A 20‑year‑old woman had been followed since age eight for idiopathic nephrotic syndrome (NS) inaugurated by cerebral venous thrombosis extended to the right jugular vein with a massive pulmonary embolism, without sequelae and without personal or family thrombotic history. Kidney biopsy was deferred because there was no kidney failure, gross hematuria, hypertension, or extra‑renal signs suggestive of secondary NS at presentation. She was treated with an oral vitamin K antagonist and oral corticosteroids with good evolution. Subsequently, she had multiple steroid‑dependent relapses and was started on mycophenolate mofetil (MMF) as background therapy to spare corticosteroids and ensure normal growth. An exhaustive thrombophilia assessment was negative: homocysteine, fibrinogen, protein C, protein S, antithrombin III, factor V Leiden, JAK‑2, cryoglobulins, anticardiolipin antibodies, lupus anticoagulant, and anti‑β2‑glycoprotein I antibodies were all normal. Anticoagulation was stopped after nine years. Several relapses occurred but were controlled with oral corticosteroids. NS remission was documented from 2017; MMF was gradually discontinued in 2019, and she remained asymptomatic without relapse.

One year later, she presented to the emergency department with acute intense diffuse abdominal pain without irradiation, associated with postprandial vomiting and bilateral lower‑limb edema for six hours. Examination showed intense epigastric tenderness with normal vital signs (BP 120/70 mm Hg, HR 83 bpm, SpO2 100% on room air) and no fever or neurological impairment. Urinalysis detected proteinuria. Hemogasanalysis showed metabolic acidosis with respiratory compensation. Labs revealed hypoalbuminemia, hypercholesterolemia, prothrombin time 90%, elevated D‑dimer, LDH, and creatine phosphokinase, with inflammatory markers (CRP 37 mg/L) and leukocytosis (26.4 × 10^3/µL); renal and liver function were normal. Urgent abdominal ultrasound showed a low‑to‑moderate intra‑abdominal effusion. Contrast‑enhanced CT demonstrated acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. She underwent emergency laparotomy: intraoperative exploration confirmed mesenteric ischemia with extensive necrosis of almost the entire small bowel, rendering resection incompatible with life. She died 48 hours later.

This case illustrates catastrophic arterial thrombosis in the setting of NS despite a negative thrombophilia work‑up. NS is a hypercoagulable state with multifactorial mechanisms, including urinary loss of anticoagulant proteins (e.g., antithrombin III, protein S), increased fibrinogen, hemoconcentration, dyslipidemia, and systemic inflammation. While venous thromboembolism is more common in NS, superior mesenteric artery thrombosis is rare but often fatal, underscoring the need for high clinical suspicion and rapid imaging when severe acute abdominal pain occurs in patients with active or relapsing NS.


A 65-year-old man developed persistent swelling and a boutonniere deformity of the right middle finger after a motorcycle fall six months earlier. He could not fully extend the finger. On exam, the finger showed edema with flexion at the proximal interphalangeal (PIP) joint and hyperextension at the distal interphalangeal (DIP) joint. Active PIP range of motion (ROM) was 45–110 degrees. X‑rays of the right hand (AP/oblique) showed no bone injury, indicating a soft-tissue problem consistent with a central slip injury. The patient underwent reconstruction of the central slip using a partial ulnar slip of the flexor digitorum superficialis (FDS) tendon. A PIP extension splint was used for 2 weeks. Active and passive PIP ROM exercises began after 2 weeks. One month after surgery, PIP ROM improved to 0–90 degrees, and by 2 months it returned to normal. Hand function, measured by the DASH score, improved markedly from 50 to 4.2.


We report a unique case of a 13-year-old boy who presented with a palpable, painless mass in the left inguinal (groin) area and no other constitutional symptoms. His medical history included prior spinal surgery with resulting immobility and a pressure sore on the left foot, but otherwise he was well. Routine blood tests were normal except for a very high erythrocyte sedimentation rate (ESR 119 mm/h), and CT scans of the chest, abdomen and pelvis showed enlarged lymph nodes below the inguinal ligament, the largest about 3.5 × 2.4 cm. Because imaging and blood tests could not rule out malignancy (for example lymphoma or leukemia), the enlarged nodes were surgically removed for definitive diagnosis. Pathology showed features consistent with unicentric Castleman disease, plasma-cell type — one of the rarest forms in children and, to our knowledge, the first reported unicentric Castleman case in the inguinal area. The patient was discharged after 14 days with a course of oral prednisolone and was followed with clinical exams, laboratory tests and whole-body CT scans every three months. After 12 months of follow-up there were no new symptoms, no new enlarged lymph nodes on exam or imaging, and no abnormal laboratory findings.


A 40-year-old HIV-positive man with reported regular ART adherence (prior year viral load 4,500 and CD4 70/mm3) presented with a two-year history of intermittent, noncyclical febrile episodes that transiently responded to NSAIDs. Over the preceding two months, he developed progressive, diffuse abdominal pain and generalized adenomegaly. Laboratory evaluation showed pancytopenia, coagulopathy, hypoalbuminemia, and elevated acute phase reactants. Initial CT of the thorax, abdomen, and pelvis demonstrated hepatosplenomegaly and generalized adenomegaly without additional parenchymal findings. A broad microbiologic workup was undertaken, including mycobacterial cultures from multiple specimen types; all were negative except an RT-PCR positive for HHV-8. Excisional biopsy of a left iliac lymph node showed features consistent with Castleman’s disease. Despite reinitiating antiretroviral therapy, clinical status deteriorated, prompting initiation of corticosteroids and ganciclovir. After approximately one week, the patient developed multiorgan failure with anasarca, rendering the instituted therapies contraindicated and necessitating discontinuation. Repeat chest CT revealed right upper lobe tree-in-bud infiltrates with bilateral pleural effusions. Concurrent abdominal imaging showed progression of hepatosplenomegaly and new-onset ascites. Forty-eight hours later, he developed fulminant hepatic failure and was transferred to the intensive care unit. He expired within hours. Tracheal aspirate culture, finalized postmortem, grew Mycobacterium tuberculosis. A percutaneous liver biopsy performed with transfusion support demonstrated non-necrotizing granulomas with otherwise preserved parenchyma. The case management and reporting adhered to the ethical principles of the WHO/Declaration of Helsinki.


A 77-year-old man has memory and thinking problems. He had a big seizure. Both hip joints popped inward into the pelvis. In the emergency room, his right leg looked shorter than the left. Both legs were turned outward. Both hips were stuck when staff gently rolled his legs. Scans and medical checks were done to get him ready for surgery. The surgeries were done in two steps. The left hip was done on day 8. The right hip was done on day 15. In both surgeries, doctors put in a support ring and a special hip socket that helps keep the joint stable. They also put in a new thigh-bone piece that does not use cement. Right after surgery, there were no problems from the operation. At 12 months, he could put full weight on his legs. His right hip score was 77. His left hip score was 79. His WOMAC score was 12. He has had no problems since the surgery.


A 16-year-old girl has a depressed gray plaque on the lower outer (lateral) part of her left thigh, about 10.5 × 8.0 cm. The area includes lighter patches and small dilated surface blood vessels (telangiectasias) around the edges, and some nearby veins are visible. The lesion has been present since birth—it was initially purplish (violaceous) and over the years became lighter and sunken. There is no difference in leg length. Vascular imaging (angioresonance) shows a vascular malformation involving the skin and the fat under the skin in that area, supplied by branches of the popliteal artery. The scan showed early filling of veins, which suggests early venous shunting; no markedly dilated draining veins were found except for a superficial draining vein along the front of the thigh. The subcutaneous tissue beneath the plaque is thinner, and there is no extension into muscle or bone.


A.P. is a 38‑year‑old woman. At age 17, her heart became big and weak. This may have started after a bad throat infection.
She stayed in the hospital for 10 months and 10 days. She was very sick and waiting for a new heart. Her heart rhythm was not dangerously abnormal. Her heart’s pump was very weak.
Doctors treated her heart failure. They also tried to prevent dangerous heart rhythms and blood clots.
Her heart got better. This kind of recovery happens in about 16 out of 100 people. The better phase lasted 4 years.
Then the disease got worse for 2 years.
After that, she was stable. She had her first baby, and the pregnancy was normal.
In the middle of her second pregnancy, her heart got worse again. It improved a few months after the birth.
In May 2017, she was doing well on medicines. These medicines relax blood vessels, slow the heart, help the body get rid of extra water, and slow the heart’s natural pacemaker. She had no limits in daily activity. She is a mother of two. She did not have a job.


An 18-year-old man came to the emergency room with new chest pain, fever, and trouble breathing when he lay down. A blood test showed strain on his heart. His heart tracing had changes that can happen when the heart is irritated. His chest X-ray made the heart look bigger than normal. An ultrasound showed the heart muscle was very thick on both sides. It also showed fluid around the heart. Blood tests pointed to a common virus called Coxsackie, which can inflame the sac around the heart. Doctors treated him, but he got worse with shortness of breath and very low blood pressure. A new heart ultrasound showed the fluid was starting to squeeze his heart, like a tight jacket. Doctors drained the fluid, but his heart stopped, and he needed a heart-lung machine to stay alive. A small piece of heart tissue did not show infection. A small skin lump on his right arm was tested. It showed a rare blood cancer linked to the Epstein–Barr virus. He started cancer medicines. His heart pumping got better. The fluid around his heart went away. The thick heart muscle slowly went back toward normal.


A 59-year-old woman has multiple sclerosis. She started a new seizure medicine called levetiracetam. A few weeks later, her vision in both eyes became blurry. The eye doctor found swelling in the clear front window of both eyes. A special eye scan confirmed the swelling. They lowered the dose of the new medicine. Her vision started to get better. They then stopped the medicine. Her vision went back to normal. The swelling went away.


A baby boy was 4 months old. He lived with his mother in a prison cell. A painful lump grew in his left armpit. A chest X-ray looked like some ribs were broken. Doctors worried he might have been hurt. The pictures also showed a pocket of pus in his armpit, damage to his ribs, a lung infection, and small spots in his lungs. He got strong antibiotics. He went home. When he was 8 months old, he got a fever. The pus spread toward his left shoulder. New chest pictures looked worse. Tests found a mold called Aspergillus fumigatus in the pus. The doctors said he had a serious mold infection. He took a strong antifungal medicine called voriconazole for 28 days. A special blood test showed his germ-fighting cells did not work well. He had a rare immune problem called chronic granulomatous disease. It was caused by a change in a gene called CYBB. His mother carried this gene change. When he was 12 months old, the mold infection came back. The treatments did not work. He died.


A 40-year-old man has HIV and takes his medicines regularly. For two years, he had fevers that came and went. In the last two months, he also had spreading belly pain and many swollen glands. Blood tests showed very low blood cells, blood that did not clot well, low blood protein, and strong signs of inflammation. A body scan showed a big liver and spleen and many swollen glands. Many germ tests were done and were negative, except one that found the HHV-8 virus. A gland sample showed a rare illness called Castleman’s disease. Even after restarting his HIV drugs, he got worse. Doctors tried steroids and an antiviral called ganciclovir. A week later, many organs started to fail and he swelled all over, so those drugs had to be stopped. A new chest scan showed small branch-like spots in the right lung and fluid around both lungs. The belly scan showed the liver and spleen got bigger and there was fluid in the belly. He went to intensive care because his liver suddenly failed. He died soon after. After his death, a lung sample grew tuberculosis. A liver sample showed tiny immune lumps called granulomas.


