Endocrine Abstracts

Objective: Clarify mechanisms determining thyroid homeostasis during pregnancy at hypothalamic-pituitary level.

Methods: Retrospective analysis of 251 pregnant women. 220/251 euthyroid without thyroxine therapy (Group 1), 31/251 thyroidectomized under thyroxine replacement therapy (Group 2). Patients under thyroxine replacement therapy with a TSH between 0.4 and 4.0 were included in the study. Patients with combined T3/T4 therapy were excluded.

Results: The median TSH, FT3, FT4 and FT3/FT4 in Group 1 vs Group 2 were: TSH 1.6 (0.9,2.3) vs 0.5 (0.3,1.7) P = <0.01, FT3 4.5 (4.0-4.8) vs (3.9-4.7) P = 0.23, FT4 14.2 (12.1-15.5) vs 16.5 (14.8-20.1) P = <0.001, FT3/FT4 0.3 (0.3-0.4) vs 0.2 (0.2-0.3) P = <0.001. We examined the correlation between FT3/TSH and FT4/TSH in the two groups. Group 1 FT4/TSH correlation: before pregnancy >r=-0.09 P = 0.38, first trimester r=0.08 P = 0.55, second trimester r=0.10 P = 0.34, third trimester r=-0.38 P = 0.02, after pregnancy r=0.04 P = 0.71. Group 1 FT3/TSH correlation: before pregnancy r=-0.01 P = 0.90, first trimester r=-0.11 P = 0.39, second trimester r=0.16 P = 0.12, third trimester r=-0.12 P = 0.49, after pregnancy r=-0.05 P = 0.65. Group 2 FT4/TSH correlation: before pregnancy r=-0.54 P = 0.008, first trimester r=-0.41 P = 0.14, second trimester r=-0.50 P = 0.009, third trimester r=-0.40 P = 0.09, after pregnancy r=-0.12 P = 0.71. Group 2 FT3/TSH correlation: Before pregnancy r=-0.21 P = 0.34, first trimester r=-0.16 P = 0.57, second trimester r=-0.39 P = 0.04, third trimester r=0.18 P = 0.45, after pregnancy r=-0.13 P = 0.70. Discussion. Taken together these results indicate that in euthyroid pregnant women T4 is less effective in suppressing TSH in the first trimester, this phenomenon is extended to T3 in the second trimester, while TSH suppression by T4 and T3 is recovered in the third trimester. In contrast, in thyroidectomized women T4 suppression of TSH is lower but was maintained in all trimesters, as well as T3 suppression that is lost only in the second trimester. These data suggest that during pregnancy the increased secretion of thyroid hormones is due not only to an increased thyroid stimulation by hCG, but also to reduced negative feedback of thyroid hormones at hypothalamus/pituitary level. The reduced variation in TSH suppression in thyroidectomized pregnant women suggest that this phenomenon may be determined by a change in deiodinase activity in euthyroid pregnant women. Since this mechanism is inhibited by T4 replacement therapy, it is reasonable to suppose that is based upon the modulation of Type 2 Deiodinase activity.