There is insufficient evidence concerning entecavir therapy for severe acute hepatitis. A study comparing entecavir and lamivudine in the treatment of exacerbations of chronic hepatitis B found that entecavir was superior in antiviral effect to lamivudine, but a tendency to prolongation of jaundice was identified.[279] Caution is required in administering entecavir to acute hepatic dysfunction associated

with jaundice. At present, more than half of Japanese patients with acute hepatitis B are infected with HBV genotype Cilomilast ic50 A. Acute hepatitis B has been shown to be more likely to be prolonged or become chronic in patients with HBV genotype A.[280-282] The usefulness of NA therapy with the aim of preventing chronic disease has yet to be established, and is not recommended

overseas either. Acute hepatitis B, with sexual transmission as the main route of infection, can be a coinfection with HIV. To avoid drug resistance, treatment of HIV infection requires the use of at least 3 antiviral agents. Of the NAs approved for the treatment of hepatitis B in Japan, lamivudine has a strong anti-HIV effect, and adefovir and entecavir have weak anti-HIV effects.[283, 284] It is therefore necessary to confirm whether coinfection with HIV is present before commencing NA therapy for acute hepatitis B, and take care to avoid HIV monotherapy. There has been some indication that entecavir monotherapy in patients with HBV/HIV coinfection, who are not receiving fully suppressive antiretroviral regimens, may lead to the emergence of drug resistant HIV strains.[283] Recommendations Selleck INCB024360 Lamivudine therapy is recommended for patients with severe acute hepatitis B, commencing before the prothrombin time goes below 40%. Lamivudine should be ceased when HBsAg testing becomes negative. Presence of coinfection with HIV should be determined before commencing lamivudine therapy. Approximately 40% of cases of fulminant hepatitis in Japan are caused by HBV.[285] The etiology of fulminant hepatitis B can be broadly

divided into rapid progressive acute infection (transient infection) and acute exacerbation in an HBV carrier. A recently devised etiological classification of acute liver failure further divides acute exacerbation in an HBV carrier into 3 categories: (1) asymptomatic or inactive carrier without click here drug exposure, (2) reactivation in asymptomatic or inactive carrier receiving immunosuppressive and/or anti-cancer drugs, and (3) reactivation by immunosuppressive and/or anti-cancer drugs in patients with resolved HBV infection (de novo hepatitis B).[286, 287] Both the pathological state and prognosis differ between patients with a rapidly progressive acute infection and those with acute exacerbation of the carrier state. The former is hepatitis in the process of clearing HBV, in which amelioration of the hepatitis can be expected as the viral load decreases.