A 15-year-old male with no prior surgeries developed four days of abdominal pain and vomiting. CT suggested a small-bowel obstruction from an internal hernia through the foramen (hiatus) of Winslow, an opening behind the stomach. He underwent urgent surgery that began as a diagnostic laparoscopy but was converted to a supraumbilical midline laparotomy because the view was poor. The surgeons reduced a herniated ileal loop; the bowel looked viable, so no resection was needed. They did not perform a preventive maneuver to lower the risk of recurrence. After surgery, he developed a pelvic fluid collection that was managed with antibiotics alone. He is currently followed in the outpatient pediatric surgery clinic.


A 19‑month‑old boy went to the emergency room because he hit his head. Doctors saw that he was fighting to breathe. They put in a breathing tube to help him. The team believed the breathing problem likely started first. It may have made him less alert, and then he fell and hit his head. Scans showed the left lung was not filling with air, like a balloon that stays flat. This made doctors think something was stuck in his airway. A CT scan showed a sudden stop in the main airway to the left lung. Doctors used a small camera to look inside. They found and removed a 2‑cm almond that was blocking the airway.


A 42-year-old woman with primary cough headache (PCH) could not tolerate oral preventive medicines because of side effects. She developed more than ten short, severe headache attacks a day after a bout of bronchitis; each attack lasted about 30 minutes, was triggered by coughing, straining or lifting, and reached 9/10 on a pain scale. Neurological exam and brain and neck imaging were normal, and she declined a lumbar puncture. Because she could not keep taking indomethacin and could not use other oral options, we offered an ultrasound-guided proximal greater occipital nerve block (PGONB) using bupivacaine. After a single, unilateral block the pain fell from 9/10 to 2/10 within 20 minutes. The block was repeated once weekly for a month; at two months both the number of attacks and their intensity had declined (about two attacks per month at 4/10), and by six months she reported no attacks. No adverse effects from the nerve blocks were observed, suggesting ultrasound-guided GON blockade can be an effective option when oral drugs are not tolerated.


A 77-year-old woman was admitted with haematemesis. CT scans showed that the third part of her duodenum bent sharply on the right side of the aorta and ran downward without crossing in front of it; the duodenojejunal junction and much of the jejunum were located on the right side of the abdomen. Upper GI endoscopy found a mucosal tear at the gastric cardia consistent with Mallory–Weiss syndrome. Seven days after the first scan the abnormal right-sided position resolved on CT, but two months later the patient had another episode of haematemesis and the duodenojejunal junction and jejunum had again shifted to the right. Because the small bowel moved back and forth rather than staying in the wrong position, true intestinal malrotation was considered unlikely. The working diagnosis was dysplasia (abnormal development) of the ligament of Treitz, meaning the ligament that normally helps fix the upper small intestine was not holding the jejunum securely. At laparotomy the ligament of Treitz was present but did not fully fix the upper jejunum to the back wall of the abdomen (retroperitoneum); the pararenal area also appeared loosely fixed and mobile on CT. These factors probably allowed the jejunum to fold and deviate to the right. Surgically the upper jejunum was tacked to the left retroperitoneum with sutures, the postoperative course was good, and the patient has remained symptom-free.


A 10-year-old boy was getting cancer medicine for leukemia. During the first phase of treatment, he got a pocket of infection in his brain. The germ was called Bacillus cereus. Doctors found it with brain scans and by testing the fluid around his brain and spine. He got better after taking antibiotics.


This is the story of a 35-year-old man with a rare condition called Carney syndrome. This condition led to a growth in his heart (a myxoma) and made his heart large and weak (dilated cardiomyopathy). Three years ago, he went to the hospital for sudden chest tightness and shortness of breath. Heart pictures showed the growth. Exams and genetic tests confirmed Carney syndrome. His symptoms got better with medicines, and he went home. No surgery was done then. Later, his chest tightness and shortness of breath got much worse. Doctors said he had very severe heart failure. Tests showed the weak, enlarged heart was still there along with the heart growth. He received a heart transplant. The transplant successfully treated his heart failure.


A 12-year-old boy with Down Syndrome and motoric disorders (diagnosed with myeloradiculopathy) was referred from Pediatrics to the Oral Medicine Department (RS Hasan Sadikin Bandung) for oral evaluation. The mother reported hospitalization for weakness of both hands and feet and difficulty maintaining the child’s oral hygiene; there was a history of a fall approximately one year prior. Extraoral findings: dysmorphic facies; cracking and desquamation of the vermilion border; cervical collar in place, precluding lymph node assessment. Intraorally, there was an irregular 1×0.7 cm ulcer with an indurated margin and a white‑yellowish base on the right lateral tongue. Additional findings included dentinal caries on tooth 63 and tooth remnants on 55, 62, 74, and 85. The 55 tooth had a sharp cusp causing occlusal trauma to the right lateral tongue. Pediatric dentistry recommended extraction of the upper and lower tooth remnants with subsequent space maintenance. Laboratory data: hyponatremia (Na 130 mEq/L) and relative lymphocytosis (46%). MRI of the cervical spine demonstrated dislocation; the mother provided informed consent for publication. Working diagnoses, based on history, clinical examination, and investigations: chronic traumatic ulcer mimicking OSCC (clinical diagnosis; indurated margin raised concern for oral squamous cell carcinoma), exfoliative cheilitis, reversible pulpitis of 63, and radix gangrene on 55, 62, 74, and 85. The patient had been hospitalized for 4 days and received paracetamol 120 mg/5 mL oral suspension and amoxicillin 125 mg/5 mL oral suspension from Pediatrics. Oral Medicine management included sodium chloride 0.9% solution, 1% povidone‑iodine mouthwash, and petroleum jelly. Caregiver instructions: cleanse the oral cavity with gauze soaked in 0.9% saline; apply 1% povidone‑iodine compresses to the ulcer three times daily as an antiseptic/anti‑inflammatory; apply petroleum jelly to moisturize the lips. Extractions of 55, 62, 74, and 85 were advised. Follow-up: at 3 days, oral lesions showed improvement; at 1 week, the lateral tongue ulcer decreased in size and lip lesions improved; at 10 days, the ulcer showed significant improvement. Two days later, the patient underwent neurosurgery and was observed in the Pediatric ICU. After two weeks in the ICU, he developed respiratory failure and died.


A 13-year-old boy presented with acute pleuritic chest pain but no other systemic symptoms. On exam, he had diminished breath sounds over the lower two thirds of the chest, and his oxygen saturation was normal (98% on room air). Chest X-ray showed a marked interstitial infiltrate similar to an image taken 4 years earlier during an illness treated presumptively with azithromycin. Chest CT demonstrated multiple bilateral ground-glass opacities with areas of “crazy paving,” involving more than 65% of the lung, which raised concern for pulmonary alveolar proteinosis (PAP). Respiratory viral testing, including SARS-CoV-2, was negative. Bronchoalveolar lavage yielded milky fluid with positive periodic acid–Schiff staining. Pulmonary function testing showed a mild restrictive pattern (FVC 77%) and a moderately reduced diffusing capacity (DLCO 48.6%). A genetic panel found no mutations linked to surfactant dysfunction. Anti–GM-CSF antibodies were strongly positive, supporting autoimmune PAP. At 20 months, he remains asymptomatic, and spirometry has normalized.


A 28-year-old male with no significant past medical history presented with a 48-hour history of two erythematous plaques with central vesicles and superficial ulceration on the flexor surface of the right arm and forearm, equidistant from the antecubital crease, associated with burning and pruritus. He denied systemic symptoms and had not self-medicated. He reported being on vacation in coastal Ecuador at the time of onset. Incisional biopsy demonstrated epidermal acanthosis, parakeratosis, and spongiosis, neutrophils within the stratum corneum, and perivascular lymphocytic infiltrates in the superficial, mid, and deep dermis. Integrating the clinical morphology, tropical travel history, and histopathology, the diagnosis of Paederus dermatitis was made. Management included antihistamines, topical corticosteroids, and cold compresses. By day 8, the eruption resolved, with residual post-inflammatory hyperpigmentation. Paederus dermatitis is an irritant contact dermatitis due to exposure to Paederus species toxin (pederin), typically producing burning, vesiculation, and superficial erosions; the histologic pattern here (spongiotic dermatitis with mixed inflammatory infiltrates) is consistent with this mechanism.


This 69-year-old man had heart bypass surgery in the past. For 2 months, he got very short of breath with light activity. Tests—a heart tracing, a blood test, and an X-ray movie with dye of the heart arteries—showed heart failure from poor blood flow after a bypass vein to the right heart artery failed. Doctors first opened a totally blocked artery on the left side of his heart. Then they used tiny natural detours between heart arteries to reach the right heart artery from the far end and open it. His breathing was better when he left the hospital. Six months later, his shortness of breath had not come back.


A 12-year-old boy with Down Syndrome and movement problems went to the mouth doctor. His face looked different. His lips were very dry. The doctor could not feel the neck glands because he wore a neck brace. Inside his mouth, there was a sore on the right side of his tongue. It was about 1 by 0.7 centimeters. The edge felt hard. The bottom looked white-yellow. A sharp baby tooth kept rubbing and biting that spot on his tongue. This made a long-lasting injury sore that can look like mouth cancer, but it was from repeated rubbing. The team gave 0.9% salt-water solution, 1% iodine mouthwash, and petroleum jelly for his lips.


A 36-year-old woman had trouble swallowing. Tests found she was born with an unusual shape of the main body artery in her chest. The artery curves to the right in a mirror-image pattern. It wraps around a main branch of the airway. The side branches of the artery come off in the reverse order from normal. Most people with this have no symptoms. Problems happen only if the artery squeezes the space in the middle of the chest. This can press on the food pipe or the windpipe. Surgery may be needed if there is strong pressure on these tubes, a bulge or a tear in the chest artery, or a pouch on the artery bigger than 2 cm. There is no one-size-fits-all treatment. Care is tailored to the person’s symptoms and body anatomy. This patient did not receive any treatment.


A male infant was delivered at 40 weeks via emergency cesarean section for fetal distress to a 33-year-old G1P1 mother. Family history was negative for congenital anomalies, aortic disease, or sudden death. Prenatal imaging showed advanced femur length (by 1–3 weeks), cardiomegaly with a cardiothoracic circumference ratio ≥0.5, an enlarged foramen ovale, and left aortic constriction near the subclavian artery basin; no other anomalies were noted. Birth measurements: 3560 g (75th percentile), length 56.5 cm (>90th), head circumference 36 cm (>90th). Apgars were 4 and 6 at 1 and 5 minutes. In the delivery room he had no spontaneous respirations, bradycardia, and cyanosis, prompting NICU admission. Physical exam revealed multiple musculoskeletal and craniofacial anomalies: severe arachnodactyly and camptodactyly of all extremities with flat soles; elbow and knee contractures; malar hypoplasia with senile facial appearance; deep-set eyes with down-slanting palpebral fissures; hypoplastic, crumpled auricular cartilage; sagging mouth; prominent coronal suture; and brachycephaly. A grade V/VI systolic murmur was audible at both upper sternal borders and the left lower sternal border with a grade III parasternal heave. The Ghent systemic score for musculoskeletal features was 11. Echocardiography demonstrated poor contractility, severe pulmonary hypertension, a dilated aortic sinus measuring 20.2 mm (Z-score 8.08 Boston, 6.37 Detroit, 5.97 Halifax), and multivalvular prolapse with dysfunction: moderate aortic regurgitation, severe mitral regurgitation, moderate tricuspid regurgitation, and moderate pulmonary valve regurgitation. Ophthalmology confirmed bilateral ectopia lentis with lens subluxation. Abdominal radiography and ultrasound identified liver herniation.

