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Updated: Jun 8, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
Published on: March 17, 2023
Parity is not related to autoimmune thyroid disease in a population-based study of Japanese-Brazilians
José A Sgarbi1, Teresa S Kasamatsu, Luiza K Matsumura
1Laboratory of Molecular Endocrinology, Division of Endocrinology, Department of Medicine, Escola Paulista de Medicina, Federal University of São Paulo, Rua Pedro de Toledo 669, São Paulo, Brazil.
Background:
It has been suggested that the female preponderance for autoimmune thyroid disease might be associated with hormonal differences, abortion, and fetal microchimerism. Findings emerging from the few epidemiological studies on this matter, however, are controversial. In this study, we investigated the hypothesis whether parity, abortion, and the use of estrogens are associated with a higher risk for thyroid autoimmunity.
Methods:
This cross-sectional population-based study examined 675 women from a Japanese-Brazilian population aged above 30 years. Thyroid peroxidase antibodies (TPOAbs), thyroglobulin antibodies (TgAbs), thyrotropin, and free T₄ were measured by immunofluorimetric assays. Urinary iodine concentration was measured using a colorimetric method. Data were analyzed in logistical regression models to obtain the odds ratio (OR) and 95% confidence intervals.
Results:
TPOAbs and TgAbs were present in 11.6% and 13.6% of women, respectively. After adjustment for age, smoking, and urinary iodine concentration, the OR for positive TPOAb (OR, 1.22 [95% confidence interval, 0.73–2.02]) and for positive TgAb (OR, 1.01 [0.63–1.62]) among women who had one or more parities did not differ from those who had never given birth. In addition, we found no association between the presence of thyroid antibodies and previous abortions or the use of estrogens.
Conclusions:
Parity, abortion, and the use of estrogens are not associated with thyroid autoimmunity in this population. These findings reinforce previous reports that advocated against a key role of fetal microchimerism in the pathogenesis of autoimmune thyroid disease.
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