Autoimmune thyroiditis (AIT) is the most common autoimmune disease impacting up to 20% of women of reproductive age [1, 2]. The disease is characterised by the presence of thyroid antibodies (TAs), and lymphocytic infiltration of the thyroid gland [1]. TAs in pregnancy increase risk of miscarriage, recurrent pregnancy loss, pre-term birth and gestational diabetes mellitus (GDM) in the absence of changes to thyroid hormones . Therefore, we aimed to explore how AIT impacts risk of maternal and fetal complications in pregnancy.
Thyroglobulin antibody positivity (TgAb+) was induced before pregnancy in Lewis rats by immunisation with porcine thyroglobulin in Freund’s adjuvant and exposure to sodium iodide in drinking water. We then explored how TgAb+ affects estrous cycling prior to pregnancy, maternal glucose tolerance on embryonic day 16 (E16), maternal thyroid parameters, placental development, and fetal survival.
Maternal TgAb+ increased maternal plasma T4 concentration by E20. However, given there was no change to thyroid stimulating hormone (TSH) concentration and no overt thyroid pathology, this may indicate reduced peripheral T4 utilisation. TgAb+ increased maternal estrous cycle length and reduced survival rate of male fetuses but did not affect pregnancy success rate or litter size. Maternal glucose tolerance on E16 was unaffected by TgAb+, however maternal random blood glucose prior to pregnancy and on E20 was increased, suggesting that TgAb+ does not increase risk of GDM in the absence of changes to TSH or presence of other pathogenic TAs. Placentas were significantly larger which was associated with increased junctional zone glycogen accumulation and altered labyrinth zone (LZ) expression of genes that regulate angiogenesis and syncytialisation. Genes important for achievement of term gestation were also reduced in the LZ.
Maternal TgAb+ should be monitored in pregnancy as it may increase risk of maternal and fetal complications in the absence of overt thyroid pathology.