Molecular testing (Sanger sequencing/PCR) of FBN1 detected a heterozygous donor splice-site variant, c.3964+1G>T in intron 32, classified as likely pathogenic per the 2015 ACMG/AMP guideline. The variant resides within the established neonatal region of FBN1 (exons 24–32) associated with the severe neonatal Marfan phenotype. Mechanistically, splice-site variants at this locus are expected to disrupt normal FBN1 splicing, compromising microfibril integrity and driving the aggressive cardiovascular phenotype observed in neonatal MFS (notably early aortic root dilation and severe atrioventricular valve regurgitation).

On day 1, he exhibited differential cyanosis with refractory hypoxemia despite >60% oxygen and clinical signs of low cardiac output. Medical management targeted afterload reduction (continuous milrinone infusion), full sedation (continuous fentanyl infusion), and diuresis to address oliguria and heart failure. Despite these measures, he progressed to respiratory failure and severe pulmonary hypertension requiring continuous invasive mechanical ventilation. Aortic and mitral regurgitation worsened, pulmonary hypertension escalated, and cardiac contractility deteriorated. Given the grave trajectory and the expectation that surgical intervention would be essential to prolong life but with limited prospects in the face of rapid progression, the family elected palliative care after multidisciplinary discussions. He developed hepatic and pulmonary congestion with pulmonary hemorrhage, progressed to multiple organ dysfunction syndrome, and died 32 days after birth.

This case documents a novel FBN1 c.3964+1G>T splice-site variant in the neonatal region, concordant with the classic neonatal MFS phenotype: severe early valvulopathy, aortic root dilation, ectopia lentis, characteristic skeletal/craniodysmorphic features, and a fulminant cardiorespiratory course with death in early infancy.


A 22-year-old woman presented with a month of painful stomatitis that made eating and drinking difficult. The illness began with a fever and pimple-like lesions on the lips. She had been vaping regularly for about one year. Examination showed no skin lesions elsewhere. The lips had serosanguineous crusts and erosions at the labial commissures that tended to bleed. Intraorally, there were multiple irregular white ulcers with yellowish borders on several sites of the oral mucosa. Anti–HSV-1 IgG was non-reactive. The diagnosis was oral erythema multiforme, likely related to vaping. Management included normal saline compresses to the lips, a dexamethasone mouth rinse mixed with hyaluronic acid, 2% miconazole cream applied to the lip corner, petroleum jelly for dry lips, and stopping vaping. Her oral condition improved within one week.


A 19-year-old woman came to the emergency department with a dangerous arrhythmia and signs that her heart was failing to pump well (cardiogenic shock). An ECG ruled out an acute heart attack, and cardiac MRI did not show cardiomyopathy. Because a hidden congenital issue was suspected, she underwent cardiac CT angiography. The scan showed ostial atresia of the right coronary artery—the opening of the right coronary artery was absent. She was referred to a specialized congenital heart disease center. An electrophysiology study pinpointed the arrhythmia to the posteromedial papillary muscle, and the focus was treated with catheter ablation. She has remained symptom-free since.


A term newborn boy had neonatal Marfan syndrome with severe heart involvement. He showed typical features: very long fingers and toes (arachnodactyly), bent fingers and toes (camptodactyly), elbow and knee contractures, an aged facial appearance, deep-set downward-slanting eyes, underdeveloped ear cartilage with a sagging mouth, a short-wide head shape (brachycephaly), and ectopia lentis (displaced eye lenses). Genetic testing identified a new FBN1 mutation affecting a splice site (c.3964+1G>T in intron 32) within the known neonatal region (exons 24–32). He developed low cardiac output due to severe mitral and aortic regurgitation and also had pulmonary hypertension. Medical management focused on afterload reduction, deep sedation to lessen cardiac work, and diuretics to treat fluid overload and low urine output. Despite treatment, the valve regurgitation, pulmonary hypertension, and poor heart pumping worsened. Surgery would likely have been required to extend survival, but given the rapid and grave progression, the family chose palliative care. Within a few months after birth, he experienced rapidly progressive heart failure and died.


A 65-year-old male presented with six months of swelling and boutonniere deformity of the right digit III following a motorcycle accident on January 1, 2023. He initially self-managed with analgesics and did not seek care. He reported inability to fully extend the right middle finger. Examination demonstrated edema and a boutonniere posture (PIP flexion, DIP hyperextension). Active PIP ROM was 45–110 degrees, with passive PIP ROM within normal limits. Radiographs of the right hand (AP/lateral) revealed no osseous pathology, supporting a soft-tissue etiology consistent with a central slip injury.

Surgical technique: Central slip defect reconstruction was performed using the partial ulnar slip of the flexor digitorum superficialis (FDS) tendon. Under anesthesia and tourniquet control in the supine position, a midlateral incision was made on the ulnar aspect of the middle phalanx centered at the PIP joint with dorsal oblique extension, and a transverse incision was made over the MCP flexion crease proximal to the A1 pulley. The ulnar digital neurovascular bundle was identified and protected. Full-thickness dorsal flaps were elevated to expose the central slip and extensor mechanism to the PIPJ. Scar and pseudotendinous tissue were excised. The central slip was not amenable to primary repair; therefore, the ulnar slip of the FDS was selected for reconstruction. The ulnar neurovascular bundle was mobilized to visualize the periosteal insertion of the A3 pulley. The extensor tendon was mobilized and tenolyzed; the dorsal PIP capsule was incised with removal of interposed tissue. The A3 pulley periosteal insertion and the volar capsule of the PIP joint were incised longitudinally. A 2–0 non-absorbable monofilament suture was placed around the ulnar FDS slip at the PIP level. Through the proximal incision, the flexor sheath and A1 pulley were incised longitudinally to expose the FDS; the ulnar slip was isolated and transected, preserving the radial slip. The previously placed 2–0 suture facilitated delivery of the distally based ulnar FDS slip distally. A 2.8‑mm dorsal-to-volar bone tunnel was drilled at the base of the middle phalanx; an elevator protected the FDP, volar plate, and volar structures. With the PIP reduced in full extension, the FDS slip was passed through the tunnel and routed through the intact proximal segment of the central slip/extensor tendon. A tendon weaver completed a Pulvertaft weave under appropriate tension with the PIP in full extension and reduction, secured with 3–0 non-absorbable suture. The capsule and central slip reconstruction margins were approximated; adhesions were released and lateral bands mobilized. Tenodesis effect, posture, stability, and motion were assessed. Wounds were irrigated, the tourniquet deflated, hemostasis obtained, and capillary refill confirmed. Skin was closed with horizontal mattress sutures. A sterile dressing and a well-padded PIP extension splint were applied to allow early DIP and MCP motion.

Postoperative course: First wound check at postoperative day 4; the patient received meloxicam 7.5 mg PO BID and doxycycline 100 mg PO BID for 3 days. A second wound visit occurred 3 days later. At 2 weeks, the back slab and external sutures were removed, and active and passive PIP ROM exercises were initiated. By 3 weeks, the wound had healed and PIP ROM was 0–90 degrees. At 1 month, PIP ROM improved to 0–100 degrees, with continued functional gains. After 7 weeks of rehabilitation, he returned to work with PIP ROM 0–110 degrees. Overall function improved substantially, with the DASH score decreasing from 50 to 4.2.

Interpretation: Clinical and radiographic findings were concordant with a chronic central slip injury producing boutonniere deformity (PIP flexion, DIP hyperextension due to dorsal apparatus disruption and volar migration of lateral bands). Reconstruction using an ulnar FDS slip via bone tunnel and Pulvertaft weave restored PIP extension and yielded progressive ROM gains and marked functional recovery.


A 39-year-old woman with peripartum cardiomyopathy underwent orthotopic heart transplantation in October 2014. Induction was basiliximab plus methylprednisolone. Maintenance immunosuppression included tacrolimus XL 7 mg daily, everolimus 1 mg twice daily, and prednisolone 5 mg/day. She had two episodes of acute rejection in the first post-transplant year, managed with methylprednisolone pulse therapy. Baseline renal function during year one was normal (creatinine 0.88 mg/dL; eGFR 102 mL/min/1.73m2). Follow-up was by the heart transplant team; routine BK polyomavirus screening (plasma PCR or urine cytology) was not performed.

In 2016, creatinine rose to 1.9 mg/dL (eGFR 32.6), with tacrolimus trough 7.2 ng/mL and everolimus 5.2 ng/mL. Calcineurin inhibitor toxicity was suspected; tacrolimus was reduced to 4 mg daily, and creatinine improved to 1.25 mg/dL (eGFR 54.1); no biopsy was obtained. In March 2017, creatinine increased to 2.69 mg/dL (eGFR 21.4) without symptoms. Vitals and exam were unremarkable; renal ultrasound showed normal size with increased echogenicity; urinalysis/culture were negative (no hematuria, pyuria, or casts); echocardiogram showed adequate cardiac function; HIV, syphilis, HBV, and HCV serologies were negative. Tacrolimus and everolimus troughs were 5.2 ng/mL and 5.98 ng/mL, respectively. Despite IV hydration and reducing tacrolimus XL to 2 mg daily, renal function did not improve, prompting biopsy.

Renal biopsy demonstrated active chronic interstitial (tubulointerstitial) nephritis associated with advanced polyomavirus nephritis. Plasma BK virus PCR was positive at 33,800 copies/mL (log 4.5). Tacrolimus was discontinued; creatinine stabilized between 2.2 and 2.4 mg/dL with declining BK viremia to undetectable. Over three years, there were no further cardiac rejection episodes. At two years of follow-up from diagnosis of BKVN, renal function was stable with creatinine 2.5 mg/dL (eGFR 23.4 mL/min/1.73m2).

Context: BK polyomavirus nephropathy, while classically described in kidney transplant recipients, can occur in non-renal solid organ transplant recipients under potent immunosuppression. Management centers on reduction of immunosuppression; maintaining an mTOR inhibitor (everolimus) while withdrawing the calcineurin inhibitor can aid viral clearance, at the potential cost of rejection risk, which was not observed here. Plasma BK viral load (log 4.5) plus biopsy-proven late-stage BKVN established the diagnosis and guided therapy.


