Introduction:We report an unusual case of extra-pulmonary tuberculosis (TB) involving the esophagus and pancreas. The case presented a diagnostic challenge with unrevealing original core biopsy and a battery of infectious, inflammatory, rheumatologic, and procedural testing. Case Description/Methods: A 54-year-old female with a past medical history of renal transplant and latent TB treated with isoniazid presented from a regional hospital for further evaluation of epigastric pain associated with 15-pound weight loss. On admission, the patient was afebrile, hemodynamically stable, with mild epigastric abdominal tenderness without rebound or guarding. Her labs were significant for mild leukocytosis, normocytic anemia, and hyponatremia. Computerized tomography of the abdomen and pelvis was remarkable for extensive retroperitoneal adenopathy, circumferential esophageal wall thickening, and a peripancreatic mass. At the transferring hospital the patient underwent a core needle biopsy of the retroperitoneal mass with pathology showing granulomatous inflammation with necrosis and no evidence of malignancy. The patient was subsequently transferred to our hospital for further evaluation. After extensive infectious and rheumatologic workup, including bronchoalveolar lavage, the patient underwent endoscopic ultrasound-fine needle aspiration, which showed an irregular 5.6 cm by 5 cm mass in the peripancreatic region with mixed features near the body and tail (Figure ). A fine needle biopsy was performed, and 45 milliliters of cloudy, yellow, purulent fluid was sent for pathology and microbiology. Gastric and distal esophageal biopsies were also sent for pathology. The final report was significant for acid-fast bacilli in the esophagus and the pancreas. The fluid analysis of the pancreas with real-time polymerase chain reaction (PCR) was positive for Mycobacterium tuberculosis. The patient was subsequently treated with rifabutin, isoniazid, pyrazinamide, and ethambutol. Discussion: Extra-pulmonary tuberculosis manifesting in the pancreas or esophagus is extraordinarily rare. Per the literature review, there are no reported synchronous pancreatic-esophageal tuberculosis cases. Esophageal tuberculosis mainly presents as an extension of pulmonary disease. Pancreatic tuberculosis generally presents as a pancreatic mass and is often misdiagnosed as a pancreatic adenocarcinoma. This case demonstrates the deceptive nature of tuberculosis and its capability to afflict the gastrointestinal system.[1900] Figure 1. Endoscopic ultrasound-fine needle aspiration of pancreatic mass.

Figure 1. (A) Magnetic resonance cholangiopancreatography (MRCP) of the pancreatic tail cyst. (B) Endoscopic ultrasound (EUS) of the pancreatic tail cyst.

Introduction: Fluoxetine is a commonly prescribed antidepressant with generalized gastrointestinal side effects that can include nausea and diarrhea. While fluoxetine is metabolized in the liver, fewer than 1% of patients develop a mild and self-limited transaminitis. Here, we present a unique case of clinically apparent drug-induced liver injury (DILI) soon after fluoxetine initiation. Case Description/Methods: A 28-year-old male with schizophrenia and bipolar disorder was admitted to the hospital due to a 3-day history of worsening right upper quadrant (RUQ) abdominal pain with a 2day history of yellowing of the skin and eyes. A thorough history revealed that he was on chronic citalopram and olanzapine therapy but was started fluoxetine (20 mg daily) 5-days prior. Additionally, he denied use of alcohol, recreational drugs, and herbal supplements, and denied a history of known liver disease. On admission, the patient was alert and oriented x4 with jaundice, scleral icterus, and asterixis. Laboratory work demonstrated WBC 15,000, platelets 235,000, ammonia 131, AST 3219, ALT 6574, ALP 181, total bilirubin 22.9, and INR 1.97. Acetaminophen and salicylate levels were unremarkable. Fluoxetine was held immediately, and the patient was empirically given N-acetylcysteine. RUQ ultrasound was unremarkable. MRCP demonstrated fatty infiltration of the liver without nodularity or biliary dilation. A thorough workup including viral hepatitis (A, B, C, E), EBV, CMV, HIV, hemochromatosis, Wilson's disease, and autoimmune hepatitis was unremarkable. A liver biopsy was performed, and pathology was consistent with mixed-pattern DILI. With the removal of fluoxetine, the patient's liver function tests and clinical symptoms continued to improve, and on hospital day 10 he was discharged in stable condition. Discussion: Transaminitis from fluoxetine is typically mild, asymptomatic, and self-limited. Our case highlights a rare instance where fluoxetine precipitated DILI. It is unclear whether polypharmacy with his other psychiatric medications, or underlying hepatic steatosis, were predisposing factors to developing fluoxetine-associated DILI. Higher awareness of fluoxetine-associated hepatotoxicity is needed and caution should be used when considering current medications and underlying liver pathology when starting this medication.

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