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A longitudinal follow-up of asymptomatic hepatitis B surface antigen-positive chinese children

✍ Scribed by Anna S. F. Lok; Ching-Lung Lai


Publisher
John Wiley and Sons
Year
1988
Tongue
English
Weight
487 KB
Volume
8
Category
Article
ISSN
0270-9139

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✦ Synopsis


Fifty-one asymptomatic Chinese hepatitis B surface antigen (HBsAg) carrier children (34 boys, 17 girls), age 1 to 15 years (median: 10 years), were prospectively followed for up to 4 years (median: 30 months) to determine the natural evolution of clinical, biochemical and virological features during the early phase of chronic hepatitis B virus infection.

Hepatomegaly was the only abnormal finding on examination, being present in five children initially and four at follow-up. Serum ALT levels were normal in 80% of the children at presentation and remained within the normal range during the study in 60%. Fluctuations in ALT levels were mild. In four of 12 instances, transient elevations in ALT levels were associated with a during early childhood (10). Beasley et al. ( 11) found a carrier rate of 7.8% among Chinese preschool children. Wu et al. (12) from Taiwan reported a series of 20 HBsAg-positive children with hepatocellular carcinoma (HCC). Thus, chronic HBV infection is a common and potentially fatal disease among Chinese children. We conducted a prospective, long term follow-up of untreated, asymptomatic HBsAg-positive Chinese children to determine the natural evolution of clinical, biochemical and virological features during the early phase of chronic HBV infection.

PATIENTS AND METHODS fall in serum hepatitis B virus DNA levels.

At presentation, 43 (84%) children were hepatitis B e antigen (HBeAg) positive; only two (7%) cleared HBeAg on follow-up. None of the eight children who were initially positive for the antibody to HBeAg reverted back to HBeAg positivity. All the children remained HBsAg positive.

In this study, we demonstrated that chronic hepatitis B virus infection in asymptomatic Chinese children is usually associated with a mild and stable liver disease despite high levels of hepatitis B virus replication. This may reflect an immunological tolerance to the hepatitis B virus induced by early exposure to the virus and accounts for the persistently high levels of hepatitis B virus replication on follow-up.


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