Azathioprine

Abstract

Drug-induced liver injury and cytomegalovirus-infection : case reportA 37-year-old man developed drug-induced liver injury and cytomegalovirus-infection during treatment with azathioprine for autoimmune hepatitis [route not stated].The man, who had a significant history of autoimmune hepatitis (AIH), primary sclerosing cholangitis (PSC), and ulcerative colitis (UC), was presented to the hospital for jaundice and fatigue. He was diagnosed with PSC eight years ago. He experienced increased levels of aspartate aminotransaminase (AST) and alanine aminotransferase (ALT). A year before the current presentation, his ALT was 145 U/L, AST was 92 U/L, alkaline phosphatase (ALP) was 245 U/L, and total bilirubin was 2.0 mg/dL. At that time, he underwent several laboratory investigations and was diagnosed with PSC/AIH overlap. He received treatment with azathioprine and concomitant therapy with prednisone. Due to financial problems, he was not consistent in administering medication. A month prior to the current presentation, his AST, ALT, ALP, and total bilirubin was elevated. His azathioprine therapy was resumed at 75 mg/day, and his prednisone dosage was increased. He complained of worsening jaundice, dark urine, fatigue, and itching at his most recent visit. He also admitted to having one incident of non-bloody emesis, but denied any stomach discomfort or diarrhoea. He denied drug or alcohol use. His outpatient therapy included azathioprine 150 mg/day. Additionally, he had received concomitant therapy with losartan/hydrochlorothiazide, mesalazine [mesalamine], prednisone, omeprazole, and ergocalciferol. He denied using any over-the-counter or herbal drugs. He recommended compliance with azathioprine and prednisone during the last month. Two weeks before the current presentation, he had increased his azathioprine dose from 75 to 150mg. His vital signs were steady. He was vigilant and aware of his surroundings, including time, location, and himself. There was no evidence of asterixis. Jaundice and scleral icterus were present. He had a smooth, non-distended, and non-tender abdomen. In the extremities, there was no oedema. During admission, his AST, ALT, ALP, and total bilirubin levels are more elevated than a month prior his admission. Following laboratory investigations revealed: INR 5.4; creatinine 1.4 mg/dL; WBC 5.2 × 10 9 /L; haemoglobin 10.3 g/dl; platelets 190 × 109; ferritin was 3668 ng/mL; IgG 995 mg/dL; IgG4 17.6 mg/dL. His model for end-stage liver disease score of 42 was noted. Eventually, he was hospitalised. His hepatitis A IgM antibody, acetaminophen level, hepatitis C virus antibody, hepatitis C RNA, core IgM antibody, and hepatitis B surface antigen were all negative. Magnetic resonance cholangiopancreatography revealed stable results of PSC with no indication of a dominant stricture. Infectious studies revealed a cytomegalovirus (CMV) polymerase chain reaction (PCR) of 100279 IU/mL with a negative herpes simplex virus PCR and a negative epstein-barr virus (EBV) PCR. The 6-thioguanine level was 218 pmol/8 x 1...