The survival rate is relatively favorable at 53% with medical therapy of acute infections, but only 16% in cases of acute exacerbation of the carrier state.[285] The prognosis is particularly poor in cases of fulminant hepatitis B occurring in patients with HBV reactivation.[288] Differentiation between acute infection and acute on chronic infection can be difficult,

even Sirolimus using HBV markers from before and after the onset of infection. For the etiological diagnosis of fulminant hepatitis B, we measure HBsAg, anti-HBs antibody, anti-IgM-HBc antibody, anti-HBc antibody, and HBV DNA levels. We can differentiate between acute infection and acute exacerbation of the carrier state through the presence of HBsAg prior to disease onset, and positive conversion of anti-HBs antibody during the disease course. If these markers are indeterminate, the anti-IgM-HBc antibody and anti-HBc antibody titers at the time of disease onset may be considered. In general, in acute infections anti-IgM-HBc antibody are positive with a high titer, whereas HBc antibody have a low titer. In carriers, the anti-IgM-HBc antibody titer is low, and the anti-HBc antibody titer is high. At present, anti-IgM-HBc antibody

titers are usually measured using the CLIA (chemiluminescent immunoassay) method, with a cut-off titer of 10.0 for differentiation between acute infection and acute on chronic infection.[289] Determination of anti-HBc antibody titers using the CLIA method is becoming more common, although this

has actually made differentiation between acute Daporinad chemical structure infection and acute on chronic infection more difficult in comparison with the earlier RIA (radioimmunoassay) and EIA (enzyme immunoassay) 1:200 dilution methods. HBV reactivation should be suspected in patients on immunosuppressive therapy or chemotherapy before or at the time of disease onset. A variety of HBV variants have been reported in association with fulminant hepatitis B, and preferably the HBV genotype, and the presence of precore and core promoter mutations should be determined. The B1/Bj genotype is common in fulminant hepatitis associated with acute infections,[5] and high incidences of core click here promoter (A1762T/G1764A) and precore (G1896A/G1899A) mutations have also been reported.[5, 60, 290-293] An association has also been reported between preS2 variants, S antigen variants, and fulminant hepatitis B.[294-296] On the other hand, no specific variants have been identified in HBV carriers developing acute exacerbation. Recommendation HBsAg, anti-HBs antibody, anti-IgM-HBc antibody, anti-HBc antibody, and HBV DNA levels should be determined in patients with fulminant hepatitis B to make the etiological diagnosis. Determination of HBV genotype and the presence of precore and core promoter mutations is also desirable. In general, acute hepatitis B is a condition that resolves naturally, with no need for treatment.