Long-term efficacy of plasma-derived hepatitis B vaccine: a 15-year follow-up study among Chinese children

Liao, Susu; Li, Rongcheng; Li, Hui; Yang, Jin-Ye; Zeng, Xinyi; Gong, Jian; Wang, Shusheng; Li, Yanping; Zhang, Kong‐Lai

doi:10.1016/s0264-410x(99)00031-6

Cited by 110 publications

(52 citation statements)

References 7 publications

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“…1 To control HBV infection, universal neonatal immunisation with the hepatitis B vaccine was introduced more than 3 decades ago, and its efficacy has been reported in many studies that have shown not only a reduction in the prevalence of childhood HBV infection, but also the presence of an anamnestic response that could maintain immunoprotection for many years. [2][3][4][5][6][7][8][9][10][11][12][13][14] Indeed, in Taiwan, following introduction of the vaccine, the incidence of hepatocellular carcinoma (HCC) in children was reduced from 0.54 to 0.20 per 100,000 children aged 6-14 years in those born before versus after the vaccination program. 15 In Hong Kong, selective active-passive hepatitis B immunization was first administered to neonates born to mothers screened positive for hepatitis B surface antigen (HBsAg) from late 1983 to 1988, 16 followed by universal neonatal HBV vaccination from November 1988, 17 and the vaccine has become widely available since.…”

Section: Introductionmentioning

confidence: 99%

Immune persistence after hepatitis B vaccination in infancy – Fact or fancy?

Lao

2016

Human Vaccines & Immunotherapeutics

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The hepatitis B vaccine has been introduced for more than 3 decades. In Hong Kong, excellent vaccine coverage through an efficient public health care system, together with supplemental programmes and easy availability of the vaccine, meant that most young pregnant women, and university students at entrance, should have been protected. Yet significant correlations in the prevalence of HBV infection with age were found in these groups of subjects, increasing from low to high endemicity rates from late teenage to the early twenties. This can only be attributed to vaccine failure, and there is cumulating evidence that several factors are involved, including the failure to respond to a primary series of hepatitis B vaccination in infancy, the waning of antibody titer with age, and loss of anamnestic response in a significant portion of the vaccinees. The duration of protection conferred by hepatitis B vaccination in infancy should be re-examined and remedial measures undertaken if its long term protection is found to be insufficient. Otherwise, the efforts to control HBV infection, especially in high endemicity regions, with universal vaccination in infancy would be rendered futile.

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Section: Introductionmentioning

confidence: 99%

Immune persistence after hepatitis B vaccination in infancy – Fact or fancy?

Lao

2016

Human Vaccines & Immunotherapeutics

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“…Serologic studies have shown that the titre of antibodies against hepatitis B surface antigen drops within the first few years after vaccination and that one-third to one-half of children vaccinated as infants will have titres below 10 IU/L by 10-15 years of age. [10][11][12] This has been misinterpreted to mean that population-level protection shows a similar dramatic drop.Long-term observational data show that vaccinated individuals -even those who have an undetectable titre of hepatitis B surface antigen -can mount an anamnestic response to contact with HBV.11,13 A recent booster trial performed 18 years after vaccination of infants in Gambia provides further evidence of persistent immunity.14 Although almost 70% of participants had no detectable antibodies at baseline, of the 181 participants who were tested 2 weeks after receiving a booster dose, 92.3% (95% CI 87.4-95.7) showed an early anamnestic response.14 The geometric mean concentration of antibodies against hepatitis B surface antigen in this group rose to 524 IU/L (95% CI 441-621), which suggests that most people who have been vaccinated can mount a protective immune response even 18 years after receiving a primary series of vaccinations in infancy. …”

mentioning

confidence: 99%

Hepatitis B immunization strategies: timing is everything

Mackie¹,

Buxton²,

Tadwalkar³

et al. 2009

Canadian Medical Association Journal

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Chronic HBV infection, with the attendant risk of cirrhosis and hepatocellular carcinoma, occurs in 1%-5% of adults and up to 90% of infants who are infected with HBV.3-5 Providing vaccinations during adolescence without offering vaccinations during infancy misses this critical period when the acquisition of a HBV infection can be the most harmful. Epidemiologic studies show that the age distribution of HBV varies by jurisdiction and suggest that roughly one-third of chronic infections are acquired during infancy and early childhood.6-9 An ideal vaccine schedule should protect against infection both in infancy, when the risk of becoming a chronic HBV carrier is highest, and in adolescence, when high-risk sexual and drugusing behaviours occur more frequently.Epidemiologic data are critical for informing decisions about vaccination. Estimating the age-specific incidence of acute infections is valuable for planning prevention measures. However, acute infections in infants and toddlers may be missed because HBV infection is often asymptomatic in young children. In many jurisdictions, the age-specific incidence of HBV infection is unknown.The controversy surrounding booster injections stems in part from the rapid drop in antibodies after completion of the primary series of injections. Serum levels of antibodies against hepatitis B surface antigen have been used to measure the initial response to vaccination (antibody levels ≥ 10 IU/L are considered protective). This marker measures response to the vaccine within the first few weeks but is not an appropriate indicator of long-term immunity. Serologic studies have shown that the titre of antibodies against hepatitis B surface antigen drops within the first few years after vaccination and that one-third to one-half of children vaccinated as infants will have titres below 10 IU/L by 10-15 years of age. [10][11][12] This has been misinterpreted to mean that population-level protection shows a similar dramatic drop.Long-term observational data show that vaccinated individuals -even those who have an undetectable titre of hepatitis B surface antigen -can mount an anamnestic response to contact with HBV.11,13 A recent booster trial performed 18 years after vaccination of infants in Gambia provides further evidence of persistent immunity.14 Although almost 70% of participants had no detectable antibodies at baseline, of the 181 participants who were tested 2 weeks after receiving a booster dose, 92.3% (95% CI 87.4-95.7) showed an early anamnestic response.14 The geometric mean concentration of antibodies against hepatitis B surface antigen in this group rose to 524 IU/L (95% CI 441-621), which suggests that most people who have been vaccinated can mount a protective immune response even 18 years after receiving a primary series of vaccinations in infancy. Universal vaccination of infantsAs of 2007, 171 of the 193 member countries of the World Health Organization (WHO) had implemented the recommendations of the Expanded Programme on Immunization to offer universal hepatitis B ...

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“…Studies meeting the following inclusion criteria were included: Application of the inclusion criteria led to the identification of one RCT [37] and nine observational studies ( [38,39,40,41,42,43,44,45,46], see . Fig.…”

Section: Group Of Persons Study Study Setting Resultsmentioning

confidence: 99%

“…The only RCT meeting all inclusion criteria [37] was performed in China, using a plasma-derived vaccine and including 649 participants (vaccine group: 308, placebo group: 341; age at vaccination: 14 months). Successful vaccination was defined as anti-HBs ≥10 IU/l after primary vaccination.…”

Section: Randomized Controlled Trialsmentioning

confidence: 99%