We report a 49-year-old woman with end-stage renal disease and advanced heart failure secondary to long-standing systemic lupus erythematosus (SLE, onset at age 13) and lupus nephritis (LN class III, then IV). Childhood LN was treated with steroids plus cyclophosphamide, later transitioned to methotrexate and then azathioprine, achieving partial remission of nephrotic syndrome; she had no immunosuppression after 2002. She was HBV- and HCV-positive. Cardiovascular SLE involvement included early coronary atherosclerosis, ischemic heart disease, and myocardial infarction at age 20. In 2007, with creatinine 2.2 mg/dL and proteinuria 2 g/day, kidney biopsy showed active and sclerotic focal proliferative LN; immunosuppression was withheld due to active HCV replication. Renal function progressively declined. Despite PCI to the RCA, she developed severe post-infarction and dilated cardiomyopathy, requiring primary-prevention ICD implantation in 2009. On a lupus and secondary cardiomyopathic background, she developed severe mitral and tricuspid regurgitation. In 2014 she underwent mitral and tricuspid valve repair and left ventricular volume reduction surgery, complicated by low cardiac output syndrome necessitating intra-aortic balloon pump support. Postoperatively, renal function worsened, prompting initiation of renal replacement therapy; she remained on dialysis for four years.

While listed for kidney transplantation, laboratory indices indicated lupus remission (C3 0.93 g/L, C4 0.4 g/L, ANA negative) but persistent circulatory insufficiency with markedly reduced functional capacity (limited to one flight of stairs) and elevated BNP 619 pg/mL (n 0–100). Pre-transplant transthoracic echocardiography demonstrated markedly enlarged LV and LA, severely reduced LV systolic function (LVEF 26%, GLS −3). Mitral ring precluded diastolic assessment. High tricuspid regurgitant flow gradient with a dilated, poorly respiratory mobile IVC suggested high probability of pulmonary hypertension.

Given the extremely low ejection fraction, cardioprotective therapy with levosimendan (a calcium sensitizer/inodilator) was instituted perioperatively. Due to transplant timing constraints, infusion (0.1 μg/kg/min) began as soon as crossmatch results were available, immediately post-dialysis, and was continued through the operation for a total of 24 h. Anesthetic management prioritized optimization of allograft perfusion, avoidance of nephrotoxins and renally excreted agents, and use of nephroprotective measures. Because of recurrent extrasystoles with prior decompensation and the need to deactivate the ICD during transplantation, a Swan-Ganz catheter was not placed. Monitoring included ECG, central venous catheter with CVP, invasive arterial blood pressure via radial arterial cannula, and cardiac ultrasound. CVP guided intravascular volume during anesthesia, and postoperative assessments incorporated focused cardiac ultrasound with IVC diameter and respirophasic variability. Fluid management followed a Goal Directed Therapy paradigm. Agents included fentanyl, triacrium, propofol, desflurane, antibiotic prophylaxis, standard immunosuppression, mannitol 25 g for nephroprotection, and 0.9% NaCl for fluid therapy.

Postoperatively, immunosuppression comprised steroids and tacrolimus; mycophenolate mofetil was discontinued due to persistent leukopenia and cytomegalovirus infection. Delayed graft function occurred, necessitating hemodialysis for almost six weeks (largely due to fluid retention). BNP rose to 2996 pg/mL and then gradually declined. Allograft biopsy at postoperative week two revealed acute rejection (AR II B, Banff 2015) with acute tubular necrosis. She was discharged on postoperative day 67 with serum creatinine 1.4 mg/dL and BNP 1794 pg/mL.

At one month post-transplant, echocardiography showed reduced LV dimensions and improved systolic performance (EF increased to 30%, GLS to −6). Tricuspid regurgitant gradient decreased, and IVC caliber and respirophasic motion normalized, indicating low probability of pulmonary hypertension. Functional status improved from NYHA III/IV to NYHA II. At five months, there was continued cardiac improvement with BNP down to 1066 pg/mL and normalization of renal function. Overall, despite a nontrivial postoperative course, perioperative levosimendan support and tailored hemodynamic and nephroprotective strategies were associated with successful kidney transplantation, progressive recovery of LV function, and stable, normal allograft function at short-term follow-up.


A 51-year-old man came to us with sudden, painful vision loss in his left eye for three days. His right eye could see clearly (20/20). His left eye could only see hand movements. The back of his left eye showed swelling of the seeing nerve, a bulge in the layer under the retina, several patches of fluid under the retina, and wrinkles in the thin lining there. An MRI scan with contrast dye of the eyes and brain showed a small lump behind the eye where the eye nerve meets the white part of the eye. Tests for cancer and immune diseases were normal. The doctors diagnosed inflammation in the back part of the eye’s white coat that forms a small lump (nodular posterior scleritis). They started high-dose steroid pills by mouth (prednisolone).


A 19-year-old woman went to the emergency room. Her heart was beating fast and uneven. Her body showed signs that her heart was not pumping enough blood. A heart tracing test showed she was not having a heart attack. A heart MRI did not show a disease of the heart muscle. A special heart CT scan then looked at her heart arteries. It showed the normal opening to her right heart artery was missing from birth. She was sent to a center that treats heart problems people are born with. Doctors did an electrical test inside her heart. They found a small hot spot on a tiny muscle that helps a heart valve. That spot was starting the bad rhythm, like a faulty spark. The team gently burned that spot to stop it. She has had no symptoms since.


This story is about a 49-year-old woman who had lupus for many years. Over time, her kidneys and her heart got weaker. She needed dialysis to do the work of her kidneys for 4 years until she could get a kidney transplant. Her heart pump was very weak before surgery. To help her heart get through the operation, doctors gave her a heart-helping medicine called levosimendan. The time after surgery had some ups and downs. But she got through it. At about one month after surgery, her heart started to work better, and her new kidney worked normally. At about five months, her heart kept improving, and her kidney function stayed normal.


A 10-year-old boy receiving chemotherapy for acute lymphoblastic leukemia developed a brain abscess during induction therapy. He had a severe headache, and brain scans (CT/MRI) showed lesions that looked like an infection. Tests on his spinal fluid directly detected Bacillus cereus, confirming the cause. He was treated with antibiotics (such as meropenem and vancomycin). His symptoms resolved, follow-up imaging showed the abscess shrinking, and he recovered well.


A 28-year-old Moroccan man developed about a month of liver-area pain along with fever, night sweats, and weight loss, which are symptoms that can suggest tuberculosis. CT and MRI showed multiple non-specific nodules in the liver. An initial needle biopsy was not conclusive, so doctors performed a laparoscopy to obtain better tissue samples. Pathology showed granulomas with caseous necrosis, confirming focal hepatic tuberculosis. He started standard anti-tuberculosis therapy: two months of four drugs, then four months of two drugs. He improved quickly, both in how he felt and in his lab results. A follow-up scan at three months showed that the liver nodules were fewer and smaller.


A 10-year-old male with high-risk early T-cell acute lymphoblastic leukaemia (initially treated per LAL SEHOP-PETHEMA 2013) experienced an early CNS relapse two years after diagnosis and began InteReALL HR 2010 induction with bortezomib. After four weeks of profound neutropenia (20 neutrophils/µL) on prophylaxis (cefepime, cotrimoxazole, fluconazole) and acyclovir for HSV-1 skin infection, he developed a severe, analgesia-refractory headache. Head CT revealed a right temporal hypodense lesion. Suspecting infection, a lumbar puncture was performed and cefepime was switched to meropenem plus vancomycin. Despite being afebrile, he showed signs of septic shock on day 1 and required PICU admission for inotropic/vasoactive support; antimicrobials were broadened with gentamicin and caspofungin. Inflammatory markers rose (CRP 312 mg/L, procalcitonin 47.58 ng/mL by day 3), with pancytopenia attributable to chemotherapy and no other major biochemical abnormalities. Blood, urine, and fecal cultures were negative; viral serologies were negative. CSF biochemistry was normal (glucose 63 mg/dL; protein 16 mg/dL; leukocytes 1/µL), but microbiology detected Bacillus cereus, susceptible to meropenem, vancomycin, linezolid, and ciprofloxacin; CSF PCR/assays were negative for HSV-1/2, HHV-6, CMV, VZV, enterovirus, parechovirus, Toxoplasma, Neisseria meningitidis, Listeria monocytogenes, Streptococcus pneumoniae, and Cryptococcus. EEG showed diffuse slowing without epileptiform activity. On day 4, once off haemodynamic support, brain MRI demonstrated two T2/FLAIR hyperintense subcortical lesions in the right temporal and parietal lobes; the parietal lesion exhibited ring enhancement post-gadolinium, both lesions had peripheral diffusion restriction, and scattered parenchymal microhaemorrhages were present—an appearance suggestive of bacterial abscess due to an atypical pathogen. Integrating imaging with direct CSF detection established the diagnosis of B. cereus cerebral abscess. After two weeks of therapy, his headache resolved with no focal neurological deficits; interval MRI showed lesion size reduction. Vancomycin and acyclovir were discontinued after three weeks, and meropenem was continued to complete six weeks, with a favourable clinical course.


A 16-year-old girl has a sunken, gray patch on her left thigh. A special scan that looks at blood vessels showed a blood vessel problem in the skin and in the layer just under the skin.


A 4-year-old boy with metastatic neuroblastoma received intensive treatment, including chemotherapy, an autologous stem cell transplant, and then an allogeneic cord blood transplant. About a month after he developed upper respiratory symptoms and tested positive for RSV, he presented on day 194 post–cord blood transplant with worsening breathing problems and was ultimately diagnosed with pulmonary veno-occlusive disease (PVOD), a rare form of pulmonary hypertension caused by blockage of small lung veins. Lung biopsy not only confirmed PVOD-related changes but also showed lung injury patterns consistent with a recent viral infection. Taken together, the timing of his RSV infection and the biopsy findings suggest RSV may have contributed to the onset of PVOD.


A 40-year-old man with HIV on treatment presented with intermittent fevers for two years. Over the prior two months, he developed progressive, diffuse abdominal pain and generalized lymphadenopathy. Laboratory tests showed pancytopenia, coagulopathy, hypoalbuminemia, and elevated inflammatory markers. CT of the chest, abdomen, and pelvis revealed only hepatosplenomegaly and widespread adenopathy. Broad infectious workup, including mycobacterial cultures from multiple specimens, was negative except for a positive HHV-8 RT-PCR. A left iliac lymph node biopsy was consistent with Castleman’s disease. Despite restarting antiretroviral therapy, his condition worsened, so clinicians initiated corticosteroids and ganciclovir. After one week he developed multiorgan failure with anasarca, making those medications unsafe. Repeat chest CT showed right upper lobe tree-in-bud infiltrates with bilateral pleural effusions; abdominal imaging showed worsening hepatosplenomegaly and new ascites. He was transferred to the ICU 48 hours later for fulminant hepatic failure and died shortly afterward. Postmortem testing grew Mycobacterium tuberculosis from a tracheal aspirate, and liver biopsy showed non-necrotizing granulomas.


