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Delayed wound healing and duodenal ulcer leading to obstructive jaundice: case report An 82-year-old man developed duodenal ulcer leading to obstructive jaundice during treatment with lenvatinib for hepatocellular carcinoma (HCC) and antiplatelet therapy with aspirin. Additionally, he experienced delayed wound healing of endoscopic sphincterotomy (EST) incision secondary to treatment with lenvatinib [routes not stated; not all dosages and times to reactions onsets stated]. The man, who had achieved hepatitis C virus eradication with ledipasvir and sofosbuvir before 2 years, had cirrhotic liver. He had undergone two courses of transcatheter arterial chemoembolisation, followed by local ablation during the previous year; however, he had developed recurrence of HCC. Therefore, he had been receiving a standard dose of lenvatinib 8 mg/day based on body weight of 59kg, without any adverse events for 3 months. However, he presented with vomiting and upper abdominal pain at the age of 82 years. He also had a medical history of coronary stent placement (3 years previously) for angina pectoris, and he had been receiving antiplatelet therapy with aspirin at a low-dose. Concomitantly, he had been receiving rabeprazole and several unspecified medications for hypertension, dyslipidaemia and type 2 diabetes mellitus. He was admitted, and he complained of abdominal discomfort in the right upper quadrant and epigastrium. He had a low-grade fever and hypertension. Mild icterus was observed on a physical examination. Laboratory tests revealed significant increase in the levels of white blood cell count and serum levels of total bilirubin, AST, ALT, direct bilirubin, alkaline phosphatase, CRP and γ-glutamyl transpeptidase. Dilatation of the common bile duct was observed on a contrast-enhanced CT, and duodenal wall thickening was observed on T2-weighted imaging. He was noted to have acute cholangitis based on the findings on admission. Therefore, the man’s treatment with lenvatinib and aspirin were discontinued. He underwent endoscopic retrograde cholangiopancreatography (ERCP), and endoscopic examination showed multiple ulcers in the bulb and descending portion of the duodenum, without any mucosal damage in the stomach. Also, it was observed that one of the duodenal ulcers was present on the swollen ampulla of Vater, from which infective bile leaked. Subsequent cholangiography revealed several inhomogeneous unfilled areas, which were compatible with pus accumulation, in the common bile duct. All the findings indicated oedematous papilla due to the duodenal ulcer (located above) leading to cholestasis. Blood culture (taken on admission) was positive for Gram-negative rod bacteria. Cholestasis and the bacteraemia resulted from cholangitis, which necessitated urgent biliary drainage. Therefore, he underwent endoscopic biliary drainage by EST, with an incision, and balloon sweeping. Enterobacter cloacae bacteraemia was detected on bile and blood cultures, and the bacteraemia improved with the biliary drainage and treatment with cefep