Search

The authors analyzed acute exacerbations of chronic hepatitis B in 24 chronic HBsAg carriers (20 with positive HBeAg, 4 with anti-HBe), more than half of whom were treated with glucocorticoids, by examining specific antigens and antibodies of the hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis delta virus (HDV), Epstein-Barr virus (EBV) and cytomegalovirus (CMV). Of 38 observed exacerbations of the disease they found in 7 (18%) deterioration after discontinuation of glucocorticoids, in 7 (18%) seroconversion of HBeAg to anti-HBe, in 9 (24%) spontaneous exacerbation of chronic hepatitis B, in 11 (29%) chronic activation, reactivation of EBV superinfection, in 3 (8%) CMV reactivation or superinfection and in one (3%) HDV superinfection. In no instance HAV superinfection was observed. Exacerbations were found five times more frequently in subjects in the stage of active viral replication (in HBeAg+ subjects) than in subjects with anti-HBe. In eight patients EBV reactivation was found after glucocorticoids withdrawal: in five patients after an average period of 5 months (range 3-7) and in three patients after an average period of 33 months (range 22-48). The results provide evidence that in addition to already known causes of acute exacerbations of chronic hepatitis B in our geographical area probably an important cause of deterioration of hepatitis is reactivation or superinfection with EBV and CMV in some patients in conjunction with previous glucocorticoid treatment.

In serum of patients with chronic hepatitis B (HB) in the stage of active viral replication HBsAg/IgM complexes were detected. Using a commercial kit AU-IGM-K Sorin Biomedica HBsAg/IgM complexes in 136 patients with chronic HB and cirrhosis of the liver were examined, incl. 89 men, 42 women and 5 children, mean age 48 +/- 17 years. With regard to the results of the serological examination for HB virus (HBV) markers the results in 54 patients with positive HBeAg and HBsAg in serum (group 1) were compared with 68 patients with positive HBsAg only (group 2) and with 14 patients with positive antibodies against HBV or unrelated to HBV (group 3). The mean positivity index of HBsAg/IgM complexes in group 1, 2 and 3 was 9.89, 1.85 and 0.50, respectively. The results suggest a significant predominance of HBsAg/IgM complexes in patients during the stage of active viral replication with positive HBeAg in serum, as compared with patients without HBeAg (p = 0.001) and the control group (p = 0.001). A similar significant difference between groups was found as regards to ALT and AST activities. We conclude that in patients with chronic HBeAg positive hepatitis and a moderately elevated transaminase activity usually also HBsAg/IgM complexes, which are closely correlated with HBeAg, are positive.

Alpha-fetoprotein (AFP) was assessed in 159 subjects with chronic liver disease, incl. 125 chronic HBsAg carriers (42 suffered from cirrhosis of the liver) and in 34 HbsAg negative cirrhotic patients. In the group of 83 patients with chronic hepatitis B a slightly elevated AFP value was recorded in 7.2%, however, during the check-up examination it was already normal. During a one-year follow up hepatocellular carcinoma (HCC) was revealed in 4 of 42 HBsAg positive cirrhoses (9.5%) and in 2 of 34 (5.9%) HBsAg negative cirrhoses, the difference was not, however, significant. Five patients with HCC had markedly elevated or rising AFP value, one patient had abnormal AFP level despite advanced HCC. All cases of HCC were diagnosed late, in one patient radical treatment was not successful. We conclude that to improve the adverse prognosis of patients with HCC it is necessary to follow-up prospectively all patients with cirrhosis of the liver by sonography twice a year and examine after the same time intervals serum AFP to detect early stages HCC where there is still some chance of successful treatment.

In 37 patients with chronic hepatitis B in the stage of active viral replication the authors tried to assess the time of seroconversion of HBeAg to anti-HBe and HBsAg to anti-HBs (21 men, 13 women and 3 boys, mean age of adults 44 years). During the 8-years investigation period seroconversion of HBeAg occurred in 19 of 37 patients (51.3%) which is an annual rate of seroconversion 6.4%. HBeAg disappeared from serum after a mean period of 82 months (range 29-228 months). After seroconversion of HBeAg the ALT and AST activity declined significantly. Acute exacerbation of hepatitis before seroconversion of HBeAg was recorded in 13 of 37 patients (35%). The mean ALT activity at the peak of exacerbation was 7.93 mu kat/l, the average duration of exacerbation was 9.8 months. Seroconversion of HBsAg occurred in 7 of 37 patients (19%). The mean annual rate of seroconversion of HBsAg was 2.4% after an average period of 98 months. During the investigation period 7 patients died (19%), four of them had a constantly positive HBeAg. The authors conclude that very low annual average seroconversion of HBeAg (6.4%) and HBsAg (2.4%) in patients with chronic hepatitis B is probably caused by previous glucocorticoid treatment.