Case summary: A 67-year-old woman with a six-year history of recurrent left lower limb swelling presented with one month of progressive dyspnea and fatigue consistent with acute exacerbation of chronic heart failure. She had no prior cardiovascular disease, trauma, or surgery; remote oral estrogen use occurred seven years earlier. Examination showed marked left leg edema, skin sclerosis, absent popliteal and distal pulses, and a palpable thrill/tremor in the left thigh. Echocardiography demonstrated cardiomegaly with moderate mitral regurgitation, severe tricuspid regurgitation, and LVEF 60%. BNP was 2853 ng/L. ECG showed sinus tachycardia (105 bpm) with left atrial enlargement. Chest CT confirmed cardiomegaly without pulmonary parenchymal disease. CTA revealed a left iliac artery aneurysm (max 32 mm), marked dilation of the CFA (27 mm) and SFA (22 mm), complex AVMs centered on the SFA with early opacification of an enlarged femoral vein, and nonvisualization of the popliteal and anterior tibial arteries. She was diagnosed with complex congenital lower-limb AVMs and acute exacerbation of chronic heart failure, NYHA class IV.

Rationale and strategy: Preoperative duplex showed CFA volume flow of 3400 ml/min, indicating a high-flow shunt. Given prior coil embolization (two coils, 20 mm x 40 cm) failed to reduce flow or swelling, the team prioritized rapid shunt reduction using a covered stent, with staged embolization to address the nidus. This approach repurposed an abdominal aortic stent graft to reduce AVM inflow and improve cardiac load while limiting operative time in the setting of heart failure.

Procedure details: To minimize access complications in dilated vessels (iliac 32 mm, CFA 27 mm, SFA 22 mm), antegrade surgical exposure of the CFA was performed under general anesthesia, placing a 14 F sheath. Complex AVMs were visualized in the SFA and profunda femoris with early venous filling. Based on a preoperative SFA mid-segment diameter of 19 mm, a 20–12 mm/120 mm aorto-uni-iliac abdominal aortic covered stent graft (MicroPort, China) was advanced over a 0.035 super-stiff wire (after popliteal access with a single-curve catheter) and deployed at the distal SFA to span the highest AVM density. Completion angiography showed marked reduction of peri-stent venous opacification with clear visualization of the popliteal artery. The femoral arteriotomy was closed with 6-0 vascular suture. The patient’s heart failure symptoms improved postoperatively, and a staged embolization was planned to limit procedure time.

Second stage and outcomes: At one week, CFA flow decreased to 1600 ml/min and BNP to 1198 µg/L. Transvenous embolization targeted the nidus and draining veins via right CFA arterial access (5 F sheath/catheter) and ultrasound-guided puncture of the AVM drainage vein (5 F venous sheath). Embolic materials included one 18–20 mm x 40 cm coil, two microcoils (4 x 42 mm, 5 x 10 mm), 3% polidocanol (6 mL), and 99% anhydrous ethanol (10 mL). Completion angiography demonstrated near-complete disappearance of AVM/shunting. At one year, leg swelling and cardiac function improved substantially: CFA flow was 780 ml/min; echocardiography showed only mild biatrial enlargement, mild mitral and tricuspid regurgitation, and LVEF 71%; BNP declined markedly.

Practical experience and limitations: In very high-flow, complex congenital lower-limb AVMs causing high-output heart failure, coil-only embolization may be insufficient to meaningfully reduce shunt volume. A covered stent can rapidly downregulate inflow and unload the heart, but often requires adjunctive embolization of the nidus and draining veins to consolidate results. Repurposing an abdominal aortic aorto-uni-iliac covered stent in the SFA is technically feasible but off-label, demands large-bore access (14 F) with surgical exposure, and may be limited by vessel size mismatch, landing zone adequacy, and the need to preserve distal perfusion. Staging is advisable in NYHA IV patients to shorten anesthesia time and manage hemodynamics. This case illustrates that an abdominal aortic stent graft coupled with targeted embolization can effectively address acute heart failure driven by complex congenital lower-limb AVMs, while highlighting device-selection and access considerations that may constrain its use.


A 12-year-old boy with Down syndrome and motor disorders was referred to the Oral Medicine clinic. On exam he had a dysmorphic face and dry, cracked lips; a cervical collar prevented assessment of his neck lymph nodes. Inside the mouth there was an irregular ulcer on the right lateral border of the tongue measuring about 1 × 0.7 cm, with a firm (indurated) edge and a white-yellow base. A sharp remnant of tooth 55 was causing repeated trauma to that part of the tongue. Based on the history and exam, the team diagnosed a chronic traumatic ulcer that clinically looked like oral squamous cell carcinoma (OSCC). Other dental problems included caries and several tooth remnants (63, 55, 62, 74, 85) that were recommended for extraction and later space maintenance. Blood tests showed low sodium and a mildly raised lymphocyte percentage, and MRI revealed a cervical spine dislocation; the patient later had neurosurgery. Treatment in hospital included paracetamol and amoxicillin, and local oral care from the Oral Medicine team: saline rinses (0.9% sodium chloride), 1% povidone-iodine mouthwash as an antiseptic, and petroleum jelly for the lips. The mother was instructed to clean the mouth with gauze soaked in saline, apply the povidone-iodine compress to the ulcer three times daily, and use petroleum jelly to moisturize the lips. The oral lesions improved over follow-up visits at 3 days, 1 week, and 10 days. After neurosurgery the patient was observed in the pediatric intensive care unit but developed respiratory failure and died.


A 25-year-old Sundanese male presented to the Dental Hospital, Faculty of Dentistry, Universitas Padjadjaran with a 4-day history of painful oral ulcerations that appeared intraorally first and extended to the lips 2 days later, exacerbated by eating and speaking. He initially self-treated with petroleum jelly without benefit, then applied triamcinolone acetonide 0.1% in orabase once daily from a pharmacy, with partial but incomplete improvement. One week prior to lesion onset he reported a febrile episode; he also reported heavy workload and approximately 1.5 months of suboptimal nutrition. He denied systemic disease, drug or food allergies, alcohol, and tobacco, but reported frequent lip-licking; childhood varicella was noted.

General examination showed normal vital signs and no lymphadenopathy. Extraoral findings: serosanguineous crusts on the lips that were painful and bled easily. Intraoral findings: irregular, diffuse-bordered erythematous lesions with pain on the upper and lower labial mucosa. Additional findings included a non-scrapable hyperkeratotic white plaque of irregular shape with diffuse borders on the left buccal mucosa near tooth 38; scrapable yellowish-white plaques on the posterior third of the dorsal tongue without underlying erythema; crenated tongue with dental impressions laterally; a painless, hard torus palatinus (~2 × 1 × 0.5 cm) at the hard palate midline; multiple teeth with caries, radix, and edentulous areas; poor oral hygiene.

Psychological assessment (DASS-21): normal depression (0), anxiety (6), and stress (6). Working diagnosis: suspected HAEM, with concurrent findings of coated tongue, frictional keratosis, crenated tongue, torus palatinus, reversible pulpitis (tooth 18), irreversible pulpitis (tooth 47), chronic apical periodontitis et causa radix (tooth 15), and edentulous teeth 28, 37, 36, and 46. Differential diagnosis for the lip lesions included exfoliative cheilitis, which lacks herpesvirus involvement. Serologic testing (IgG anti–HSV-1) was indicated to support the diagnosis. Baseline OHRQoL (OHIP-14) was 35 (moderate).

Initial management combined non-pharmacologic and pharmacologic therapy. Non-pharmacologic: oral hygiene instructions (brush teeth and tongue twice daily with a soft-bristled brush and non-detergent toothpaste), hydrate with ≥2 L water/day, consume a balanced diet, avoid acidic, spicy, hard, and MSG-containing foods, and cease lip-licking and peeling. Pharmacologic: topical lip compresses with 0.9% NaCl at least three times daily and triamcinolone acetonide 0.1% in orabase applied thinly to the lips three times daily; a daily multivitamin was prescribed.

At 2-day follow-up, pain had decreased though serosanguineous crusts persisted. Serology returned positive for anti–HSV-1 IgG, ratio 6.32 (positive >1.1). A definitive diagnosis of HAEM (herpes-associated erythema multiforme) was established based on history, clinical findings, and serology. Existing therapy was continued, and acyclovir 200 mg orally five times daily for 7 days was added.

At 5 days after the prior visit, there was significant improvement with excellent healing of all oral lesions. Final OHIP-14 was 4, and physical, psychological, and social conditions normalized after 7 days of treatment. The patient was referred for definitive dental and oral care in periodontics, dental conservation, oral surgery, and prosthodontics. Written informed consent and institutional approval were obtained; the case complies with the Declaration of Helsinki.

Context: HAEM is an immune-mediated mucocutaneous reaction pattern commonly triggered by HSV-1. Positive HSV-1 serology in the appropriate clinical context, together with characteristic labial crusting and diffuse labial mucosal erythema, supports the diagnosis. Management typically combines topical corticosteroids and systemic antiviral therapy, along with supportive oral care and trigger avoidance.


A 78-year-old woman enrolled in a community pharmacy personalised dosage system (PDS/SPD) presented at medication pickup reporting several months of asthenia, weakness, dizziness, and confusion, limiting her usual ambulation. There were no new medicines in the SPD register. On-site vitals with an Omron Complete device showed SBP 96 mmHg, DBP 52 mmHg, HR 69 bpm, raising concern for symptomatic hypotension possibly related to her regimen. Her active medications and doses were: doxazosin 2 mg q24h (0-0-1) for hypertension; losartan 100 mg q24h (1-0-0) for hypertension; manidipine 20 mg q24h (0-1-0) for hypertension; simvastatin 40 mg q24h (0-0-1) for hypercholesterolemia; acetylsalicylic acid 100 mg q24h (1-0-0) for secondary prophylaxis; omeprazole 20 mg q24h (1-0-0) for ulcer prevention; pregabalin 100 mg q12h (1-0-1) for neuralgia; torasemide 10 mg q24h (1-0-0) for edema; dulaglutide 1.5 mg weekly; insulin glargine 74 IU q24h (1-0-0); insulin lispro 20 IU q24h (0-1-0) for diabetes; brimonidine 1 drop q12h (1-0-1) for ocular hypertension.

Renal function by CKD-EPI yielded eGFR 30 ml/min/1.73 m2. Dose appropriateness was assessed against product information and a consensus guideline for drug use in renal impairment from the University of Barcelona Faculty of Pharmacy practical pharmacy group (ATC-organised, with overdose symptom summaries and risk stratification by eGFR). Based on eGFR 30 ml/min/1.73 m2, antihypertensive agents losartan and manidipine required dose adjustment; pregabalin also warranted renal dosing, and torasemide was recognised as potentially contributing to low BP. The team prioritised adjusting antihypertensives first and proposed deferring changes to pregabalin until after reassessing response.

Intervention: A report to the primary care physician recommended reducing losartan to 50–75% of standard dose for eGFR 30–59 ml/min/1.73 m2 and adjusting manidipine for eGFR 15–30 ml/min/1.73 m2. The PCP implemented losartan 50 mg q24h and manidipine 10 mg q24h. The PCP also substituted pregabalin 100 mg q12h with gabapentin 300 mg q12h.

Follow-up over two months showed improved BP values and resolution of the initial symptoms. Gabapentin 300 mg q12h was verified as appropriate for eGFR ~30 ml/min/1.73 m2 (recommended total daily dose 300–900 mg for eGFR 30–60). Overall, the case suggests symptomatic hypotension related to cumulative antihypertensive effect in the setting of stage 3b CKD by eGFR, with clinical improvement after renal dose adjustment of losartan and manidipine and subsequent regimen optimisation.


