In a prospective study of maternal-fetal transmission of hepatitis B virus in 125 healthy mothers who were carriers of hepatitis B surface antigen (HBsAg), preliminary results showed that the most important determinant in such transmission was the presence of hepatitis B e antigen in the mother. HBsAg was detectable by solid-phase radioimmunoassay in 33% of amniotic fluid samples, 50% of cord blood samples, 71% of breast milk samples, and 95.3% of samples of gastric contents from newborns. The presence of HBsAg in gastric aspirate from the infants immediately after birth in almost all cases suggests a universal mechanism of infection by the oral route during delivery. In light of these findings, precautions such as possible elective cesarean section, routine gastric aspiration of the newborn, avoidance of breast-feeding, etc., should be taken to avoid perinatal transmission.
Materno-fetal transmission of hepatitis B was studied in 97 healthy carriers of hepatitis B surface antigen (HBsAg). Antepartum transmission occurred in at least 10 per cent. Intrapartum'transmission may have occurred in about 40 per cent as a result of swallowing of the infective fluid by the baby during delivery, and maternofetal transfusion during labour. Person to person transmission after delivery played a minor role. The presence of hepatitis B associated e antigen (HBeAg) in 48 per cent of maternal serum correlated strongly with the subsequent presence of antigen in the infants. There was a linear association between the incidence of antigens in cord blood and the duration of the first stage of labour, with a significant association when labour exceeded nine hours. Caesarean section is recommended if mothers have HBeAg; likewise amniocentesis and breast feeding should be discouraged if mothers have HBeAg.
Summary
Materno‐fetal transmission of hepatitis B was studied in 97 healthy carriers of hepatitis B surface antigen (HBsAg). Antepartum transmission occurred in at least 10 per cent. Intrapartum transmission may have occurred in about 40 per cent as a result of swallowing of the infective fluid by the baby during delivery, and materno‐fetal transfusion during labour. Person to person transmission after delivery played a minor role. The presence of hepatitis B associated e antigen (HBeAg) in 48 per cent of maternal serum correlated strongly with the subsequent presence of antigen in the infants. There was a linear association between the incidence of antigens in cord blood and the duration of the first stage of labour, with a significant association when labour exceeded nine hours. Caesarean section is recommended if mothers have HBeAg; likewise amniocentesis and breast feeding should be discouraged if mothers have HBeAg.
A double‐blind randomized placebo‐controlled study to prevent hepatitis B infection in 235 babies born to chronic hepatitis B, HBeAg carriers was carried out. Babies in three treatment groups all received heat‐inactivated hepatitis B vaccine. In addition multiple doses of HBIG and a single dose of HBIG were given in pups I and II respectively. After three years of follow‐up, 4/60 (Group I), 3/64 (Group II), and 1/64 (Group III) developed chronic infection. For those who escaped chronic infection, other hepatitis events also occurred. They were transient HBs‐antigenaemia, anti‐HBc conversion and significant rise in anti‐HBs titre without seroconversion for anti‐HBc. It was deduced that 30% of babies born to hepatitis carriers are naturally protected from chronic infection. Immunization, with vaccine only, protects another 46%. The addition of single and multiple doses of HBIG protects another 10% and 5%, respectively. 2% acquired intrauterine infection and 7% failed to respond to the most intensive immunization schedule.
A double‐blind, randomised dose‐response study was carried out to evaluate the immunogenicity of a plasma‐derived, heat‐inactivated hepatitis‐B vaccine in newborn infants of mothers who were HBsAg‐positive but HBeAg‐negative.
Four groups of 15 babies each were vaccinated at birth and at the age of 1 and 2 months with 0.1, 0.25, 0.6 and 3 μg, respectively. The anti‐HBs conversion rate was 100% at 3 and 6 months in the group immunized with 3 × 3 μg. In comparison with the 3‐μg group, the anti‐HBs conversion rate for the 0.6‐ μg group did not change significantly, but the geometric mean titre was significantly lowered (p<0.005). In the 0.1‐μg and 0.25‐μg groups, however, the anti‐HBs conversion rate was significantly reduced (p<0.05). This implies that the optimum dosage for this vaccine should be between 0.6 to 3 μg. Protective efficacy need to be proven before vaccine dosages are lowered for high risk newborns.
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