Background: Thyroid autoimmunity is more common in females than in males. One possible explanation for this female preponderance may be the effect of oestrogens on the immune system. It has also been suggested that foetal microchimerism involving transfer of foetal cells into maternal tissue during pregnancy may play an important role. Objective: We investigated the association between the presence of circulating thyroid autoantibodies and previous pregnancy. parity and the use of oral contraceptives (OCs) and hormone replacement therapy (HRT) in a population cohort. Methods: We examined 3 712 women randomly selected from the general population. Serum was analysed for thyroid peroxidase antibody (TPO-Ab) and thyroglobulin antibody (To-Ab) using assays based on an RIA technique (DYNO test). Data were analysed in logistic regression models to adjust for possible confounders. Women previously treated for thyroid disease or with pregnancy within 1 year prior to the study were excluded from the analyses. Results: In both Univariate and multivariate models and whether the presence of TPO-Ab and Tg-Ab was investigated alone or in combination. findings were negative with respect to an association between circulating thyroid antibodies and previous pregnancy, number of pregnancies, parity and previous abortion. There was no association between thyroid autoantibodies and use of OCs. Women aged 60-65 years receiving HRT now or previously had a lower prevalence of Tg-Ab (univariate. P = 0.01; multivariate, P = 0.02). No such association was observed between HRT and TPO-Ab. Conclusion: In this population study there was no association between previous pregnancy, parity and thyroid antibodies, which argues against the role of microchimerism as a trigger of thyroid autoimmunity. Exogenous oestrogens may reduce aspects of autoimmunity.
Pedersen, I. B., Laurberg, P., Knudsen, N., Jørgensen, T., Perrild, H., Ovesen, L., & Rasmussen, L. B. (2006). Lack of association between thyroid autoantibodies and parity in a population study argues against microchimerism as a trigger of thyroid autoimmunity. European Journal of Endocrinology, 154(1), 39-45. https://doi.org/10.1530/eje.1.02070