Liver cirrhosis: case reportA 65-year-old man developed hepatic cirrhosis during the treatment with methotrexate for psoriatic arthritis (PsA). The man, who had large volume ascites, presented to hospital. Three months prior to admission, he had presented to another hospital with a diagnosis of non-alcoholic steatohepatitis (NASH) induced cirrhosis and was discharged with spironolactone and furosemide. He had a medical history of type 2 diabetes mellitus and PsA, both diagnosed a decade earlier. During the previous five years, he had normal levels of glycated haemoglobin (HbA1C). He had been receiving methotrexate [route not stated] once weekly for the past six years (cumulative dose of approximately 5g) along with sitagliptin and metformin. Upon presentation, he was afebrile. He had lower extremities oedema, large volume ascites, palpable liver and spleen as well as spider nevi in the torso and palmar erythema. His laboratory tests revealed elevated GGT, bilirubin concentration and ALP. His serum albumin and INR were 2.8 g/dL and 1.17, respectively. Prior to the initiation of methotrexate, he had normal liver function tests including ALT/AST/ALP/ GGT/INR and albumin. Ultrasonography of the abdomen showed ascites, splenomegaly, cirrhotic liver and a patent portal vein. Chest X-Ray revealed right sided pleural effusion. An ascites paracentesis showed 383 cells, with 10% neutrophis and serum albumin gradient (SAAG) of 2.5 mg/dL, compatible with portal hypertension ascites. Abdomen CT scan showed a cirrhotic liver with splenomegaly, ascites and portosystemic collaterals. Upper gastrointestinal endoscopy showed portal hypertensive gastropathy, but no oesophageal or gastric varices. Liver biopsy showed micronodular cirrhosis with lymphocytic infiltrates in fibrous septa and features of cholestasis at the periphery of cirrhotic nodules; no steatosis, pericellular fibrosis, ballooning or interface hepatitis were noted. According to histological examination and clinical history, end-stage liver disease was diagnosed.Methotrexate was discontinued. The man received high doses of spironolactone and furosemide to control the accumulation of ascites. However, he developed renal failure. Subsequently, spironolactone and furosemide were discontinued. A large volume paracentesis were initiated. After eight months of his initial diagnosis, he died due to spontaneous bacterial peritonitis.