypercoagulability from both nephrotic syndrome and COVID-19 infection, we did not initiate anticoagulation therapy. Patient was discharged home after 4 days at only 700 g (0.7 kg) above her baseline weight, as estimated by her recent weight at a PCP visit 2 months prior to admission.
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Patient was in complete remission within 3 weeks of starting corticosteroids and urine protein was still negative after 6 weeks of therapy. Her coagulation profile and thyroid studies normalized without intervention; however, she remains positive for both IgM and IgG SARS-Cov-2 antibodies. Despite these positive results, she had still remained asymptomatic from a COVID-19 perspective at her follow up visit.
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data/test_raw_data/en_test/multiclinsum_test_en/fulltext/multiclinsum_test_168_en.txt
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A 32-year-old female with non-diabetic chronic kidney disease was on regular hemodialysis for 3 years, via a right forearm arteriovenous fistula. The patient was admitted to our department due to involuntary movement for 5 days. Starting 5 days prior to admission, the patient’s shoulder and neck displayed a resting tremor, which became increasingly severe, with the limbs beginning to move uncontrollably. The patient’s vital signs were stable, with no complaints of headache, fever, blurred vision or mental disorder. Myodynamic examination and deep tendon reflexes in both legs were normal, and the Babinski reflexes were suspiciously positive. Significant fluctuation of blood creatinine levels (predominantly due to inadequate dialysis), along with altered hyperthyroidism [intact parathyroid hormone (iPTH) levels of almost 3200 pg/mL], were reported 1 week ago with no accompanying history of hypertension, DM, respiratory tract infection, fever, stoke, liver disease, hypoxia or toxic fume exposure. Brain magnetic resonance imaging (MRI) was performed 5 days after the onset of symptoms in the local hospital, and showed symmetrical T2-weighted imaging (T2WI; Fig. ) and T2/fluid-attenuated inversion recovery (T2FLAIR; Fig. ) hyperintense non-hemorrhagic lesions in bilateral basal ganglia, as well as corona radiata lesions showing mild diffusion restriction. Both T1-weighted imaging (T1WI) and diffusion-weighted images (DWI) were normal.
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Blood analysis immediately after admission revealed high levels of uremic toxins (urea nitrogen 25.80 mmol/L, serum creatinine 1206 μmol/L, uric acid 548 μmol/L, phosphorus 1.88 mmol/L, calcium 2.33 mmol/L,anion gap 23.9 mmol/L), and severe hyperthyroidism (iPTH 2487 pg/mL). Bicarbonate, arterial blood gas indices, hemoglobin, albumin, lactic acid, B-vitamins and liver function were all normal.
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The patient was diagnosed with UE as a symptom of bilateral basal ganglia lesions. She did not suffer from DM or other diseases such as cerebrovascular events, intoxication or hyperlactacidemia. Thus, UE was possibly due to a combined effect of uremic toxins and hyperthyroidism. The patient was treated with high frequency and high flux dialysis (4 h hemodiafiltration with APS 15 uc dialyzer, 4 times per week), hyperbaric oxygen therapy (1.5 h per day), declining parathyroid hormone (1 μg of calcitriol injection every 2 days), and treatment for symptom relief (2 mg of haloperidol, 2 mg of clonazepam and 2 mg of benzhexol administered orally twice per day). Gradually, the symptoms reduced in frequency, and the amplitude of involuntary movement decreased. Fourteen days after admission, a subsequent brain MRI revealed high signal in the bilateral basal ganglia on T2WI and T2FLAIR , which were significantly weaker compared to the initial MRI signal.
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About 1 month later, the patient achieved complete remission and restoration of normal body movement, and was discharged. Upon discharge, blood test results showed relatively stable uremic toxins (urea nitrogen 10.48 mmol/L, serum creatinine 641.5 μmol/L, uric acid 435 μmol/L, phosphorus 1.43 mmol/L, calcium 2.30 mmol/L,anion gap 15.9 mmol/L), and relieved hyperthyroidism (iPTH 1609 pg/mL). Brain MRI was performed again upon follow-up, with T2WI and T2FLAIR showing an almost complete resolution of the lesions with slightly hyperintense signal in the bilateral basal ganglia.
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