Acute-on-chronic liver failure in HIV infection: two cases

1. Viral load [HIV-1 RNA copies/mL] CD4+ Th cells [x mL1] ALT [U/L] AST [U/L] Total bilirubin [mg/dL] -GT [U/L] TPT [%] PTT [s] CASE I Pre-acute 33,200 657 14 12 0.9 18 90 28 Fatty liver After HAV infection ND ND 619 520 3.1 139 56 40 Hepato- splenomegaly CASE II Pre-acute 304 243 46 31 1.3 87 90 30 Fatty liver After Ecstasy abuse ND ND 54 49 1.9 107 23 69.8 Hepato- splenomegaly • Acute-on-chronic liver failure in HIV infection: two cases • Canbay1, R. Gieseler2, M. Kullmer1, K. Radecke 1, B. Ross1,R. Noppeney 1, G. Gerken1, and U. Treichel1 • 1 Dept of Gastroenterology and Hepatology, Universiy Clinic Essen, and 2 LTBH Medical Research Institute, Beverly Hills, CA, USA Background Acute liver failure, as charcaterized by acute liver insufficiency, hepatorenal syndrome, and hepatic encephalopathy, is termed acute-on-chronic liver failure (AOC) when pre-damaged organ is affected. Indeed, >50% of all HIV+ patients present with non-specific hepatic alterations such steatosis, siderosis, reactive hepatitis, or cholestasis which are currently attributed to multifactorial causes. We here present two patients with long-lasting HIV-infection under anti-retroviral therapy (ART) who developed AOC after (i) acute infection with HAV, or (ii) methamphetamine (“Ecstasy”) abuse. Cases I: Approx. 1 wk. after visiting an area endemic for HAV, a 39-yr.-old male (stage A2) became icteric, showed elevated liver enzymes, and was tested IgM-positive for HAV. Previous examinations had dem-onstrated normal transaminase activities while hepatic steatosis had been suspected. He developed liver failure-associated complications including renal failure as well as pleural and pericardial effusion. II: A 33-yr.-old male (stage A3), known for ethanol abuse and suspected alcoholic liver disease. Approx. 24 hrs. after Ectasy abuse, he developed both liver failure and lactic acidosis (12 U/L). Results Both patients suffered from fatty liver in the pre-acute stage as suspected by ultrasound assessments. After developing symptoms of liver failure, ART was discontinued. The patients recovered clinically with normalized laboratory parameters in follow-up (cf. Tab. 1). Tab. 1: Virology / Clinical Chemistry / Hemostaseology Stage Sonography Conclusions Because in HIV+ patients the liver may be pre-damaged despite inapparent laboratory parameters, such individuals are likely to develop AOC when subjected to acute risk factors such as the hepatitis viruses or toxic drugs. Therefore, firstly, vaccination against hepatitis A and B should be strongly urged. Secondly, with respect to ART, liver parameters have to be closely monitored.