Tumor Necrosis Factor Alpha Inhibition for Inflammatory Bowel Disease after Liver Transplant for Primary Sclerosing Cholangitis.

BACKGROUND: Outcome data regarding the use of tumor necrosis factor alpha inhibitors (anti-TNFα) in patients with inflammatory bowel disease (IBD) after liver transplant (LT) for primary sclerosing cholangitis (PSC) are scant. METHODS: We performed a retrospective chart review to investigate outcomes among a series of post-liver-transplant PSC/IBD patients receiving anti-TNFα therapy at Henry Ford Health System ((HFHS), Detroit, MI). RESULTS: A total of five patients were treated with anti-TNFα agents for IBD after LT for PSC from 1993 through 2015. Two patients were treated with adalimumab, and three were treated with infliximab. Three patients were hospitalized with severe posttransplant infections. Two patients developed posttransplant lymphoproliferative disease (PTLD); one of these patients died due to complications of PTLD. CONCLUSION: Anti-TNFα treatment following LT worsened the disease course in our patients with concurrent PSC/IBD and led to serious complications and surgical intervention. Larger studies are needed to evaluate the side effects and outcomes of the use of such agents in this patient population. Until then, clinicians should have a high threshold to use anti-TNFα therapy in this setting.

A Rare Case of Intraductal Papillary Mucinous Neoplasm of the Biliary Duct in a Patient with Prostate Adenocarcinoma.

Intraductal papillary mucinous neoplasms (IPMNs) are mucin-producing papillary neoplasms of the pancreatic or biliary ductal system that exhibit variable cellular atypia and cause ductal dilation. There are few reported cases of IPMN arising from the biliary tree in the literature. It has a higher propensity to undergo malignant transformation compared to IPMN arising from the pancreatic duct. An 80-year-old male underwent cross-sectional tomography (CT) imaging of the abdomen for evaluation of prostate adenocarcinoma, which revealed an incidental 2.3 × 2.7 cm soft tissue mass centered at the porta hepatis with diffuse dilatation of the left intrahepatic biliary ductal system and mild prominence of the right intrahepatic ductal system. Endoscopic ultrasound showed 2 adjacent hilar masses involving the common hepatic duct and the left hepatic duct with protrusion of the tissue into the lumen of the duct and upstream ductal dilatation. Endoscopic retrograde cholangiopancreatography revealed a large filling defect in the common hepatic duct extending into the left hepatic duct. A large amount of clot and soft tissue with a fish-egg appearance was retrieved. The patient underwent left hepatic lobectomy, radical resection of the common hepatic duct with Roux-en-Y hepaticojejunostomy to the right hepatic duct. Histopathological examination of the resected specimen revealed intraductal papillary mucinous neoplasm with diffuse high-grade dysplasia. Follow-up CT scan of the abdomen 2 months after the surgery was negative for any masses.

A rare case of splenic lymphoma in a patient with polymyositis manifesting as gastric variceal bleeding.

We report an unusual case of upper gastrointestinal bleeding due to isolated gastric variceal bleeding in a patient with splenomegaly who was subsequently diagnosed with diffuse large B-cell lymphoma. The patient is a 47-year-old male with a history of polymyositis who presented to the emergency room with complaints of lightheadedness and melena for 2 days. On initial presentation, the patient had positive orthostatic vital signs. He was found to be anemic with presenting hemoglobin of 5.8 g/dl (compared with 13.4 g/dl 4 months prior to presentation). The patient was aggressively resuscitated with intravenous fluid and blood transfusions. An emergency esophagogastroduodenoscopy was performed which showed isolated gastric varices in the fundus of the stomach, with no active bleeding or high-risk stigmata. Abdominal computed tomography revealed focal splenic vein thrombosis and splenomegaly with ill-defined hypodensities. Portal and superior mesenteric veins were patent. Mild edema was seen surrounding the spleen and non-specific abdominal lymphadenopathy was also reported. A surgical consultation recommended an urgent splenectomy. Pathology of the removed spleen revealed diffuse large B-cell lymphoma. Positron emission tomography-computed tomography revealed lymphomatous disease in the thorax, abdomen, pelvis and bone marrow. The patient was subsequently started on chemotherapy.

A rare case of central nervous system tuberculosis.

