Childhood vaccination and type 1 diabetes.
ABSTRACT A link between childhood vaccinations and the development of type 1 diabetes has been proposed.
We evaluated a cohort comprising all children born in Denmark from January 1, 1990, through December 31, 2000, for whom detailed information on vaccinations and type 1 diabetes was available. Using Poisson regression models, we estimated rate ratios according to vaccination status, including the trend associated with the number of doses, among all children and in a subgroup of children who had siblings with type 1 diabetes. Given recent claims of clustering of cases of diabetes two to four years after vaccination, we also estimated rate ratios during the period after vaccination.
Type 1 diabetes was diagnosed in 681 children during 4,720,517 person-years of follow-up. The rate ratio for type 1 diabetes among children who received at least one dose of vaccine, as compared with unvaccinated children, was 0.91 (95 percent confidence interval, 0.74 to 1.12) for Haemophilus influenzae type b vaccine; 1.02 (95 percent confidence interval, 0.75 to 1.37) for diphtheria, tetanus, and inactivated poliovirus vaccine; 0.96 (95 percent confidence interval, 0.71 to 1.30) for diphtheria, tetanus, acellular pertussis, and inactivated poliovirus vaccine; 1.06 (95 percent confidence interval, 0.80 to 1.40) for whole-cell pertussis vaccine; 1.14 (95 percent confidence interval, 0.90 to 1.45) for measles, mumps, and rubella vaccine; and 1.08 (95 percent confidence interval, 0.74 to 1.57) for oral poliovirus vaccine. The development of type 1 diabetes in genetically predisposed children (defined as those who had siblings with type 1 diabetes) was not significantly associated with vaccination. Furthermore, there was no evidence of any clustering of cases two to four years after vaccination with any vaccine.
These results do not support a causal relation between childhood vaccination and type 1 diabetes.
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ABSTRACT: We analysed 2,643 suspected adverse drug reactions (ADRs) in children from birth to 17 years reported for immunization in Denmark over a decade with respect to age and gender, type of vaccines, type and seriousness of ADRs. Eighty percent of ADRs were reported in children below 2 years of age. One half of all reported ADRs were of the type "general disorders and administration site conditions". The largest share of serious ADRs was from the category "nervous system disorders" (33% of serious ADRs). The reported rate of ADRs for children's immunization programmes (MMR® and Ditekipol/Act-Hib®) was 70 per 100,000 vaccine doses and for the serious ADRs, 10 to 25 per 100,000 vaccine doses. More than one half of all suspected ADRs reported for Danish children were related to national immunization programmes and almost one third of these were serious. However, viewed in relation to the large exposure rates and the benefits of avoiding risky child diseases, the numbers are small. Health authorities should put more efforts into enlightening parents about this issue.
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ABSTRACT: Environmental factors are the main contributors to type 1 diabetes (T1D) pathogenesis, yet they remain unidentified. Enteroviruses are proposed candidate triggers due to temporal correlations between infection and T1D autoimmunity and to detection of viral proteins in diseased islets. However, such correlations are not universal and may be relatively uncommon. Furthermore, evidence of a cause–effect relationship is lacking, as infection of non‐obese diabetic mice with Coxsackie enteroviruses can either trigger or blunt disease. The proposed mechanisms are either non‐antigen‐specific (i.e. β‐cell destruction and release of sequestered antigens, islet inflammation) or antigen‐specific (i.e. epitope mimicry, by which immune responses to enteroviruses may be diverted against homologous β‐cell antigens). The case for the latter mechanisms is even less stringent, as there is little evidence of promiscuous antigen recognition at the single T‐cell level. Other infectious agents may thus be implicated. Demonstration of their role will require fulfilling the Koch's postulates, namely isolation of the agent preferentially in T1D patients, including before disease onset; and T1D induction when the agent is inoculated into mice. The same is needed for cross‐reactive T cells to support epitope mimicry mechanisms. Generation of alternative (humanized) mouse models that could be challenged with candidate microbes is needed.Diabetes Obesity and Metabolism 09/2013; 15. · 5.46 Impact Factor
- Revista medica de Chile 05/2013; 141(5):595-601. · 0.37 Impact Factor