Esophageal Variceal Bleed in a HIV Patient Secondary to Non-Cirrhotic Portal Hypertension After Didanosine Use

Abstract

Purpose: We present a case of a HIV patient presenting with hematemesis secondary to esophageal varices, who was subsequently found to have noncirrhotic portal hypertension (NCPH) likely secondary to previous didanosine use. A 59 year old male with a history of HIV on ART since 1985, presented to our hospital with an episode of large volume hematemesis, and pre-syncopal symptoms. He was first diagnosed with HIV in 1985. He was initially started on monotherapy with zidovudine. In 1988, he entered a study for didanosine (ddI) and remained on this monotherapy till 1999. He then received stavudine monotherapy from 1999 until 2001, and then switched to his current therapy of abacavir, lamivudine, and efavirenz. With treatment he has had an undetectable viral load and CD4 count above 400. On presentation he had a Hct drop from 40 to 32. Emergent EGD demonstrated 3 large cords of esophageal varices with stigmata of recent bleeding. Banding ligation was performed with no further bleeding. He had no prior history of liver disease or ETOH abuse. His hepatitis serologies, BMI, LFT's, albumin, PT/INR were all normal. He had a mild thrombocytopenia. Abdominal US demonstrated patent hepatic and portal vasculature, normal appearing liver, and mild splenomegaly with small ascites. Transjugular liver biopsy was performed demonstrating a normal hepatic venous pressure gradient of 4 mmHg. Liver biopsy showed hepatocellular disarray, portal fibrosis, hepatoportal sclersosis with no steatosis, bridging fibrosis or cirrhosis. These findings are consistent with non-cirrhotic portal hypertension likely secondary from his previous prolonged exposure to didanosine. Chronic liver disease in HIV infected patients is increasing in occurrence, often secondary to co-infection with hepatitis B/C, alcohol abuse, fatty liver disease, or medication-induced hepatotoxicity. Non-cirrhotic portal hypertension can be due to portal vein thrombosis, nodular regenerative hyperplasia, incomplete septal cirrhosis, vasculitides, schistosomiasis, or idiopathic (hepatoportal sclerosis). Recent case series and case control studies have shown an association between HIV patients on ART and NCPH. Suspected causes in these patients include medication affect specifically long term ddI therapy versus direct affect from HIV. In HIV patients presenting with upper GI bleed, esophageal varices needs to be considered even in the absence of cirrhosis as NCPH is a potential complication of the ART treatment or HIV itself.