United States

Abstract Title

Use of Hypercalcemia and Vitamin D Levels in the Diagnosis of Sarcoidosis

Background
Sarcoidosis is a granulomatous disorder that most often affects the respiratory system, but can involve tissues throughout the body. The disease may cause hypercalcemia (termed sarcoidosis associated hypercalcemia (SAHC)) as macrophages within the granulomas secrete 1α-hydroxylase resulting in conversion of 25(OH)D to 1,25(OH)2D. Renal injury can be seen in sarcoidosis secondary to hypercalcemia or as a direct result of granuloma formation in the kidneys. 

Case Presentation
A 65 year old female with past medical history notable for CKD II, HTN, DMII, and asthma-COPD overlap syndrome presented to the emergency department for the second time in one month due to hypercalcemia. The patient noted mild generalized fatigue and non focal weakness. Her medications included metformin, semaglutide, and a multivitamin. Laboratory evaluation revealed Ca of 12.2, ionized Ca of 6.1, phosphorus of 7.7, PTH of 18.3, and Cr of 3.2 from a baseline of 1.0 (GFR = 56). PTHrP from her prior hospitalization earlier in month revealed 25(OH)D wnl, 1,25(OH)2D wnl, kappa/lambda ratio mildly elevated, SPEP wnl, UPEP wnl, and urine Ca wnl. Workup of humoral hypercalcemia of malignancy included CT chest, abdomen, and pelvis, and colonoscopy which were all non-revealing. On hospital day 10 a kidney biopsy was performed and eventually revealed non-necrotizing granulomas consistent with sarcoidosis. The patient was started on prednisone with slow normalization of calcium and creatine levels.

Discussion
The classic lab profile of SAHC of normal/low PTH, low 25(OH)D and high 1,25(OH)2D is actually not seen in most cases. Hypercalcemia itself is present in only 6% of patients with sarcoidosis. Elevated PTH is not consistent with SAHC and should prompt a search for a source of PTH secretion. Of patients with SAHC, one study found that 84% of patients had reduced 25(OH)D levels, with only 11% having correspondingly elevated 1,25(OH)2D levels. Potential confounders of vitamin D measurements include supplementation, dietary intake, and sun exposure. Of note, our patient previously discontinued vitamin D supplementation, but was still taking a multivitamin which contained vitamin D. Thus, in a patient with hypercalcemia and kidney injury but with an equivocal workup, low 25(OH)D can support a diagnosis of sarcoidosis, but elevated 1,25(OH)2D provides little diagnostic value. However, 25(OH)D has several confounders, and this case illustrates that it is neither completely sensitive nor specific, and biopsy is still necessary to establish a diagnosis.

AMA Research Challenge 2025 

Use of Hypercalcemia and Vitamin D Levels in the Diagnosis of Sarcoidosis

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poster

Introduction: Muir-Torre syndrome (MTS) is a rare phenotypic variant of Lynch syndrome with approximately 200 reported cases occurring in both sexes, having a male-to-female ratio of 3:2. It is characterized by both visceral malignancies (colorectal and endometrial tumors) and dermatological neoplasms (sebaceous adenoma, sebaceous adenocarcinoma, keratocanthomas and basal cell carcinoma with sebaceous differentiation). Sebaceous adenomas are the most common dermatological manifestations on the head and neck, particularly the periocular area. In MTS, 56% of skin lesions occur after diagnosing visceral malignancy, 6% co-occur, and 22% occur before a visceral malignancy diagnosis. MTS is most commonly associated with MSH2 mutations and rarely with MLH1 and MSH6, also found in Lynch Syndrome.
Case Description: This is the case of a 64-year-old female patient with a medical history of cecal adenocarcinoma. At the age of 60, she underwent a screening colonoscopy, which revealed a large polypoid carpeted mass. The mass was surgically removed through hemicolectomy, and the pathology reported 3.1cm intramucosal well-differentiated stage 0 adenocarcinoma. Due to a family history of endometrial carcinoma in her mother, breast cancer in her sister, and colon cancer in her cousin, subsequent genetic testing was recommended, revealing an MSH6 mutation, confirming the diagnosis of Lynch syndrome. The patient also underwent a prophylactic hysterectomy with B/L salpingo-oophorectomy. Four years later, the patient developed a lesion on her right lower eyelid, which was surgically excised and later identified as a sebaceous adenoma with MSH6 gene mutation, indicating Muir-Torre syndrome (MTS). Based on the Mayo MTS score & the MSH6 mutation, the diagnosis of MTS was supported. Later, the patient underwent a colonoscopy to rule out colon cancer, which revealed two small sessile polyps, each measuring 2 mm, in the mid-sigmoid colon.
Conclusion: This case emphasizes the importance of early identification of patients with Muir-Torre syndrome (MTS), as they are at a higher risk for developing multiple primary malignancies, including GI, gynecological, and dermatological tumors. MSH6 mutations are linked to the late onset of Lynch syndrome, which explains why the patient developed malignancy later in life. It highlights the crucial role of ophthalmologists, dermatologists, and gastroenterologists in regular cancer screening and surveillance for the timely detection and management of MTS.