A.P. is a 38‑year‑old woman who developed dilated cardiomyopathy at age 17, likely on the background of infectious myocarditis after a throat infection. She was hospitalized for 10 months and 10 days with severe heart failure and a very low ejection fraction while being evaluated for heart transplantation. There was no clearly dangerous arrhythmia. Treatment focused on heart failure care and on preventing arrhythmias and blood clots.
Her heart function recovered—a remission seen in about 16% of patients—and that improvement lasted 4 years. She then had a two‑year worsening, followed by several stable years and a normal first pregnancy. During her second pregnancy, she experienced a flare in the second trimester with postpartum dilated cardiomyopathy that lasted a couple of months, then improved.
As of May 2017, she was stable on guideline‑based therapy (an ACE inhibitor, a beta‑blocker, diuretics, and an If‑channel blocker), reported no limitation in physical activity, and was a mother of two and unemployed.


A 13-year-old male from Cusco with recurrent respiratory papillomatosis (RRP) since age two (tracheostomy at age three) and a maternal history of genital papilloma presented after 16 days of predominantly nocturnal respiratory difficulty, inspiratory laryngeal stridor, and moderate dysphonia. He had previously received azithromycin and supplemental oxygen without improvement. On exam, there was mild subcostal retraction, decreased vesicular breath sounds over the left hemithorax, and scant wheezes predominating on the right; he required 4 L/min oxygen via binasal cannula. Laboratory studies showed WBC 8.03 × 10^3/μL, platelets 209 × 10^3/μL, hemoglobin 13.2 g/dL, and CRP 36.6 mg/L. Imaging included a chest study and head and neck tomography; chest tomography visualized several pulmonary cysts. Forty-eight hours after admission, he developed worsening stridor and respiratory distress, prompting emergent OR transfer for tracheostomy, microlaryngoscopy, and excision of papillomatous lesions. Intraoperative findings demonstrated extensive papillomatous disease with appendicular tumor-like lesions and ventricular bands involving the epiglottis, glottic surface, vocal cords, subglottis, and trachea to ring 5. Histopathology showed koilocytotic atypia consistent with HPV and mild focal dysplasia. Postoperatively, he was managed in the PICU with respiratory monitoring and was weaned off oxygen within 48 hours. He received a single intravenous dose of bevacizumab 400 mg and showed prompt clinical improvement. He completed a seven-day hospitalization with normalization of oxygen saturation and progressive oxygen weaning, then was transferred for ongoing care. He also received respiratory therapy. On telemonitoring at eight months, there was no evidence of recurrence or intercurrent events. Clinical context: RRP is typically HPV-related (often low-risk types) and can cause multifocal papillomas leading to airway stenosis; anti-VEGF therapy such as bevacizumab is used off-label to reduce angiogenesis and disease recurrence, and in this case was associated with a favorable short- to mid-term outcome.


A full‑term male newborn, 2 days old and delivered by cesarean section, presented with a congenital right scrotal swelling. On arrival he appeared well perfused and stable. Examination showed the right testis was enlarged, tense, non‑tender, and visibly reddish with excoriated overlying skin. Transillumination was negative on the right and positive on the left; both hernia openings were normal. Doppler ultrasound showed the right testis was enlarged with a heterogeneous, darker appearance and no detectable blood flow; the left testis looked normal, with only a small amount of fluid. He was taken urgently to surgery. Intra‑operatively, the right testis was frankly nonviable due to intravaginal torsion, with minimal hydrocele. Surgeons removed the right testis (orchidectomy) and fixed the left testis in place (contralateral orchidopexy) to reduce the risk of future twisting.


Patient: 27-year-old woman, 16 weeks pregnant, with beta thalassemia major on monthly transfusions. Iron chelation was stopped during pregnancy.

Presenting concerns: Since early pregnancy she had swollen, bleeding gums and bad breath. Exam showed dry, exfoliative lips and generalized gingival enlargement with redness, soft tissue, dark red rounded margins, easy bleeding, pain, and true periodontal pockets on the labial, buccal, palatal, and lingual surfaces. She had never seen a dentist for these issues. No other systemic illnesses were reported. Hematology showed anemia with abnormalities and evidence suggesting infection.

Assessment: Gingival enlargement and chronic periodontitis associated with pregnancy and beta thalassemia major.

Management: Multidisciplinary dental care included 3% hydrogen peroxide rinses, a chlorine dioxide spray mouthwash, a course of antibiotics, professional calculus removal (scaling/root planing), and oral hygiene instructions. Medical care continued monthly transfusions; iron chelation remained on hold during pregnancy.

Outcome: After about three months of coordinated care, symptoms and clinical findings improved satisfactorily.


A 71-year-old patient with untreated, long-standing vitiligo presented with a 6-month history of right-eye visual loss and bilateral hearing loss, right-predominant. During admission he endorsed chronic headaches, intermittent fever, significant unintentional weight loss, generalized asthenia, and skin thickening. Initial ophthalmologic assessment: RO visual acuity reduced to light perception with impaired color discrimination; LO visual acuity 20/200. There was an afferent pupillary defect in both eyes and hyperemic eyelid margins. Anterior segment (both eyes): hyperemic bulbar conjunctiva, ciliary injection, cornea with peripheral nummular subepithelial infiltrates, aqueous anterior chamber without cellularity, normal iris, and lenses with nuclear opacities. Fundus, RO: pale (++) optic disc with approximately 50% excavation, slightly blunted nasal margin, attenuated/“raised and thinned” vasculature, macular area with scattered pigment. Fundus, LO: 2+ vitreous haze; edematous, hyperemic optic disc with blurred margins; peripapillary streaked hemorrhages; excavation not assessable; thinned vasculature; macular area with scattered pigment. Impression at that time documented right optic atrophy and left anterior optic neuritis. Workup for ocular–neurologic disease included evaluation to exclude tuberculosis, herpes, ANCA and non-ANCA vasculitides, and sarcoidosis. Lumbar puncture: opening pressure within normal limits; CSF protein 54 mg/dL. Nerve conduction velocities showed a polyradiculoneuropathy with moderate–severe axonal degeneration involving all four extremities, greater in the lower limbs. Contrast-enhanced MRI of the brain and orbits showed no optic nerve enhancement and no intracranial masses, but did reveal sinusitis and meningeal enhancement. Sarcoidosis was further disfavored by a normal ACE level and a whole-body gamma scan without hypermetabolic foci. On repeat ophthalmologic evaluation, there was progression with persistent right optic atrophy and left anterior optic neuritis. High-dose pulse corticosteroids were initiated, followed by a taper. The patient experienced clinical and functional improvement, particularly in neurologic and ophthalmologic parameters.


Who: A 20-year-old Arabic man who practices martial arts. Problem: Pain in the back of his left thigh for 5 weeks. He tried medicines and physical therapy, but they did not help. Doctors said it was not a trapped-nerve problem in the hamstring. He stopped all sports. Treatment: He did a gentle seated nerve-glide exercise four times a day for three days in a row. He also learned better posture. Pain before treatment: 5 out of 10 at rest. 7 out of 10 with activity. Pain after 3 days: 2 out of 10 at rest. 4 out of 10 with activity. Knee scores got better. Pain part went from 22 to 61. Function part went from 30 to 80. After 2 months, he felt fully recovered and returned to sports with no problems.


A 67-year-old patient with no significant past medical history presented with declining overall health marked by progressive hoarseness (dysphonia) and difficulty swallowing (dysphagia). Imaging showed a large nasopharyngeal/neck mass. Biopsy confirmed grade 1–2 follicular non-Hodgkin lymphoma. CT of the neck, chest, abdomen, and pelvis found a nasopharyngeal mass measuring about 70 × 40 mm with extension to 60 mm. Bone marrow biopsy and the pre-treatment evaluation were normal. The patient received four cycles of rituximab plus CHOP without response, followed by three cycles of rituximab plus DHAOX, with persistence of the mass. Repeat biopsy then showed loss of B‑cell infiltration and the presence of AL amyloid deposits. Serum protein immunoelectrophoresis detected immunoglobulin M. PET imaging demonstrated a hypermetabolic nasopharyngeal process. The patient is currently being treated with bortezomib, prednisone, and bendamustine.


A 77-year-old male with a history of moderate cognitive impairment presented after a tonic–clonic seizure at home. On arrival to the ED he was hemodynamically unstable in a postictal state with suspected intrapelvic bleeding, triggering activation of the polytrauma code (for physiology rather than mechanism). He was stabilized with intravenous fluids and transfusion of packed red blood cells, and a pelvic girdle was applied. Once stable, examination showed shortening of the lower limb compared with the contralateral side, external rotation, and joint blockage on log-roll testing in both limbs, with functional impotence of both hips. Neurologic assessment was initially limited. There were no external injuries; distal foot pulses were present, and he could move his upper limbs. Chest and AP pelvic radiographs were obtained; the pelvic film demonstrated bilateral femoral dislocation, and a reduction procedure was performed. Computed tomography angiography was then used to exclude vascular injury (none identified). 3D-CT reconstructions revealed bilateral transverse acetabular fractures per Letournel, bilateral longitudinal iliac wing fractures, and intrapelvic protrusion of both femoral heads. Bilateral supracondylar femoral traction was applied and pelvic traction was removed. The patient was operated on hospital day 8, in accordance with the service protocol to delay acetabular fracture surgery approximately 7 days to allow fibrosis at the fracture site and reduce intraoperative bleeding. Given anticipated operative duration, a staged approach was selected. Perioperatively, both procedures were performed under general anesthesia with tranexamic acid to limit bleeding and cefazolin prophylaxis (2 g pre-op, then 1 g q8h for 24 h). Postoperatively, enoxaparin 40 mg SC daily was administered for 7 weeks. The left hemipelvis was addressed first due to greater radiographic protrusion and concern that a soft-tissue hematoma could complicate femoral head extraction (risk of vascular injury/bleeding). With the patient in lateral decubitus, a posterolateral approach was used. A Moore’s autograft was placed in the acetabular background (fracture focus). A Burch-Schneider Reinforcement Cage (Zimmer Biomet) was implanted, anchored to the ischium and ilium; dissection of the gluteus minimus and medius was required to position the femoral head. The ischial fixation was secured with screws, and fluoroscopy confirmed component positioning. A cemented dual-mobility acetabular construct was then implanted, followed by a non-cemented femoral stem. Closure included the capsule and pelvic musculature with transosseous trochanteric sutures. Seven days later, the right side was performed in lateral decubitus. The longitudinal iliac wing fracture was addressed first via the first window of the ilioinguinal approach and fixed with a six-hole anatomical plate. The hip reconstruction then mirrored the left: anti-protrusion ring with a cemented dual-mobility acetabular component and a non-cemented femoral stem. The authors note that anti-protrusion rings are indicated for acetabular fractures equivalent to pelvic discontinuity (AAOS type IV acetabular defects), requiring ischial and iliac anchorage, and are not indicated for isolated anterior or posterior wall fractures without acetabular floor involvement. During admission, the patient remained in bed with mobilization to prevent pressure ulcers. After the second operation and as tolerated, he transferred using a wheelchair; in bed he had unrestricted range of motion. He was discharged at 4 weeks and remained non–weight bearing until 6 weeks, then progressed to loading with a cane. Loading was delayed to allow initial consolidation of the acetabular background graft to support the ring and because bilateral involvement precluded practical partial weight bearing. At 12 months, he was fully weight bearing with a cane, with Harris Hip Scores of 79 (left) and 77 (right), WOMAC 12, and no postoperative complications. He reported occasional discomfort and a mild right-sided limp, had full range of motion on examination, and no episodes of instability since surgery.


