\s=b\ Twenty-three infants born to asymptomatic hepatitis B surface antigen (HBsAg) carrier mothers were followed up to determine the vertical transmission of hepatitis B virus. Four infants became positive for HBsAg within four months after birth. Three showed hepatic dysfunction; liver biopsy specimens demonstrated mild chronic hepatitis in one and persistent hepatitis in another. In six infants followed up for more than six months after birth, antibody to HBsAg (anti-HBs) without antigenemia could be detected. Antigenemia of cord blood strongly suggested that hepatitis B viral infection of the infant would occur. HBsAg was also demonstrated in breast milk by radioimmunoassay in three cases. These findings indicate that vertical transmission of hepatitis B virus occurs in many infants born to asymptomatic HBsAg carrier mothers, and that some of them become persistent carriers or develop chronic hepatitis without showing any signs suggesting hepatic involvement.(Am J Dis Child 131: [644][645][646][647] 1977) Vertical transmission of hepatitis B virus occurs when the mother has suffered from acute hepatitis during late pregnancy or within the first two months postpartum.1-In contrast, if the mother is an asympto¬ matic carrier of hepatitis surface antigen (HB"Ag), vertical transmis¬ sion from the mother to her baby occurs rarely if at all. '-" Recent studies in Taiwan7 and in Japan"-demon¬ strated frequent antigenemia in in¬ fants born to asymptomatic HB^Ag carrier mothers.This prospective study was initiated in 1971 to determine whether vertical transmission of hepatitis virus occurs from asymptomatic HB^Ag carrier mothers to their infants.
SUBJECTS AND METHODSPregnant women who visited the De¬ partment of Obstetrics at the University of Tokyo from 1971 through 1974 were tested for the presence of HB,Ag in their sera. Those who were positive for HBsAg at least twice during more than a threemonth interval were followed up. Any patients showing signs or symptoms sug¬ gesting hepatitis or elevated serum glu¬ tamic oxaloacetic transaminase or glu¬ tamic pyruvic transaminase levels were excluded. Thirty-three of the asympto¬ matic HB.Ag carrier mothers subsequently were delivered of live infants. Twentythree of these consented to their infants being followed up regularly at the Depart¬ ment of Pediatrics.At delivery, specimens of cord blood from the umbilical artery were collected, with precautions to avoid contamination with maternal blood, and were tested for HB.Ag. Breast milk obtained during the first week following delivery was also tested for the presence of HB.Ag. Physical examinations were done monthly on these infants; their sera were tested for HB.Ag, antibody to HB.Ag (anti-HB.), transami¬ nase values, and thymol turbidity at inter¬ vals of one to three months thereafter.HB.Ag was determined by the immune adherence hemagglutination method and in some specimens also by radioimmunoassay, using the solid phase method. The presence of Anti-HB. was tested by the passive hemagglutination method. HB.Ag subtype...
An analysis of the variations in the clinical course of hepatitis B (HB) was attempted with mathematical simulation. Hepatitis B could be regarded as an ecosystem consisting of liver cell, hepatitis B virus and immunity, which were integrated by Dudley's hypothesis. The reason for the variations in the clinical course of hepatitis B were found to be the variations of immunological power destroying liver cells and of the absorption of HB virus.
Non‐A non‐3 hepatitis with recurrent aggravation was also studied. The effect of treatment with transfer factor and interferon for chronic hepatitis were simulated, and the dynamics of these treatments were analyzed.
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