ESPE Abstracts (2015) 84 P-1-101

Does Type 1 Childhood Diabetes Start In Utero?

Zvi Larona,b,c, Christiane Hampea,b,c & Lester Shulmana,b,c

aSchneider Children’s Medical Center, Petah Tikva, Israel; bSackler Faculty of Medicine, Tel-Aviv University, Tel Aviv, Israel, cUniversity of Washington, Seattle, Washington, USA

Background: In the last decades a rapid increase in the incidence of childhood type I diabetes (TIDM) has been reported worldwide. To stop the progressively advancing process immunosuppressive and nutritional trials have been made, but failed. Epidemiological studies by our group performed in several countries have shown that the season during which children who developed TIDM were born differed from that in the general population; suggesting that the initial trigger for TIDM was more likely to occur during the yearly viral epidemics.

Objective and hypotheses: To test the above hypothesis we collected maternal and cord blood sera from 107 healthy pregnant women (mean age 30.7 years) in winter during a viral season.

Method: We tested for GAD 65 autoantibodies, and anti-rota and cox B3 antibodies.

Results: GAD 65 Ab and rotavirus Ab present in both maternal and cord blood correlated with an odd ratio of 6.89 (95% CI: 1–46.7). For five, 22 and 17 pregnancies antibodies to GAD 65, rotavirus and CoxB3, respectively, were detected in cord blood only and not in the maternal serum. In ten pregnancies, rotavirus antibody titres in the cord blood exceeded those in the corresponding maternal serum by 2.5–5-fold.

Conclusion: The concurrent presence of GAD 65 antibodies in cord blood and their mothers may indicate autoimmune damage to islet cells during gestation, caused by cross-placental transmission of viral infections, or antibodies. If the continuing study will confirm our findings pregestational antiviral vaccination will cause prevention or at least reduction in the incidence of childhood TIDM.

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