Endocrine Abstracts

Introduction: Thyroid autoimmunity (TAI) commonly defined as the presence of thyroperoxidase antibodies (TPOAbs) and/or thyroglobulin antibodies (TgAbs) affects up to 15 percent of women of reproductive age and is a well-known risk factor of pregnancy loss. One of the possible explanations of obstetrical complications might be the disturbed process of placentation caused by thyroid antibodies. To test this hypothesis, we evaluated placental hormonal function and placental angiogenic factors in women with TAI.

Materials and methods: 91 hypothyroid pregnant women and 39 healthy pregnant controls were enrolled to the study. Patients were divided into two groups: positive for TPOAbs/TgAbs (n=58) and negative for TPOAbs/TgAbs (n=33). All hypothyroid women were diagnosed before pregnancy or at the 1st trimester of pregnancy and treated with L-thyroxine to maintain TSH<2.5 mIU/l. Maternal thyroid function tests (TSH,fT4,fT3) were established every month throughout pregnancy and angiogenic placental factors: proangiogenic placental growth factor (PlGF), and 2 antiangiogenic factors: soluble vascular endothelial growth factor receptor 1 (sFlt-1), soluble endoglin (sEng) as well as placental hormones: estradiol, progesterone, and human chorionic gonadotropin were determined at each trimester.

Results: Obstetrical and neonatal outcomes did not differ between the groups. TAI negatively impacted placental hormone secretion. Group 1 characterized by lower estradiol concentration compared to group 2 in the 1st trimester: 1682.00 vs 2440.00 pg/mL, P=0.016 and lower progesterone concentration compared to controls in the 2nd trimester: 37.00 vs 50.25 ng/mL, P=0.003. Thyroid autoimmunity was connected with unfavorable placental angiogenic factors profile. Antiangiogenic sEng was higher in group 1 than in group 2 in all three trimesters (1st trimester: 6.79±2.18 vs 5.73±1.41, P=0.026, 2nd trimester: 5.81±1.76 vs 4.68±0.75, P=0.022, 3rd trimester: 7.80 vs 5.60 ng/mL, P=0.003). In group 1 positive correlation between TPOAbs and sFlt-1 in the 3rd trimester: rho=0.31, P=0.040, and negative correlation between TgAbs and estradiol in the 3rd trimester, and between TgAbs and PIGF in 1st trimester was found (rho=-0.29, P=0.043, and rho=-0.27, P=0.037, respectively).

Conclusion: Our preliminary results suggest that thyroid autoimmunity can negatively influence placental development and function, but further research is needed.