This report describes a 49-year-old woman with long‑standing systemic lupus erythematosus (SLE) who developed progressive kidney and heart failure and was listed for kidney transplantation after four years on dialysis. Her SLE began in childhood with lupus nephritis and she had prior immunosuppressive treatments; she was also hepatitis B and C positive. She had early heart disease, including a heart attack at age 20, later developed ischemic and dilated cardiomyopathy, received an ICD, and underwent mitral and tricuspid valve repair with left‑ventricle surgery; after that operation her kidney function worsened and dialysis was started. Before transplant she had severe heart dysfunction (LVEF about 26%, high BNP) and signs suggesting possible pulmonary hypertension, so the team added perioperative cardioprotective therapy with levosimendan. Levosimendan infusion (0.1 µg/kg/min) began after a dialysis session when the donor match was confirmed and continued through the first 24 hours after surgery. Anesthesia and postoperative care focused on protecting the new kidney and careful fluid and hemodynamic management; invasive pulmonary artery catheterization was avoided because of her ICD and unstable rhythm history. The postoperative course was complicated: she experienced delayed graft function requiring hemodialysis for roughly six weeks, had a biopsy‑proven acute rejection episode with acute tubular necrosis, and developed leukopenia and cytomegalovirus infection that led to changes in immunosuppression. BNP rose after surgery but then gradually fell; she was discharged on day 67 with serum creatinine 1.4 mg/dL. By one month after transplant there was measurable improvement in heart size and function (EF up to ~30%, better strain measurements), lower pressures suggesting less pulmonary hypertension, and better exercise tolerance (NYHA III/IV to II). At five months she had continued improvement in heart function, BNP down to about 1066 pg/mL, and normal kidney function.


A 23-year-old male with a 23 pack-year smoking history, no alcohol use, and no illicit drug use presented with 2 hours of sudden severe frontal headache, nausea, vomiting, and chest heaviness. He was distressed but alert and oriented. Vitals: BP 178/103 mmHg, RR 26/min, T 38.9°C, HR 87/min, SpO2 94%. Exam: normal vesicular breath sounds; cardiovascular and abdominal exams inconclusive; neurological exam notable for neck stiffness, dilated but light-reactive pupils, normal plantar reflexes, and no focal deficits. ECG showed ST-segment elevation >2 mm in V2–V5, consistent with STEMI; he received a 300 mg aspirin load and was urgently transferred for PCI. Troponin was elevated at 1.48 mg/dl (normal <0.16 mg/dl). Femoral-access coronary angiography demonstrated normal coronary arteries with TIMI 3 flow. Post-angiography ECG showed normal sinus rhythm with LVH; echocardiography revealed normal ventricular function without RWMA. Subsequent workup found lymphocytosis and mildly elevated CRP. Non-contrast CT brain demonstrated a cisternal subarachnoid haemorrhage with extension anterior to the right temporal lobe. Abdominal ultrasound was negative for polycystic kidney disease; cerebral CT angiography was planned to exclude aneurysm. Nimodipine 60 mg q4h was initiated with a BP target of 160/100 mmHg. On day 2, he acutely deteriorated with cardiac arrest; after CPR, GCS was 6, and he was intubated and mechanically ventilated in the ICU. Owing to instability, repeat CT brain and planned cerebral CTA were not performed. He received multidisciplinary ICU care with NG feeding, IV fluids, antibiotics, a proton pump inhibitor, and nimodipine. On day 8, he developed ventricular fibrillation and, despite CPR and more than five defibrillation attempts, could not be resuscitated and died.


This child is 2 and a half years old and has a condition called NF1. She had diarrhea with blood. Doctors used a small camera to look inside her large intestine. The inner lining looked red and irritated from the bottom (anus) to the start of the large intestine (cecum). The usual fine pattern of tiny blood vessels was hard to see. Small tissue samples showed long-lasting swelling. This fits a disease of the large intestine called ulcerative colitis. A special lab test (PCR) on the tissue found a virus called CMV.


A 69-year-old male with prior CABG presented with 2 months of severe dyspnea on mild exertion (NYHA III). ECG showed ST depression in II, III, aVF, and V4–6; NT-proBNP was 2640 pg/mL. Echocardiography demonstrated LV systolic dysfunction with LVEF 30%. His history included an inferior STEMI in 2009 with severe 3-vessel disease (proximal LAD CTO, 90% mid/distal LCx stenoses, 95% mid RCA stenosis) treated with CABG (LIMA–LAD; sequential SVG to OM1, OM2, and PL). Current angiography via 6 Fr left radial access showed patent LIMA–LAD and SVG–OM1/OM2, but complete occlusion of the sequential SVG to PL. The native LM was occluded at the ostium and the native RCA was occluded in the mid segment with bridging collaterals. The strategy was to treat the native RCA CTO. Dual arterial access was obtained with an additional 6 Fr right femoral sheath. The right and left coronaries were engaged with 6 Fr AL 0.75 (Launcher; Medtronic) and 6 Fr EBU 3.5 (Launcher; Medtronic) guide catheters, respectively. An antegrade approach from the left radial artery failed: neither a Fielder XTR nor a Gaia 3 with a Finecross microcatheter could enter the distal true lumen. A parallel wire technique with a Crusade microcatheter and two Gaia 3 wires also failed. The team then switched to a retrograde approach via septal channels from the LAD through the occluded left coronary system. A Gaia 3 crossed the occluded LM and LAD to reach the distal LAD true lumen. A Sion wire was exchanged via a Finecross into the distal LAD, followed by dilation of the LM and proximal LAD with a 2.0 × 15 mm balloon. Septal surfing technique (SST) was then used to identify a viable septal channel. A Sion wire, supported by a 150-cm Finecross, was advanced retrogradely through a distal septal branch into the distal RCA. A Gaia 3 traversed the RCA CTO retrogradely into the proximal RCA true lumen and was advanced into a Guidezilla guide extension catheter positioned in the antegrade guide. The Finecross was delivered to the antegrade guide and an RG3 wire was externalized. The CTO segment was predilated with a 2.0 × 15 mm balloon and stented with two overlapping DES (2.5 × 38 mm and 3.0 × 38 mm), achieving an excellent angiographic result with TIMI 3 flow in all distal branches. Dyspnea was relieved at discharge, and at 6-month follow-up there was no recurrence of dyspnea.


A 67-year-old woman with years of left leg swelling developed new symptoms of heart failure and was diagnosed with complex, congenital arteriovenous malformations (AVMs) in the lower limb. These abnormal vessel connections create high-flow shunts that can overload the heart. After a prior coil embolization failed to help, the team used an abdominal aortic stent graft (repurposed in the leg) to quickly reduce blood flow through the AVM, then performed staged embolization to target the AVM nidus and draining veins. Her heart failure and leg swelling improved, with blood flow in the common femoral artery falling stepwise and heart function markers getting better over time. The article highlights real-world lessons and limits: coils alone may not control very high-flow AVMs; covered stents can promptly lower shunt flow but usually need follow-up embolization; and staging helps reduce risk in patients with severe (acute) heart failure.


A 2‑day‑old term male neonate, delivered by cesarean section at a private hospital, was referred for a congenital right scrotal swelling and presented to our children’s hospital one day later. On ED arrival he was well hydrated, pink on room air with good perfusion. Physical exam: right hemiscrotum with an enlarged, tense, non‑tender, visibly reddish testis and overlying skin excoriation; transillumination negative on the right and positive contralaterally; both hernial orifices normal. Laboratory studies were obtained, and urgent inguinoscrotal Doppler ultrasonography demonstrated an enlarged right testis measuring 15.6 × 9.4 mm with heterogeneous hypoechoic echotexture, prominent rete testis, and absent intratesticular color Doppler flow. The left testis was normal in size, shape, and echotexture; there was minimal hydrocele. The patient underwent urgent scrotal exploration. Intra‑operatively there was frank necrosis of the right testis secondary to intravaginal testicular torsion, with minimal hydrocele. A right orchidectomy and contralateral orchidopexy were performed. Contextually, perinatal testicular torsion often presents at or shortly after birth and Doppler evidence of absent flow with heterogeneous hypoechoic parenchyma correlates with nonviability; salvage rates are low when presentation is delayed. Contralateral orchidopexy is commonly performed to mitigate future torsion risk.


A teenager was getting treatment for a blood cancer called non-Hodgkin lymphoma. He developed very high blood fats (triglycerides). This made a lab test say his sodium was low, even though his body sodium was okay. Think of it like the blood looked milky with fat, which can trick the test. Doctors thought this was a side effect from two cancer medicines: asparaginase and a steroid (prednisone). They used a standard checklist and decided the side effect was definitely from those medicines. He was treated with a low-fat eating plan and medicines that lower blood fats. The cancer drugs were not stopped because that part of his treatment had already reached its planned end. His blood fats went back to normal in about two weeks, and he had no problems.


This report is about a woman with abnormal blood vessel connections in her left leg that she was born with. Her left leg stayed swollen for a long time. She then started having signs of heart trouble. At age 67, doctors confirmed the leg problem was complex and present since birth. The team used a special tube made for the big belly artery, plus a blocking procedure, to slow the bad blood flow in her leg. This was done to help her sudden heart failure caused by the leg problem. The report explains what worked well and what did not.


At 32 weeks of pregnancy, a routine scan found one small lump inside the baby’s heart. It caused no symptoms. This was the only problem seen. Doctors watched it with clinic visits until 39 weeks plus 1 day. Then the baby was delivered by C-section (a surgery to deliver the baby). After birth, the child had checkups on day 1, day 7, day 30, month 7, and month 12. At each visit, the child’s growth and behavior were healthy for age. The heart lump stayed the same size; it did not grow or shrink. By 1 year old, there were no signs of a related condition called tuberous sclerosis complex.


