Risk of type 1 diabetes in childhood and maternal age at delivery, interaction with ACPI and sex

Bottini, Nunzio; Meloni, T; Lucarelli, P.; Amante, A.; Saccucci, Patrizia; Gloria‐Bottini, F.; Bottini, E.

doi:10.1002/dmrr.521

Cited by 14 publications

(14 citation statements)

References 36 publications

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“…The remaining 32 articles (9–15,19–43) contained information from 37 independent studies, as information from five centers was taken from one article (14) and information from two centers was taken from another (15). An investigator from each of the 37 studies was invited to provide raw data (or estimates from prespecified analyses), but one author (20) could not be contacted.…”

Section: Resultsmentioning

confidence: 99%

“…In one study (19), the odds ratio per 5-year increase in maternal age was extrapolated from the odds ratio per 1-year increase, combined between males and females, and was available only after adjustment for number of abortions and gestational age. In another (20), the odds ratio per 5-year increase was estimated from the following maternal age categories (15–21, 22–31, 32–41, 42–49, 50–55 years).…”

Section: Methodsmentioning

confidence: 99%

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Maternal Age at Birth and Childhood Type 1 Diabetes: A Pooled Analysis of 30 Observational Studies

et al. 2009

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OBJECTIVEThe aim if the study was to investigate whether children born to older mothers have an increased risk of type 1 diabetes by performing a pooled analysis of previous studies using individual patient data to adjust for recognized confounders.RESEARCH DESIGN AND METHODSRelevant studies published before June 2009 were identified from MEDLINE, Web of Science, and EMBASE. Authors of studies were contacted and asked to provide individual patient data or conduct prespecified analyses. Risk estimates of type 1 diabetes by maternal age were calculated for each study, before and after adjustment for potential confounders. Meta-analysis techniques were used to derive combined odds ratios and to investigate heterogeneity among studies.RESULTSData were available for 5 cohort and 25 case-control studies, including 14,724 cases of type 1 diabetes. Overall, there was, on average, a 5% (95% CI 2–9) increase in childhood type 1 diabetes odds per 5-year increase in maternal age (P = 0.006), but there was heterogeneity among studies (heterogeneity I2 = 70%). In studies with a low risk of bias, there was a more marked increase in diabetes odds of 10% per 5-year increase in maternal age. Adjustments for potential confounders little altered these estimates.CONCLUSIONSThere was evidence of a weak but significant linear increase in the risk of childhood type 1 diabetes across the range of maternal ages, but the magnitude of association varied between studies. A very small percentage of the increase in the incidence of childhood type 1 diabetes in recent years could be explained by increases in maternal age.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Maternal Age at Birth and Childhood Type 1 Diabetes: A Pooled Analysis of 30 Observational Studies

et al. 2009

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“…It is unclear whether an "immunologic" stress (for example a rubella infection or a maternal immune reaction against "foreign" fetal antigen) is necessary, or whether general stress (for example amniocentesis, complicated delivery) is the causative factor [149,157]. Protective factors appear to include being a firstborn child, having a low birth weight, or having a short birth length [158][159][160][161][162]. However, increased maternal age was associated with a longer duration of breast feeding.…”

Section: Perinatal Factors and Postnatal Growthmentioning

confidence: 97%

Environmental factors in the development of Type 1 diabetes

Peng

Hagopian

2007

Rev Endocr Metab Disord

113

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Environmental factors appear to play an important role in the pathogenesis of childhood-onset type 1 diabetes (T1D). The most important factors are thought to be infectious, dietary, perinatal, and psychosocial. Enteroviruses (especially Coxsackie B virus), breastfeeding, the early presence or lack of certain foods, birth weight, childhood over-nutrition, maternal islet autoimmunity, and negative stress events have been shown to be related to the prevalence of T1D. However, clear conclusions to date are limited because most studies lacked power to detect exposure/disease associations, were not prospective or long-term, did not start in infancy, had imprecise or infrequent exposure estimates, had confounding exposures, and failed to account for genetic susceptibility. In addition to the identification of specific antigenic triggers, several more general hypotheses, including the accelerator and hygiene hypotheses, are testable approaches worth pursuing.

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“…We have reported an association of ACP1 with immunological diseases like type 1 diabetes mellitus (TIDM), Crohn’s disease (CD) and allergy [16,17,18,19,20,21] and some data suggest an opposite pattern of association between Th1 and Th2 classes of immunological disease [22] and between sexes [16, 18]. …”

Section: Introductionmentioning

confidence: 99%

ACP1 and Th Class of Immunological Disease: Evidence of Interaction with Gender

Gloria‐Bottini

Bottini

Renzetti

et al. 2007

Int Arch Allergy Immunol

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Background: Data collected by our group in the past years indicate a relationship between ACP1 genetic polymorphism and susceptibility/resistance to immunological diseases. Recent observations suggest that through modulation of ZAP-70 activity, the enzyme may influence T cell activation. In view of the current interest in gender differences in autoimmune diseases we reviewed our data to enlighten possible effects of gender on the relationship between ACP1 and class of immunological disease. Methods: We studied three samples of subjects with allergic disorders of a total of 299 subjects, 71 subjects with Crohn’s disease and 188 children with type 1 diabetes. Three-way contingency tables were analyzed by a log linear model and two-way contingency tables by χ² test. Results: There is an association between ACP1 and allergy (Th2 class) that depends on gender: the presence of the ACP1*A allele seems to make females more susceptible to allergic manifestations as compared to males. ACP1 is also associated with Crohn’s disease and type 1 diabetes: the relationship between this class (Th1) of immunological diseases and ACP1 depends on gender. The presence of *A allele seems to make females less susceptible to this class of diseases as compared to males. Conclusions: The ACP1*A allele which is associated with low ACP1 activity appears responsible for a complex relationship involving gender, ACP1 and Th1/Th2 orientation. Low ACP1 activity influencing ZAP-70 activity and in turn T cell activation seems to have opposite effects on Th1/Th2 orientation depending on gender.

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Risk of type 1 diabetes in childhood and maternal age at delivery, interaction with ACPI and sex

Cited by 14 publications

References 36 publications

Maternal Age at Birth and Childhood Type 1 Diabetes: A Pooled Analysis of 30 Observational Studies

Maternal Age at Birth and Childhood Type 1 Diabetes: A Pooled Analysis of 30 Observational Studies

Environmental factors in the development of Type 1 diabetes

ACP1 and Th Class of Immunological Disease: Evidence of Interaction with Gender

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