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Liver injury: case report A 61-year-old man developed drug-induced liver injury (DILI) while receiving treatment with diltiazem for angina and warfarin as an anticoagulant [dosages, routes and time to reaction onset not stated]. The man on maintenance dialysis was hospitalised with hepatobiliary enzymes abnormality and jaundice. He had been started on haemodialysis 3 years earlier for diabetic nephropathy. He had undergone coronary artery bypass grafting (CABG) 7 months earlier for unstable angina. The laboratory results showed a biliary tract and liver disease. An abdomen CT scan revealed swelling of his liver and oedema of the periportal space, without biliary obstruction. He had been using aspirin, alfacalcidol, carvedilol, esomeprazole, nicorandil, linagliptin, prasugrel, rosuvastatin, and precipitated calcium carbonate for above 2 years. Diltiazem and warfarin had been initiated after his CABG 7 months earlier. Considering the possibility of DILI, all drugs were discontinued from day 1 of admission; however, his liver function continued to deteriorate. Subsequently, CT scan revealed significant atrophy of liver with massive ascites. He was diagnosed with DILI due to diltiazem and warfarin, by exclusion based on blood test findings and clinical course. On day 46, liver biopsy revealed piecemeal necrosis, fibrotic enlargement, and proliferation of bile canaliculi were noted in the portal area. On the second side, within the hepatic lobule, very slight lymphocytic infiltration, and a very small amount of hepatocellular necrosis were identified. These studies were consistent with mixed-type DILI, specifically cholestatic injury. On day 8, his Model for End-Stage Liver Disease (MELD) score was 32, and symptoms equivalent to grade 1 hepatic encephalopathy were noted. Hence, liver transplantation was suggested, but he was unfit for transplantation because of his renal and cardiac complications. The man was initiated on cell-free concentrated ascites reinfusion therapy (CART) on day 45 for the management of ascites while awaiting liver regeneration. He was discharged from the hospital on day 67 because his general condition was stabilised by CART. After the discharge, haemodialysis was continued and CART was performed according to his symptoms. Further, he developed an umbilical hernia 131 days after discharge, and enterectomy was performed. Albumin was 2.1–2.5 g/dl from the onset of DILI until enterectomy and remained above 2.5 g/dL thereafter. CART was withdrawn 206 days after discharge. His abdominal CT scan revealed that his liver had regenerated and enlarged, which was considered to be the cause of the decreased ascites. More than 1 year later, his albumin was >3 g/dl, prothrombin time was