Volume 3, Number 3, December 2002 97 C ASE REPO RT INTRODUCTION Viral hepatitis is a systemic infection that causes the inflammation and necrosis of hepatocytes, causing an array of clinical, biochemical, immunoserological, and morphological changes. 1 It is estimated that 316 million people carry the virus in the world, 170 of which reside in the Asia-Pacific region. In Southeast Asia, including Indonesia, the prevalence is relatively high, ranging between 6 and 16%. 2 Viral hepatitis shows a range of clinical signs and laboratory manifestations, from unapparent illness, asymptomatic infection, to culminant disease with a very high mortality rate (>80%). 1,2 A French hepatogastroenterologist stated that acute liver failure is characterized with clinical signs of encephalopathy, while early acute liver failure is defined as a reduction in prothrombine ratio to less than 50% the normal value in a patient with acute hepatitis. In the Netherlands, a patient is considered to have early acute Early Acute Liver Failure In Severe Acute Hepatitis B Gontar A. Siregar Division of Gastroentero-Hepatology, Department of Internal Medicine, Faculty of Medicine, University of North Sumatera/Adam Malik Hospital, Medan, Indonesia ABSTRACT Early acute liver failure is defined by the presence of a drop below 50% of the normal prothrombine ratio, jaundice, and clotting factors of less than 50% in any patient with acute liver disease. Clinical features and laboratory manifestations of viral hepatitis range from unapparent disease, asymptomatic infection, to culminant disease, which has the highest mortality rate of up to over 80 %. We report a case of a 22-year old man who was treated in a private hospital with early acute liver failure caused by hepatitis B infection. The diagnosis was based on clinical symptoms and laboratory test results such as jaundice, hepatomegaly, ascites, 34% prothrombine ratio, elongated prothrombine time (37,1 seconds), hypoalbuminemia (1,9 g/dL), hyperbillirubinemia (total billirubin 26,35 mg/dL, direct billirubin 16,66 mg/dL, HbsAg (+), IgM anti- HBc (+), IgM anti HAV (-), and anti HCV (-). The patient suffered from jaundice for 6 weeks and on the third week, he suffered from ascites. He had improved clinical condition and laboratory test results with conservative therapy after the seventh week. At the end of the tenth week, the patient’s clinical condition and laboratory test results had reached normal, with HBsAg (-) and HBsAb (+). Whether or not interferon should have been given to this patient is still arguable. Key words: Early acute liver failure, Severe acute hepatitis B liver failure if there is jaundice and a clotting factor of less than 50%. 3 Serological diagnosis of acute hepatitis B is estab- lished if HBsAg and IgM anti-HBc are found in the patient’s serum. 1-4 There is no specific treatment for distinguishable acute viral hepatitis. Nevertheless, hospitalization is advisable for possible focused treatment and care as well as pre- vention of transmission to other members of the family and the community. The patient is given a low fat, high carbohydrate, and high protein diet. Immunotherapy may alleviate complaints and assist the normalization of liver function. 5 CASE REPORT T, a 22-year old, male college student living in Medan was hospitalized in a private hospital from May 8, 2002 with a chief complaint of yellow eyes since the previous