Exploring Muir-Torre Syndrome: A rare case study of Eyelid Sebaceous Adenoma in a Lynch syndrome patient

Background
Anabolic androgenic steroids (AASs) are known to cause hepatotoxicity, with significant concern for inducing cholestasis and vanishing bile duct syndrome (VBDS). The risk is increased when combined with other supplements, such as the X-39 patch, containing copper. VBDS is a rarely reported but serious complication of AAS use, characterized by cholestasis and histological evidence of intrahepatic bile duct loss. Diagnostic confirmation requires a liver biopsy, showing the loss of at least 50% portal tracts. 

Case Presentation
A 27-year-old male with a history of low testosterone levels, being treated with testosterone supplementation, presented to the emergency department with symptoms of pruritus and jaundice. The patient was also reportedly using the X-39 patch for general wellness support. On physical examination, the patient appeared icteric. Laboratory studies revealed elevated liver enzymes – aspartate transaminase (AST) 152 U/L, alanine transaminase (ALT) 227 U/L, alkaline phosphatase (ALP) 216 U/L, total bilirubin level of 32.6 mg/dL, elevated WBC (17.6×109/L), and platelet count (657×109/L). His initial copper level was markedly elevated at 3,248 μg/dL. USG, MRI, and MRCP of the abdomen were unremarkable. Liver biopsy was negative for malignancy but demonstrated cholestatic hepatitis with mild focal portal chronic inflammation with stage-1 fibrosis. The infectious and autoimmune workups were unremarkable. Cytomegalovirus PCR depicted low-level viremia. The hepatitis panel was negative. Anti-nuclear antibodies were negative, with a mildly elevated anti-smooth muscle antibody. Ceruloplasmin level was within normal limits, while alpha-1 antitrypsin was slightly elevated. The patient was managed with immediate cessation of testosterone supplementation, along with penicillamine to chelate copper. Supportive care for symptom relief was provided – colestipol, hydroxyzine, and gabapentin for pruritus, and ursodeoxycholic acid for prevention of gallstone formation. Following treatment, the patient's copper level decreased to 402 μg/dL. Serial liver function tests showed gradual improvement over weeks, with normalization of bilirubin and significant reductions in AST and ALT levels. 

Discussion: 
VBDS is often a diagnosis of exclusion in patients with elevated ALP levels (≥2 times the upper limit of normal) when other causes of cholestasis are ruled out. Our case is only the fourth documented instance linking AAS use to this condition, and the first case ever to report the association of VBDS to the X-39 wellness patch, alongside AAS. While most cases improve with time, severe VBDS can lead to acute liver failure and death. Clinicians should maintain a high index of suspicion for drug-induced liver injury, particularly in patients using testosterone and wellness supplements.

