At postpartum, increased TGF-β1 is related to a less pronounced anti-TPO increase as compared to the 3rd trimester, suggesting an immunosuppressive role for TGF-β1. During pregnancy and postpartum, oestradiol, cortisol, and TGF-β1 are associated with suppression of thyroid autoantibodies.

No abstract

There is inconsistency in the literature regarding the management of women diagnosed with subclinical hypothyroidism (SCH) during pregnancy in the postpartum period. The purpose of our study was to assess the need for continuation of levothyroxine (LT4) treatment after delivery. We conducted a retrospective cohort study of 114 women with new-onset SCH during pregnancy and at 1-year follow-up postpartum. Criteria for continuation of LT4 after delivery were breastfeeding, thyrotropin (TSH) levels at diagnosis >5 mIU/L, positive antithyroid antibodies and LT4 dose before delivery >50 μg/day. On treatment initiation, mean TSH ± SD was 5.24 ± 2.55 mIU/L. One year after delivery, most patients (86/114) were still on LT4. This was related to TSH levels at the initiation of treatment in gestation (p = 0.004) and inversely related to primiparity (p = 0.019). In the group of patients who stopped LT4 postpartum, treatment was reinstated in 11 out of 39 (28.2%) due to SCH relapse (mean TSH ± SD = 9.09 ± 5.81 mIU/L). Most women in our study continued treatment after delivery, and a considerable number of women who had discontinued LT4 restarted treatment postpartum. These results stress the need to reassess thyroid function at 6 to 12 months postpartum.

The effective management of Graves' disease (GD) during pregnancy is crucial for maternal and neonatal well-being. Conventional treatment of GD during pregnancy includes antithyroid drugs (ATDs) and surgery, ideally during the second trimester. We report a 27-year-old woman with GD and we present the course of GD during her three consecutive pregnancies. During the first pregnancy, thyrotoxicosis was successfully treated with low doses of antithyroid drugs; in the second pregnancy, thyrotoxicosis was only controlled at the third trimester; while in the third pregnancy, our patient presented with treatment-resistant thyrotoxicosis, which was finally managed with corticosteroids in adjunction with ATDs. Although hyperthyroid, the patient maintained her fertility. Resistance to ATD is a rare condition and in our case was adequately controlled with corticosteroids.

Betamethasone (BM) administration in pregnancy has been shown to reduce the incidence and severity of neonatal respiratory distress syndrome. Its known diabetogenic impact, combined with placental insulin resistance, leads to a transient increase in glycemia. However, its effect on glucose homeostasis in pregnancy has not been adequately investigated. We closely monitored and assessed the glycemic profile of 83 pregnant women, with normal glucose metabolism, who were given BM during their hospitalization due to threatened premature labor. A significant change in the glycemic profile in most patients was noted, lasting 1.34 ± 1.05 days. Sixty-six of eighty-three women were eventually treated with insulin to maintain glycemia within acceptable limits. The mean ± SD insulin dosage was 12.25 ± 11.28 units/day. The need for insulin therapy was associated with higher BM doses and the presence of marginal values in the 75-g oral glucose tolerance test (OGTT) at 60 min. Our study demonstrates, following BM administration, the need for increased awareness and individualized monitoring/treatment of pregnant women with normal-yet marginal-values in the 75-g OGTT.