Duodenal Hemangioma as a Complication of Portal Hypertension

Abstract

Portal hypertensive duodenopathy (PHD) is an uncommon outcome of portal hypertension (PHTN) and can present wither as incidental finding or associated with anemia from gastrointestinal bleeding. A 75-year-old male with well controlled HIV presented with symptomatic anemia (Hb 5.2 mg/dL). He had a history of variceal bleeding one year prior for which he had a liver biopsy and was diagnosed with cryptogenic cirrhosis and obstructive portal venopathy. The esophageal varices were ligated and obliterated. Four months ago, MRI for hepatoma surveillance showed portal vein thrombosis, managed conservatively. On this admission, his medications were Atripla, Aspirin, Omeprazole and Nadolol. Panendoscopy and capsule endoscopy were non-diagnostic. Repeat endoscopy showed a nodule in the bulb and third portion of duodenum, one of which was oozing blood. This was treated with argon plasma coagulation (APC) and hemostatic clips. They were histologically confirmed as hemangioma. Surveillance endoscopy showed a new nodule in the duodenal bulb. Pathology showed mild chronic duodenitis with focal gastric metaplasia and duodenal mucosa with focally increased vessels, consistent with hemangioma. A third surveillance endoscopy also demonstrated a nodule in the bulb with actively oozing and was treated with APC. PHD presenting as erythema, telangiectasia, ulcers, or varices has been reported with a prevalence of up to 51.4%. Also, there have been two case reports of duodenal polyps, presenting as bleeding and as an incidental finding, respectively. Histologically, PHD has been associated with angiogenesis, congestion, edema, apoptosis, fibrosis and villous changes. Duodenal hemangiomas are very rare vascular malformations with only 22 reported cases. Our case is the first to describe PHD-associated recurrent duodenal hemangioma, presenting with bleeding and anemia, in a patient with portal vein thrombosis. The relapsing nature of this lesion, in absence of recurrence of esophageal varices, suggests upregulated angiogenesis. The possible hemodynamic changes associated with successful variceal ligation and portal vein thrombosis may also contribute to development of duodenal hemangioma. While endoscopic management is effective, repeat endoscopy may be required given recurrence. The definitive management of duodenal hemangioma would likely involve therapies beyond treatment of PHTN with B-blockers or Transjugular intrahepatic portosystemic shunt, such as liver transplantation.Figure 1Figure 2