Testosterone-induced Vanishing bile duct syndrome associated with X-39 wellness patch: A rare case report

This is a case of a patient who underwent an elective laparoscopic cholecystectomy after previously presenting with acute cholecystitis. His operation was complicated by a high common hepatic duct (CHD) injury requiring complex surgical repair. This case highlights the importance of early recognition of this type of injury and the utility of a Kasai portoenterostomy as an operative repair in high CHD injuries in the absence of a viable extrahepatic duct viable for repair.

Surgical Management of a Complex High Hepatic Duct Injury: A Case Report

Diaphragmatic hernias result from a defect in the diaphragm that allows abdominal contents to herniate into the thoracic cavity. The most common cause is acute trauma, particularly blunt force trauma, more than penetrating trauma. Congenital causes are the second most common cause. Such as Bochdalek and Morgagni hernias. There are other types and the most uncommon is a spontaneous diaphragmatic hernias (SDH). This paper presents a novel case of SDH, leading to gastric fundus protrusion and incarceration, resulting in abscess formation. The patient’s medical history did not suggest trauma or congenital anomalies, making this case an acquired SDH, with fewer than 40 documented occurrences. Diagnosis is often delayed due to the overlap of symptoms with other conditions, and SDH frequently presents with nonspecific gastrointestinal or respiratory symptoms. Imaging, particularly CT, is crucial for diagnosis. The patient underwent successful repair using a transabdominal robotic approach with the Da Vinci Xi system, marking the first documented case of SDH repaired exclusively with robotic techniques. This case highlights the importance of considering SDH in patients with unexplained thoracoabdominal pain, particularly in the absence of trauma, and demonstrates the efficacy of robotic surgery in minimizing complications and reducing morbidity in such cases.

Trans-abdominal Approach in a Spontaneous Diaphragmatic Hernia: A Case Report

Introduction
Intracholecystic papillary neoplasm (ICPN) is a rare, visibly distinct lesion arising
from the gallbladder lining and projecting into its lumen. It is often discovered
incidentally when asymptomatic but may sometimes cause symptoms such as pain,
jaundice, weight loss, or ascites. ICPN is very rarely reported in Nepal, highlighting
the need for careful evaluation and management.
Presentation of case
We report a 63-year-old man diagnosed incidentally with ICPN during routine
evaluation. The patient had no symptoms such as abdominal pain. He underwent
laparoscopic cholecystectomy and recovered well without complications.
Discussion
ICPN is a preinvasive gallbladder tumor that can show different histologic patterns,
typically appearing as papillary or polypoid growths. Imaging like ultrasound and CT
can suggest ICPN, but a definitive diagnosis requires surgical removal and
microscopic confirmation. Intraoperative frozen section assessment of tumor invasion
and margins is helpful for surgical decision-making, as demonstrated in this case.
Early diagnosis and surgery generally result in better outcomes than those seen in
invasive gallbladder cancer.
Conclusion
Because ICPN is rare and often presents subtly, a thorough clinical workup with
appropriate imaging is essential. Early surgical intervention supported by
intraoperative pathology evaluation can improve prognosis and patient outcomes.

