ABSTRACT
The long-term changes in the HBeAg/anti-HBe system were examined in 55 children with chronic type B hepatitis (52 patients) or cirrhosis (three patients) during a follow-up period of two to 10 years. At the time of presentation, positive reactions to HBeAg were seen in 46 children, and to anti-HBe in nine. Spontaneous seroconversion from HBeAg to anti-HBe occurred in 13 of 38 patients (average annual rate 16%), mainly those with acute onset of hepatitis B or with features of active liver disease at presentation and with a focal distribution pattern of hepatitis B core antigen in the liver. Normalization of transaminase activity and disappearance of histologic features of activity were the rule in patients in whom seroconversion occurred, but the exception in those who maintained persistently HBeAg-positivity. In contrast to the favorable evolution of illness observed in children showing anti-HBe seroconversion, three of nine patients who had anti-HBe-positive reactions at presentation were found to have liver cirrhosis, and a fourth patient had features of active hepatitis throughout the observation period. Because delta antigen was detected in the liver in two of these patients, it is conceivable that etiologic cofactors could have influenced their course of chronic hepatitis.
Subject(s)
Antibodies, Viral/analysis , Hepatitis B Antigens/analysis , Hepatitis B e Antigens/analysis , Hepatitis B/immunology , Adolescent , Alanine Transaminase/metabolism , Child , Child, Preschool , Chronic Disease , Female , Follow-Up Studies , Hepatitis B/drug therapy , Hepatitis B/pathology , Hepatitis B virus/immunology , Humans , Immunosuppressive Agents/therapeutic use , Infant , Liver/enzymology , Male , Prospective StudiesABSTRACT
Hepatitis B virus markers were studied in serum and liver of 24 children with chronic hepatitis. All patients had evidence of active virus replication, as shown by hepatitis B core antigen in the liver cell nuclei, independently of the severity of histologic lesions. Furthermore, 19 of 24 patients had hepatitis B e antigen in serum, and most patients showed a diffuse pattern of HBcAg distribution in the liver. In all 24 children, the presence of immunoglobin G bound to the liver cell surface paralleled the activity of virus replication, but it did not correlate with the severity of liver lesions. During a follow-up period of two to four years, the virus replication persisted in all eight patients receiving immunosuppressive therapy, whereas in 5 of 16 untreated patients we observed a seroconversion to antibody to HBeAg, which is currently regarded as a favorable event for the prognosis of the disease.