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Prevention and control of perinatal hepatitis B virus transmission in ...

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Vryheid RE, Yu ES, Mehta KM, McGhee J. The decl<strong>in</strong><strong>in</strong>g prevalence <strong>of</strong> <strong>hepatitis</strong> B <strong>virus</strong><strong>in</strong>fection among Asian <strong>and</strong> Pacific Isl<strong>and</strong>er children. Asian Am Pac Isl J Health 2001; 9:162-178.This article provides a review <strong>of</strong> the literature on the decl<strong>in</strong>e <strong>of</strong> <strong>hepatitis</strong> B <strong>virus</strong> (HBV) <strong>in</strong>fection<strong>in</strong> Asian <strong>and</strong> Pacific nations hav<strong>in</strong>g universal <strong>hepatitis</strong> B immunization programs. Papers on theepidemiology <strong>of</strong> HBV <strong>in</strong>fection <strong>and</strong> <strong>hepatitis</strong> B immunization programs <strong>in</strong> Asian <strong>and</strong> Pacificnations were located by search<strong>in</strong>g MEDLINE <strong>and</strong> libraries for publications <strong>in</strong> English, <strong>and</strong> bycontact<strong>in</strong>g <strong>hepatitis</strong> B experts. High endemicity for HBV <strong>in</strong> Asian <strong>and</strong> Pacific nations was partlycaused by a cycle <strong>of</strong> high <strong>in</strong>fectiousness, <strong>per<strong>in</strong>atal</strong> <strong>transmission</strong>, <strong>and</strong> chronic <strong>in</strong>fection from earlyages. Higher prevalence <strong>of</strong> <strong>in</strong>fection has been found <strong>in</strong> men, some families, communities, <strong>and</strong>ethnic groups, <strong>and</strong> <strong>in</strong> people with high risk behaviors <strong>and</strong> situations, such as attend<strong>in</strong>g day care,gett<strong>in</strong>g <strong>in</strong>jections, or shar<strong>in</strong>g personal items. Incidence <strong>of</strong> acquisition <strong>of</strong> <strong>in</strong>fection is about 2%-5%per year. Prevalence <strong>of</strong> HBV <strong>in</strong>fection was decl<strong>in</strong><strong>in</strong>g <strong>in</strong> some nations before commenc<strong>in</strong>g <strong>hepatitis</strong>B immunization programs, probably because <strong>of</strong> improvements <strong>in</strong> medical practices <strong>and</strong> liv<strong>in</strong>gconditions. Twenty-seven <strong>of</strong> 34 Pacific <strong>and</strong> East <strong>and</strong> Southeast Asian nations have atta<strong>in</strong>ed > 70%<strong>hepatitis</strong> B vacc<strong>in</strong>ation coverage <strong>in</strong> <strong>in</strong>fants, <strong>and</strong> twelve have documented reduc<strong>in</strong>g <strong>in</strong>fection orliver cancer to fractions <strong>of</strong> their former rates. But the immunization programs may be caus<strong>in</strong>gnatural selection <strong>of</strong> mutant <strong>hepatitis</strong> B <strong>virus</strong>es, necessitat<strong>in</strong>g study <strong>of</strong> the mutants, <strong>and</strong> modification<strong>of</strong> serological tests <strong>and</strong> vacc<strong>in</strong>es. Practical implications for U.S. health pr<strong>of</strong>essionals are:<strong>in</strong>creas<strong>in</strong>g HBV screen<strong>in</strong>g <strong>and</strong> <strong>hepatitis</strong> B vacc<strong>in</strong>ation <strong>of</strong> adolescents <strong>and</strong> adults from Asian <strong>and</strong>Pacific nations can prevent many <strong>in</strong>fections <strong>and</strong> disease cases; most children com<strong>in</strong>g from highcoverage Asian <strong>and</strong> Pacific nations will be immune <strong>and</strong> few <strong>in</strong>fected; we can learn much fromthese successful programs; <strong>and</strong> we should still make efforts to immunize Asian <strong>and</strong> Pacificchildren <strong>in</strong> the United States, <strong>and</strong> help Asian <strong>and</strong> Pacific nations which do not yet have highlysuccessful <strong>hepatitis</strong> B immunization programs.Wang JS, Chen H, Zhu QR. Transformation <strong>of</strong> <strong>hepatitis</strong> B serologic markers <strong>in</strong> babies born to<strong>hepatitis</strong> B surface antigen positive mothers. World J Gastroenterol 2005; 11:3582-3585.The aim was to better underst<strong>and</strong> the cl<strong>in</strong>ical significance <strong>of</strong> <strong>hepatitis</strong> B serologic markers <strong>in</strong>babies born to <strong>hepatitis</strong> B surface antigen (HBsAg) positive mothers, the <strong>in</strong>cidence <strong>of</strong> maternalserologic markers <strong>of</strong> <strong>hepatitis</strong> B via placenta <strong>and</strong> its transformation <strong>in</strong> these babies were<strong>in</strong>vestigated. Mothers with positive HBsAg were selected <strong>in</strong> the third trimester <strong>of</strong> pregnancy. Theirbabies received immunoprophylaxis with <strong>hepatitis</strong> B immunoglobul<strong>in</strong> <strong>and</strong> <strong>hepatitis</strong> B vacc<strong>in</strong>e afterbirth, <strong>and</strong> were consecutively followed up for <strong>hepatitis</strong> B serologic markers <strong>and</strong> HBV DNA atbirth, mo 1, 4, 7, 12, <strong>and</strong> 24. Forty-two babies entered the study, <strong>in</strong>clud<strong>in</strong>g 16 born to <strong>hepatitis</strong> B eantigen (HBeAg)-positive HBsAg carrier mothers <strong>and</strong> 26 to HBeAg-negative HBsAg carriermothers. Apart from four babies born to HBeAg-positive carrier mothers <strong>and</strong> demonstratedpersistent positive HBeAg eventually became HBV carriers, all other babies developed anti-HBsbefore 12 mo <strong>of</strong> age. Among the other 12 babies born to HBeAg-positive carrier mothers, HBeAgwas detected <strong>in</strong> 7 at birth, <strong>in</strong> 4 at mo 1, <strong>and</strong> <strong>in</strong> none <strong>of</strong> them thereafter. No antibody response to thetransplacental HBeAg was detected. Among the babies born to HBeAg-negative carrier mothers,anti-HBe was detected 100% at birth <strong>and</strong> mo 1, <strong>in</strong> 88.5% at mo 4, <strong>in</strong> 46.2% at mo 7, <strong>in</strong> 4.2% at mo12 <strong>and</strong> none <strong>in</strong> mo 24. Among all the immunoprophylaxis-protected babies born to either HBeAgpositiveor HBeAg-negative carrier mothers, anti-HBc was detected <strong>in</strong> 100% at birth, mo 1 <strong>and</strong> mo4, <strong>in</strong> 78.9% at mo 7, <strong>in</strong> 36.1% at mo 12 <strong>and</strong> <strong>in</strong> none at mo 24. HBeAg can pass through humanplacenta from mother to fetus <strong>and</strong> become undetectable before 4 mo <strong>of</strong> age, but no antibodiesresponse to the transplacental HBeAg can be detected till mo 24 <strong>in</strong> the immunoprophylaxisprotectedbabies. The sole existence <strong>of</strong> anti-HBe before 1 year <strong>of</strong> age or anti-HBc before 2 years <strong>of</strong>age <strong>in</strong> babies born to HBsAg carrier mothers may simply represent the transplacental maternalantibodies, <strong>in</strong>stead <strong>of</strong> <strong>in</strong>dicators <strong>of</strong> HBV <strong>in</strong>fection status.42

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