Hepatitis B immunity in children vaccinated with recombinant hepatitis B vaccine beginning at birth: a follow-up study at 15 years.

BACKGROUND: The duration of protection after hepatitis B vaccination of infants is unknown. We determined antibody to hepatitis B surface antigen (anti-HBs) and response to a booster dose 15 years after vaccination among Alaskan children born to hepatitis B surface antigen-negative mothers. These children had protective anti-HBs concentrations when tested after receiving a three-dose series of 2.5 microg recombinant hepatitis B vaccine starting at birth. METHODS: Participants received 5 microg of recombinant hepatitis B vaccine. Sera were collected at baseline, 10-14 days and 1 month after vaccination, and tested for antibody to hepatitis B core antigen (anti-HBc) and anti-HBs. An anamnestic response was defined as an anti-HBs increase within 15 days, from either undetectable to >/=10 mIU/mL, or, if the baseline concentration was detectable, a 4-fold increase. RESULTS: None of 37 participants (mean age 14.6 years) were anti-HBc positive. An anamnestic response (GMC=254 mIU/mL, range 16-2767 mIU/mL) was observed in 18 (51%) of 35 participants who had sera collected within 15 days after the booster. CONCLUSIONS: In this small study, half of children who had received hepatitis B vaccine starting at birth did not have evidence of immune memory as measured by development of anamnestic responses to booster vaccination. Additional studies are needed to assess whether this indicates susceptibility to infection and whether persons vaccinated starting at birth may benefit from a hepatitis B vaccine booster to maintain long-term protection.

Asymptomatic Helicobacter pylori infection and iron deficiency are not associated with decreased growth among Alaska Native children aged 7-11 years.

INTRODUCTION: Alaska Native children have high Helicobacter pylori infection and iron deficiency prevalences, and their average height-for-age is lower than US reference populations. During a clinical trial to determine the impact of H. pylori treatment on iron deficiency, we evaluated the effects of H. pylori infection and treatment on growth. MATERIALS AND METHODS: We measured height and weight for children aged 7-11 years in western Alaska using village-based measuring devices. H. pylori infection was determined by urea breath test and iron deficiency using serum ferritin. Children with H. pylori infection and iron deficiency entered the treatment phase and received iron alone or iron plus triple therapy for H. pylori. Follow-up evaluations occurred at 2, 8, and 14 months. We evaluated the association between baseline H. pylori infection and growth; among children in the treatment phase, we also assessed the effect of H. pylori resolution on growth. RESULTS: At baseline, 566 (87.1%) of 650 children were infected with H. pylori. Neither height and weight, nor body mass index differed by H. pylori infection status. Of 189 children in the treatment phase, 20 (10.6%) were uninfected at all three follow-up periods, and 54 (28.6%) were uninfected for one or two periods. Compared with continuously infected children, children in these two groups had little evidence of improvements in any of the measured growth outcomes. CONCLUSIONS: H. pylori infection is not related to growth among Alaska Native children aged 7-11 years. Growth deficiency should not be considered an indication for H. pylori therapy.

A controlled, household-randomized, open-label trial of the effect that treatment of Helicobacter pylori infection has on iron deficiency in children in rural Alaska.

BACKGROUND: Helicobacter pylori infection and iron deficiency are prevalent in disadvantaged populations worldwide. Previous small or uncontrolled studies have reported that successful treatment of H. pylori infection may resolve iron deficiency or anemia. METHODS: We screened 68% of children 7-11 years old living in 10 western Alaska villages. The 219 children with iron deficiency (serum ferritin level, <22.5 pmol/L [<10 microg/L]) and H. pylori infection (diagnosed on the basis of (13)C-labeled urea breath tests) were enrolled in a household-randomized, unblinded trial. All children received iron supplementation for 6 weeks; children in the intervention group also received a 2-week course of treatment for H. pylori infection plus another 2-week course of treatment if the infection had not resolved at 2 months after treatment initiation. RESULTS: At 2 months after treatment initiation, 32% of children in the intervention group and 39% of children in the control group had iron deficiency. At 14 months after treatment initiation, 65% of children in the intervention group and 72% of children in the control group had iron deficiency (adjusted relative risk [ARR], 0.90 [95% confidence interval [CI], 0.74-1.1]); in addition, 22% of children in the intervention group and 14% of children in the control group had anemia (ARR, 1.6 [95% CI, 0.86-2.9]). Results were similar when children were compared by H. pylori infection status. CONCLUSIONS: In a high-prevalence population, treatment and resolution of H. pylori infection did not improve isolated iron deficiency or mild anemia up to 14 months after treatment initiation.

A randomized trial of triple therapy for pediatric Helicobacter pylori infection and risk factors for treatment failure in a population with a high prevalence of infection.

BACKGROUND: Few trials of treatment for Helicobacter pylori infection have been conducted in high-prevalence or pediatric populations, and risk factors for treatment failure are poorly understood. METHODS: As part of a study evaluating the effect of H. pylori therapy on iron deficiency, we conducted a household-randomized, open-label treatment trial involving children aged 7-11 years in 10 villages in western Alaska. We screened 690 children, of whom 219 with iron deficiency and H. pylori infection (determined on the basis of positive results of the 13C urea breath test) were enrolled in the treatment phase of the study. These 219 children received treatment with iron sulfate alone (the control group) or with iron sulfate combined with a 2-week course of lansoprazole, clarithromycin, and amoxicillin (the intervention group). Children in the intervention group who were allergic to amoxicillin or macrolides received metronidazole. Children in the intervention group who did not respond to treatment were re-treated with a 2-week course of metronidazole-based quadruple therapy. RESULTS: Two months after initiating therapy, 34% of 104 children in the intervention group and 0.90% of 111 children in the control group tested negative for H. pylori. Among children in the intervention group, risk factors for treatment failure were lack of metronidazole (adjusted odds ratio [aOR], 145), fewer treatment doses (aOR, 0.74), larger household population (aOR, 1.5), and lower body mass index (aOR, 0.69). These 4 variables predicted most of the variation in H. pylori infection status. Among 50 children who were re-treated, 84% tested negative for H. pylori at the 8-month follow-up visit, including those with poor treatment compliance. CONCLUSIONS: Among disadvantaged populations with a high prevalence of H. pylori infection, the response to standard treatment regimens may be low. Treatment compliance, household crowding, and re-treatment may influence treatment success. Metronidazole may be appropriate first-line therapy.