Intracranial abscess is an extremely rare form of central nervous system (CNS) tuberculosis (TB). We describe a case of central nervous system tuberculous abscess in absence of human immunodeficiency virus (HIV) infection. A 82-year-old Middle Eastern male from Yemen was initially brought to the emergency room due to altered mental status and acute renal failure. Cross-sectional imaging revealed multiple ring enhancing lesions located in the left cerebellum and in bilateral frontal lobe as well as in the inferior parietal lobe on the left. The patient was placed on an empiric antibiotic regimen. Preliminary testing for infectious causes was negative. Chest radiography and CT of chest showed no positive findings. He was not on any immunosuppressive medications and human immunodeficiency virus (HIV) enzyme immunoassay (EIA) test was negative. A subsequent MRI one month later showed profound worsening of the lesions with increasing vasogenic edema and newly found mass effect impinging on the fourth ventricle. Brain biopsy showed focal exudative cerebellitis and inflamed granulation tissue consistent with formation of abscesses. The diagnosis of CNS TB was finally confirmed by positive acid-fast bacilli (AFB) cultures. The patient was started on standard tuberculosis therapy but expired due to renal failure and cardiac arrest.

Liver Injury Secondary to Anti-TNF-Alpha Therapy in Inflammatory Bowel Disease: A Case Series and Review of the Literature.

Background. Biologic therapy to inhibit tumor necrosis factor-alpha (TNF- α ) is an effective, safe treatment for patients with inflammatory bowel disease (IBD). All TNF- α inhibitors have been associated with liver toxicity, but many of these cases have been reported in patients receiving therapy for rheumatologic disease. Herein we report the first single-center case series of TNF- α antagonist related liver injury in patients with IBD. Methods. A retrospective case series was performed at the Henry Ford Inflammatory Bowel Diseases Center. IRB approval was obtained. Results. 2 patients were treated with infliximab, whereas the 3rd patient was treated with adalimumab for IBD. All 3 patients had negative viral markers, normal autoimmune serologies, and normal biliary imaging studies. Liver biopsy was performed in all 3 patients, and evidence of portal inflammation was seen. Liver enzymes normalized after discontinuation of therapy in all patients, and no long term effects have been observed. One patient was successfully transitioned from infliximab to adalimumab without relapse of either IBD or liver injury. Conclusion. Liver injury secondary to TNF- α antagonist is an underrecognized, important clinical entity with potentially serious consequences. The mechanism of drug-induced injury is idiosyncratic. Larger cohort studies are needed to establish risk factors and injury patterns related to hepatotoxicity in these patients.

Acute respiratory distress syndrome: A rare presentation of amantadine toxicity.

PATIENT: Male, 64 FINAL DIAGNOSIS: Acute Respiratory Distress Syndrome (ARDS) Symptoms: Generalized myoclonic jerks • impaired concentration • memory decline • visual hallucinations MEDICATION: Amantadine HCl Clinical Procedure: - Specialty: Toxicology. OBJECTIVE: Adverse events of drug therapy. BACKGROUND: Amantadine is indicated for treatment of influenza A infection, Parkinson disease and extrapyramidal reactions. Amantadine overdose affects mainly cardiovascular and central nervous systems. Amantadine-induced respiratory failure has not been described in previous case reports but it is a potential known side effect. CASE REPORT: We describe the case of a 64-year-old African American male with end stage renal disease who was prescribed amantadine at a dose for normal kidney function (300 milligrams per day) for no clear reasons. PATIENT's serum level of amantadine drawn on admission was found to be 6200 nanogram per deciliter (ng/dl) with normal range being 700-1000 ng/dl. Amantadine hydrochloride is not actively metabolized in humans; is mainly excreted unchanged in urine by glomerular filtration and tubular secretion (90% of the ingested dose). It tends to accumulate in patients with impaired renal function; poorly excreted in patients on hemodialysis and has a large volume of distribution. CONCLUSIONS: Our patient with impaired renal function was prescribed a much higher dose and eventually presented with high serum concentration of amantadine and neurological manifestations suggestive of amantadine toxicity. He developed sudden onset respiratory failure and pulmonary edema which is described as a potential lethal complication of amantadine toxicity. Since there is no specific etiology for his respiratory failure, this could represent the first reported case of Amantadine-induced Adult Respiratory Distress Syndrome (ARDS).