An incidental finding of Intracholecystic Papillary Neoplasm- A rare case report

Background: 
Extramedullary plasmacytoma (EMP) is a rare form of plasma cell neoplasm characterized by monoclonal plasma cell infiltration without systemic evidence of multiple myeloma. It represents 1.6-4% of all plasma cell tumors. The most common sites of involvement are the upper respiratory and gastrointestinal tracts, while anterior chest wall involvement is rare and can mimic other common thoracic malignancies. Here, we report a case of a 50-year-old man presenting with a large anterior chest wall mass diagnosed as extramedullary soft tissue plasmacytoma occurring years after blunt thoracic trauma. Plasmacytoma should be considered in the differential diagnosis of anterior chest wall masses, especially when associated with a history of trauma and presence of invasive features on imaging. A combination of clinical presentation, imaging, and biopsy is critical for diagnosing atypical soft tissue neoplasms.
Case Presentation: 
A 50-year-old man presented with a progressively enlarging anterior chest wall mass, initially noticed 5–6 years after blunt thoracic trauma. The mass remained stable for years but rapidly increased in size over six months, causing dyspnea, dysphagia, and odynophagia. Physical examination revealed an 18 cm, firm, non-mobile mass with superficial venous prominence. The initial differentials included thymoma, teratoma, thyroid neoplasm, and lymphoma. However, the history of trauma, chronic presentation, recent progression, and normal tumor markers raised suspicion for a soft tissue or bony lesion. Contrast-enhanced CT showed a lobulated, calcified mass in the superoanterior mediastinum with scattered enhancement, sternal erosion, invasion of the first rib, anterior chest wall extension, and tracheal compression. Laboratory workup revealed hemoglobin 11.6 g/dL, calcium 9 mg/dL, creatinine 0.8 mg/dL, and normal TSH, LDH, β-hCG, and AFP levels, but urine electrophoresis demonstrated an M spike with significantly elevated free kappa light chains (1956.2 mg/L). Histopathology showed diffuse sheets of plasma cells with eosinophilic cytoplasm and eccentric nuclei. Immunohistochemistry was positive for CD138, MUM1, CD56, and kappa light chain, consistent with a diagnosis of kappa-restricted extramedullary plasmacytoma.
Discussion: 
This case demonstrates a rare post-traumatic extramedullary plasmacytoma with extensive local invasion, highlighting the need to consider plasma cell neoplasms in the differentials of anterior mediastinal masses. In this case, scar tissue from prior injury may have created a permissive microenvironment, allowing delayed plasma cell proliferation. Imaging revealed aggressive features suggestive of soft tissue plasmacytoma, and biopsy confirmed the presence of plasma cells. While radiotherapy is the primary treatment modality, chemotherapy may also be used in combination based on the tumor characteristics.


Post-Traumatic Extramedullary Plasmacytoma Presenting as an Anterior Chest Wall Mass

Abstract Title : 
An Uncommon Case of BRAF V600E–Mutated Colorectal Adenocarcinoma in an African American Patient: Case Report and Therapeutic Implications 
Background:
BRAF V600E mutations occur in 8% to 15% of colorectal cancers (CRC) and are linked to aggressive tumors, poor prognosis, and chemotherapy resistance. These mutations occur less frequently in African American patients (1.8% to 6.4%). Early molecular profiling is essential to guide personalized treatment. Case Presentation A 77-year-old African American man with hypertension and type 2 diabetes presented with fatigue and iron deficiency anemia. Colonoscopy identified a transverse colon mass; biopsy confirmed invasive adenocarcinoma. Molecular testing revealed a BRAF V600E mutation with loss of MLH1 and PMS2. The patient underwent right hemicolectomy, which showed a 5.0 × 3.5 × 1.2 cm high-grade tumor invading through the muscularis propria into the subserosal fat (pT3) with lymphovascular invasion. Five of 15 lymph nodes were positive (pN2a), and a contrast-enhanced computed tomography (CT) scan showed no distant metastasis consistent with stage IIIC (T3N2aM0). He completed 12 cycles of FOLFOX (oxaliplatin, leucovorin, and 5-fluorouracil) per National Comprehensive Cancer Network (NCCN) guidelines with mild peripheral neuropathy. Carcinoembryonic antigen (CEA) is being monitored. A post-treatment CT is pending to assess distant metastasis and treatment response. 
Discussion:
BRAF V600E mutation causes aggressive tumor behavior, rapid progression, and resistance to treatment. In metastatic colorectal cancer (CRC), BRAF inhibitor monotherapy is ineffective due to epidermal growth factor receptor (EGFR)–mediated resistance. Combination therapies targeting BRAF and EGFR, such as encorafenib plus cetuximab, have shown improved outcomes. Our patient completed 12 cycles of FOLFOX, the standard first-line chemotherapy for stage IIIC CRC without distant metastasis. Post-treatment imaging will guide next steps; if metastases are found, targeted therapy with BRAF and EGFR inhibitors will be considered. The phase III BEACON trial demonstrated median survival of 9 months and response rates up to 26% with encorafenib plus cetuximab, with or without the MEK (mitogen-activated protein kinase kinase) inhibitor binimetinib. MEK inhibitors increased response rates from 10% with doublet therapy to 21% with triplet therapy. The BREAKWATER trial showed first-line encorafenib, cetuximab, and chemotherapy improved response to 60.9% versus 40.0% with chemotherapy alone, with durable disease control in 69% and no added toxicity. Early genomic testing enables timely, personalized therapy. Though BRAF mutations are less frequent in African American patients, comprehensive molecular profiling is essential to detect early mutations and guide appropriate treatment. Addressing disparities in testing and access remains key to improving outcomes in this aggressive CRC subtype.

