Cloxacillin-induced acute vanishing bile duct syndrome: A case study and literature review.

Ductopenia is often regarded as a chronic process where ≥50% of portal tracts lack bile ducts, which is also known as vanishing bile duct syndrome (VBDS). One aetiology is drug-induced liver injury. Cloxacillin, an antistaphylococcal penicillin, typically causes "bland" cholestasis. We present the first case of cloxacillin-induced acute ductopenia or VBDS and a review of published cloxacillin-induced liver injuries. A 66-year-old woman with no prior liver disease, but known penicillin allergy, was treated for postcarotid angioplasty staphylococcal infection with 6 weeks of cloxacillin. She presented with a 2-week history of weakness and jaundice. Laboratory work-up showed elevated liver enzymes with a cholestatic pattern, hyperbilirubinemia and eosinophilia. She required ICU transfer for hypotension and was started empirically on prednisone. Liver biopsy revealed severe centrilobular cholestasis, mild necroinflammation and ductopenia with epithelial injury, but no ductular reaction. Two months later she was discharged on hydrocortisone and ursodiol with persistently elevated alkaline phosphatase and bilirubin. She was considered for liver transplantation but died of liver failure 4 months later. Four additional articles were found with histopathologic descriptions of cloxacillin-related liver injury. These included portal inflammation, cholestasis and mild necroinflammation. Clinical features were reported in two cases; both had mild symptoms with cholestatic liver enzymes and hyperbilirubinemia. Both patients recovered completely within 10-60 days. Cloxacillin-induced cholestasis can be secondary to acute ductopenia, which can result in worse clinical outcomes than previously described "bland" cholestasis. Liver biopsy is recommended to identify cases with acute VBDS.

Value of liver biopsy in anorexia nervosa-related transaminitis: A case study and literature review.

Anorexia nervosa (AN) is a complex eating disorder that affects multiple organs. 60% of patients have liver injury with transaminitis. The mechanism of liver injury in AN remains unclear. We present a case of a 19-year-old female with AN was admitted to our hospital with marked transaminitis but near normal liver histology on biopsy. Her transaminitis eventually improved as she regained weight. We also conducted a literature review of similar cases to delineate the clinicopathologic spectrum of liver injury in AN patients. English published cases of adult AN patients with elevated transaminases who underwent a liver biopsy or autopsy were selected. 32 cases (including ours). All except four patients were female, with median age of 26.5 years and median body mass index 11.9 kg/m2 . Presentations mainly included hypoglycemic coma and weight loss. 63% of patients had severe transaminitis (AST >15x ULN). Other lab findings included elevated international normalized ratio (72%) and hypoalbuminemia (47%). Microscopically, all cases showed intact hepatic architecture. Fibrosis was reported in 12 cases and necroinflamfmation in 8, but only half of each had severe transaminitis. AN patients display a wide spectrum of liver histopathology which often does not correlate with the degree of transaminitis. In severe persistent AN-related transaminitis, liver biopsy is useful to assess the degree of liver injury and to exclude other potential etiologies.