A previously healthy 13-year-old male presented with 3 days of acute bilateral pleuritic chest pain, mild non-productive cough, no dyspnea, mild rhinorrhea, and a single febrile episode (38°C). Pain localized to the costal margins, was worse with cough, and improved with paracetamol. He denied constitutional symptoms, syncope, or exercise limitation and regularly canoed twice weekly. There were no reported infectious exposures, environmental/occupational inhalational exposures, or family history of cardiopulmonary disease. A prior chest radiograph 4 years earlier during an acute illness showed a marked interstitial infiltrate; he was presumptively treated with azithromycin and had no follow-up.
On admission, temperature was 37.8°C, SpO2 99% on room air, HR 93 bpm, RR 15/min, and BP 115/66 mmHg (85th percentile). Exam revealed diminished breath sounds in the lower two thirds of the chest without adventitious sounds; there was no respiratory distress, clubbing, cyanosis, or abnormal heart sounds. Chest radiograph again showed a marked interstitial infiltrate comparable to the prior film. Thoracic CT demonstrated multiple bilateral ground-glass opacities involving >65% of the lung parenchyma, suggestive of pulmonary alveolar proteinosis (PAP). Respiratory viral testing was negative, and he remained clinically stable in the ED. He was discharged on empiric amoxicillin–clavulanate and azithromycin with symptom resolution and referred to a pediatric respiratory clinic.
Outpatient workup showed positive ANA at 1/89 (fine speckled) with other autoantibodies negative and immunoglobulins within normal limits. Bronchoalveolar lavage returned milky fluid with positive periodic acid–Schiff staining; microbiology including mycobacterial studies was negative. Spirometry demonstrated a mild restrictive ventilatory defect with reduced FVC 2.92 L (77% predicted) and FEV1 3.21 L (69.9% predicted) with a normal FEV1/FVC ratio (109%). DLCO (SB) was moderately reduced at 13.8 ml/min/mmHg (48.6% predicted). A surfactant dysfunction genetic panel identified no pathogenic variants. GM-CSF antibody testing was positive, supporting a diagnosis of autoimmune PAP (AI-PAP). At 20 months, he remains asymptomatic and physically active; repeat testing showed FVC 4.03 L (81.3%), FEV1 3.71 L (87.5%), FEV1/FVC 91.96%, and DLCO (SB) 25.54 ml/min/mmHg (83.7%). Given stable, improving physiology and absence of symptoms, treatment was deferred with ongoing surveillance.
Context: AI-PAP is mediated by neutralizing anti–GM-CSF antibodies that impair alveolar macrophage–mediated surfactant clearance, producing intra-alveolar lipoproteinaceous material that is PAS-positive and radiographically manifests as diffuse bilateral ground-glass opacities (often with a “crazy paving” pattern). Standard therapies include whole lung lavage and GM-CSF replacement; however, observation is appropriate in stable, minimally symptomatic patients, as in this case.


A 38-year-old male with a three-year history of exertional chest tightness and dyspnea re-presented with progressive orthopnea and decompensated heart failure. Three years prior, outpatient echocardiography had identified a left-sided intracardiac echogenic mass consistent with myxoma, prompting admission. Physical examination at that time noted auricular hyperpigmentation with multiple brown-black macules. Abdominal imaging reported extracardiac findings, and genetic testing revealed TTN and PRKAR1A mutations. The diagnosis of Carney complex (CNC) with cardiac myxoma was established by clinical findings, imaging, and genetics. He improved with symptomatic therapy but declined definitive surgery.

On re-presentation (September 20, 2023), exam showed jugular venous distension, cardiomegaly with leftward/downward displacement, an irregular rhythm, a 2/6–3/6 mitral murmur at the left sternal border (fourth intercostal space), bilateral mid-to-lower lung wet rales, hepatomegaly (firm liver palpable 3 fingerbreadths below the xiphoid and 2 fingerbreadths below the costal margin), and mild bilateral pitting edema. ECG demonstrated atrial fibrillation (average ventricular rate ~150 bpm) with abnormal Q waves in V1–V3. Transthoracic echocardiography showed global cardiac enlargement, dilation of the aortic sinus and main pulmonary artery, small-to-moderate mitral regurgitation, and an irregular echogenic mass measuring 54 × 43 mm in the left chamber attached to the atrial septum. LV systolic function was severely depressed (LVEF 23.1%, FS 10.9%). The working diagnosis was end-stage heart failure due to dilated cardiomyopathy (DCM) in the setting of CNC with a cardiac myxoma. Given concomitant end-stage DCM and intracardiac tumor, heart transplantation was pursued when a suitable donor became available.

Operative course: Median sternotomy was performed with cardiopulmonary bypass. Exploration confirmed global cardiomegaly, most pronounced in the LV, with poor contractility. Diseased native right atrium, left atrium, right ventricle, and left ventricle were resected, revealing a gray-white mucoid mass consistent with myxoma. Standard orthotopic heart transplantation anastomoses were completed (including left atrial cuff, great vessels, and caval anastomoses) using continuous Prolene sutures (3/0 and 5/0), with meticulous hemostasis. After rewarming and aortic unclamping, the graft resumed sinus rhythm spontaneously. Assisted circulation was weaned uneventfully. Histopathology of the explanted tissues confirmed DCM and cardiac myxoma.

Postoperative course: On postoperative day (POD) 1, urine output was 1200 mL; hs‑troponin T was 796.70 ng/L; NT‑proBNP 10,798 pg/mL; WBC 17.15 × 10^9/L. Echocardiography demonstrated normal ventricular wall thickness and morphology with LVEF 65% (FS 35%). Immunosuppression and anti-infective therapy included IV methylprednisolone sodium succinate 0.25 g, cefoperazone/sulbactam 2 g, supportive nutrition, and hepatoprotective therapy. On POD 3, steroids were transitioned to oral prednisone acetate 25 mg; mycophenolate mofetil 0.5 g PO was initiated for rejection prophylaxis; caspofungin acetate 50 mg IV was added for antifungal prophylaxis. Urine output increased to 2000 mL; hs‑troponin T decreased to 390 ng/L; NT‑proBNP decreased to 7877 pg/mL; WBC 12.15 × 10^9/L. On POD 7, tacrolimus 1 mg PO was introduced with therapeutic drug monitoring (blood level 10.90 ng/mL), and prednisone was tapered to 10 mg. Clinical status steadily improved. By late postoperative follow-up (October 20, 2023), echocardiography was unremarkable; hs‑troponin T was 85 ng/L; NT‑proBNP 210 pg/mL; other labs were within normal limits. The patient was discharged in excellent condition and has remained clinically stable on outpatient follow-up.

Interpretation: This case illustrates CNC with PRKAR1A mutation manifesting as atrial myxoma and end-stage DCM, compounded by atrial fibrillation and severe LV systolic dysfunction (LVEF 23.1%). Orthotopic heart transplantation effectively addressed both the intracardiac tumor and the refractory heart failure, with prompt normalization of graft function and favorable early outcomes under standard triple immunosuppression.


A 19-month-old boy came to the emergency department after falling from a highchair and hitting his head. On exam he had severe, unexplained breathing trouble that required tracheal intubation (a tube placed into the windpipe to help him breathe). The team suspected that the breathing problem had caused an altered state of consciousness and led to the fall and head injury. Imaging of the chest showed complete collapse (atelectasis) of the entire left lung and an abrupt cutoff of the left main bronchus about 12 mm from the lung hilum (the area where the bronchus enters the lung). Rigid bronchoscopy found and removed a 2 cm almond that was stuck in the left main bronchus. Earlier signs included very fast breathing and heart rate, low oxygen levels despite bag-mask ventilation, visible chest retractions, and decreased breath sounds on the left. The mother reported the child had an intense coughing episode a few days earlier that resolved without treatment; the child had never eaten almonds before and likely swallowed this one by accident. After the almond was removed the child improved steadily, was extubated 24 hours later, moved from intensive care to the pediatric ward, and made a full recovery of respiratory function.


A 12-year-old boy presented with one week of acute-onset headache and polyuria–polydipsia. Past history was unremarkable. On first assessment: height 146.5 cm (M), weight 30 kg (−1.4 SD). He was at the onset of puberty with bilateral gonadal length 3.2 cm and penile length 6.2 cm (M). Visual assessment, including OCT, was normal. Polyuria reached 113 ml/kg/day with nocturnal enuresis and intake approximately 3.8 L/m²/day. Initial labs were consistent with central diabetes insipidus: serum sodium 140 mEq/L, plasma osmolality 287 mOsm/kg, urine osmolality 179 mOsm/kg. Basal pituitary axes were otherwise intact: IGF-1, PRL, free T4, cortisol, FSH, and LH within reference ranges. MRI with and without contrast demonstrated apoplexy within a Rathke cleft cyst (T1/T2 hyperintense lesion measuring 15 × 6 × 11 mm). The anterior pituitary enhanced homogeneously. The posterior pituitary bright spot was absent. There were no radiologic features suggestive of craniopharyngioma. DI improved significantly with vasopressin therapy. A multidisciplinary team (endocrinology, neurosurgery, radiology) elected conservative management given the absence of compressive symptoms, early pubertal status, and normal baseline endocrine testing apart from DI. Serial MRI over nine months showed stability (12 × 11 × 10 mm), and subsequent surveillance at two years remained stable (11 × 12 × 11 mm) with slight size reduction at three years (7 × 10 × 6 mm). Over three years, the patient maintained normal pubertal progression and a stable hormonal profile on routine testing, with persistently normal vision. Growth velocity declined from −0.8 SD to −1.1 SD, prompting evaluation for acquired GH deficiency. At 14 years 9 months, two GH stimulation tests demonstrated partial GH deficiency: propranolol–glucagon peak 19.3 µUI/ml and insulin tolerance test peak 10.0 µUI/ml. GH therapy led to improved growth velocity from −1.1 SD to 0.2 SD over one year. Overall, this case illustrates that RCC apoplexy in a pubertal child can present with abrupt DI due to posterior pituitary/stalk dysfunction, while sparing anterior pituitary function initially. In the absence of mass effect or broader hypopituitarism, conservative management with structured clinical, biochemical, and radiologic follow-up is appropriate; delayed, isolated partial GH deficiency may emerge, warranting dynamic testing and treatment.


A 17-year-old male with no significant past medical or family history was referred from Dentistry after an incidental nasal foreign body (NFB) was detected during preoperative orthodontic planning with dental radiographs and cone beam computed tomography (CBCT) without contrast. He was entirely asymptomatic, denying nasal obstruction, rhinorrhea, epistaxis, foul odor, hyposmia, halitosis, facial pain, discomfort, or sleep disturbances. The parents recalled a prior event at age seven when he inserted an object into his nose; an anterior rhinoscopy was attempted at that time, and removal under sedation was recommended, but the family did not follow up and assumed spontaneous expulsion given the absence of symptoms. Nasal endoscopy of the right cavity showed a deviated nasal septum with inferior turbinate hypertrophy; the mucosa was erythematous and mildly edematous. A foreign body was visualized, lodged and adherent to the floor of the nasal cavity beneath the inferior turbinate, partially covered with mucus/crust, with a shiny surface suggesting a metallic nature. Lateral and frontal radiographs demonstrated a circular radiopaque object along the nasal floor consistent with a metallic snap button; adjacent bony structures were normal. CBCT confirmed the foreign body and mild surrounding inflammation, without significant bony erosion or sinus involvement. With informed consent, removal was performed under local anesthesia in a semi-sitting position to mitigate the risk of airway dislodgment. After decongestion with xylometazoline 0.1% and topical anesthesia with lidocaine spray (10 mg/spray) in the right nostril, a hook was used to disengage the foreign body, which was then extracted with bayonet forceps. The procedure was uncomplicated with minimal bleeding controlled by saline irrigation, and post-removal inspection showed no significant tissue injury. The retrieved object was a metallic snap button (1 cm diameter) with substantial corrosion and biological deposits, consistent with long-term retention—likely over a decade. The patient was discharged in stable condition with 0.9% sodium chloride nasal irrigations and had an unremarkable two-week follow-up.