An Uncommon Case of BRAF V600E–Mutated Colorectal Adenocarcinoma in an African American Patient: Case Report and Therapeutic Implications

Authors: 
Muneeba Ali, MD, Lubaba Mukhtar, MD, Warda Naqvi, MD, Muhammad Ayub, MD. 

Background:
Today, we present the case of Mollaret’s meningitis in a 49-year-old male who was acutely distressed with a severe headache and associated back pain upon presentation to the emergency department. Remarkably, he experienced a complete resolution of symptoms within 24 hours of admission. This case provides an opportunity to highlight the clinical behavior of this rare condition, the critical role of detailed history-taking , the importance of maintaining a high index of suspicion in patients with a history of viral meningitis, and the eventual bold decision to discontinue all intravenous management in a patient exhibiting signs of meningitis, provided the symptomatology is consistent with a diagnosis of Mollaret’s meningitis.

Case Presentation:
A 49-year-old male with a past medical history of viral meningitis presented to the emergency department (ED) with the chief complaint of a gradually worsening headache, associated with lower back pain. A lumbar puncture was performed, revealing cerebrospinal fluid with 180/μL red blood cells, 228/μL white blood cells, a glucose level of 37 mg/dL, and a protein level of 152 mg/dL. His symptoms surprisingly resolved completely within 24 hours. HSV-2 was detectable on CSF DNA PCR, and his clinical course was highly consistent with Mollaret’s meningitis. All intravenous therapy was discontinued, and the patient was discharged home on oral valacyclovir 1 g every 8 hours to complete a 10-day course.

Discussion:
Mollarets Syndrome or benign recurrent aseptic meningitis collectively refers to two distinct medical conditions which are Mollaret’s meningitis and Mollaret's lymphocytic meningitis. Mollaret’s meningitis is characterized by recurrent episodes, which typically goes away within a week or so, whereas Mollaret's lymphocytic meningitis is a recurrent chronic inflammation of the meninges.

Symptoms of moderate syndrome typically include meningeal signs, as well as various neurological symptoms including confusion, altered consciousness, seizures, paresthesia and cranial nerve palsies. However, these symptoms vary between episodes and may not always be present. The most implicated causative organisms are varicella-zoster virus (VZV) and herpes simplex virus (HSV). Autoimmunity and genetic factors also play a role in pathogenesis.

The diagnosis of Mollaret’s syndrome often proves to be a challenge, as there are no specific diagnostic tests available for this rare neurological disorder. CSF analysis is usually a critical lab test to diagnose the syndrome and usually shows elevated levels of lymphocytes and protein in the CSF. Viral testing can identify the underlying causative agent.

Treatment of Mollaret’s syndrome usually includes managing the acute episode and preventing further attacks. The literature regarding the use of antiviral therapy in an acute episode or as longer term prophylaxis is currently mixed.

The Back Burn: A Case Report of Mollaret’s Meningitis in a Young Male.

Background: Intracranial hypertension (IH) is a rare but serious complication of growth hormone (GH) therapy. Incidence is roughly 13 per 100,000 cases. Risk factors for GH-induced IH include obesity, chronic renal failure, and Turner Syndrome. Blindness and intractable headache are primary concerns. GH therapy discontinuation is commonly sufficient for resolution of IH, but some patients require additional therapies. Most cases resolve within 12 months of GH discontinuation with favorable outcomes. We describe an unusual case of a very prolonged course of IH after GH therapy.

Case Presentation: A 19-year-old non-obese female developed persistent intracranial hypertension at age eleven within two months of starting GH therapy (0.264 mg/kg/week) for GH deficiency. Initially, she presented with new-onset headaches, pulsatile tinnitus, visual obscurations, and bilateral grade 1 papilledema. Lumbar puncture (LP) revealed an opening pressure of 44 cm H2O, and neuroimaging revealed a congenital hypoplastic transverse sinus. Despite promptly discontinuing GH therapy, symptoms remained persistent eight years later (opening pressure: 29 cm H2O; elevated OCT RNFL measurements: OD 120 um, OS 121 um). Her course was resistant to multiple standard diuretics (acetazolamide, topiramate, furosemide) and she was treated with repeated LPs for symptom relief. Her headache phenotype evolved into chronic migraine (16 days/month, MIDAS=69, severe) with medication overuse headache.

Discussion: Through our literature review of 169 reported cases, we found that symptom onset of GH-induced IH was typically within three months. Growth hormone discontinuation alone was often sufficient for symptom resolution, but up to 43% of patients underwent additional treatments– most commonly with acetazolamide, but interventions also included serial LPs, and, rarely, ventriculoperitoneal shunts. The prognosis is favorable. In those with detailed data, an estimated 95% reported resolution by 6 months and 98% by 12 months. Two cases reported complete resolution at 2 years after discontinuation. At 8 years, our patient’s duration is unusually prolonged. Although CSF pressures have improved over time, this is the longest persistence of GH-induced IH to the best of our knowledge. IH is an uncommon event during GH treatment, but our patient's course demonstrates the potential for long-lasting and debilitating adverse effects. Routine ophthalmological monitoring and a high index of suspicion is essential for early recognition, enabling timely interventions to prevent vision loss and headache disability.

Eight-Year Persistence of Growth Hormone-Induced Chronic Migraine and Intracranial Hypertension

Abstract Title
A Clot Conundrum: Reassessing Interstitial Lung Disease as Pulmonary
Embolisms with Aubagio Use
Background
Interstitial lung disease and pulmonary embolism are rare side effects reported post
teriflunomide use. Based on a trial evaluating the potential long-term effects of teriflunomide, reports of such adverse reactions have emerged from the TOWER extension study1 as well as several case studies2,3,4 . There are case reports of suspected pneumonia with a CT angiogram performed upon lack of clinical improvement, with pulmonary embolisms found there after. Here we report a case of suspected interstitial lung disease in the setting of teriflunomide use and upon further investigation, multiple pulmonary embolisms were discovered.
Case Presentation
A 46 year old female with a past medical history of multiple sclerosis, who was started on Teriflunomide four years prior, presented with progressive dyspnea, with persistent deoxygenation for one year based on an Apple watch monitoring device. The patient had several CT chest without contrast studies that were suggestive of interstitial lung pneumonitis prompting discontinuation of Teriflunomide and initiation of steroids. When the patient had no clinical improvement, a CT Angiogram with contrast later revealed extensive pulmonary artery emboli at multiple levels. Transthoracic echocardiogram revealed significant right heart strain. She was then started on a heparin drip and underwent a bilateral pulmonary endarterectomy.
Following this, the patient was started on oral anticoagulation and was continued on steroids.
Discussion
There have been a few reported cases of either interstitial lung disease and pulmonary embolism linked to Aubagio use in multiple sclerosis patients. In our case, a patient presumed to have interstitial lung disease was later diagnosed with multiple pulmonary embolisms. A more comprehensive evaluation of potential side effects could have resulted in earlier, more effective treatment. Thus, we caution against solely attributing symptoms to one side effect and recommend early consideration of multifactorial and broader adverse effects of Aubagio.

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Exploring Muir-Torre Syndrome: A rare case study of Eyelid Sebaceous Adenoma in a Lynch syndrome patient

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