Thyroid hormones are crucial for a normal pregnancy and intrauterine fetal development, particularly development of the central nervous system. In the pregnant women there is an increase in thyroxine and triiodothyronine production in response to the estrogen-stimulated rise in the thyroid hormone transport protein, thyroxine-binding globulin. Also, in the first trimester, there is a transient inhibition of thyrotropin, which is mediated, via the negative feedback system, by an increase in thyroid hormones that are stimulated by hCG. Moreover, a large plasma volume, and thus altered distribution of thyroid hormones, increased thyroid hormone metabolism, together with increased renal clearance of iodide are responsible for higher thyroid hormone requirements in pregnancy. The fetus thyroid gland starts functioning after the first trimester. The most important maternal thyroid hormone for the fetus is thyroxine, because it crosses the placental barrier and achieves the fetus. The consequent fetal consumption of maternal thyroid hormone is an additional stimulus to increase maternal thyroid hormone secretion to ensure adequate fetal thyroid hormone availability. Such a new physiological demand requires an adequate iodine intake by pregnant women. The diagnosis of thyroid disease in pregnancy is still based upon serum TSH concentration. Due to the physiological changes occurring during pregnancy, including the increase in hCG and thyroxine-binding globulin levels, TSH normal levels are lower in pregnancy than in nonpregnant women. If internal pregnancy-specific TSH reference ranges are not available, a simple clinical way for TSH reference interval in the first trimester of pregnancy could be calculated as the reference interval for the nonpregnant population decreased by 0.5 mU/L in the upper limit (for most centers ~4 mU/L). In patients with primary hypothyroidism taking levothyroxine, lowering TSH to <2.5 mU/L has been recommended not only to pregnant women but also for women planning to become pregnant.
Thyroid Function in Pregnancy / Delitala, A.; Maioli, M.; Dessole, F.; Petrillo, M.; Capobianco, G.. - (2022), pp. 1-16. [10.1007/978-3-030-98777-0_1]
Thyroid Function in Pregnancy
Delitala A.
Writing – Original Draft Preparation
;Maioli M.Data Curation
;Dessole F.Formal Analysis
;Petrillo M.Writing – Review & Editing
;Capobianco G.Writing – Review & Editing
2022-01-01
Abstract
Thyroid hormones are crucial for a normal pregnancy and intrauterine fetal development, particularly development of the central nervous system. In the pregnant women there is an increase in thyroxine and triiodothyronine production in response to the estrogen-stimulated rise in the thyroid hormone transport protein, thyroxine-binding globulin. Also, in the first trimester, there is a transient inhibition of thyrotropin, which is mediated, via the negative feedback system, by an increase in thyroid hormones that are stimulated by hCG. Moreover, a large plasma volume, and thus altered distribution of thyroid hormones, increased thyroid hormone metabolism, together with increased renal clearance of iodide are responsible for higher thyroid hormone requirements in pregnancy. The fetus thyroid gland starts functioning after the first trimester. The most important maternal thyroid hormone for the fetus is thyroxine, because it crosses the placental barrier and achieves the fetus. The consequent fetal consumption of maternal thyroid hormone is an additional stimulus to increase maternal thyroid hormone secretion to ensure adequate fetal thyroid hormone availability. Such a new physiological demand requires an adequate iodine intake by pregnant women. The diagnosis of thyroid disease in pregnancy is still based upon serum TSH concentration. Due to the physiological changes occurring during pregnancy, including the increase in hCG and thyroxine-binding globulin levels, TSH normal levels are lower in pregnancy than in nonpregnant women. If internal pregnancy-specific TSH reference ranges are not available, a simple clinical way for TSH reference interval in the first trimester of pregnancy could be calculated as the reference interval for the nonpregnant population decreased by 0.5 mU/L in the upper limit (for most centers ~4 mU/L). In patients with primary hypothyroidism taking levothyroxine, lowering TSH to <2.5 mU/L has been recommended not only to pregnant women but also for women planning to become pregnant.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
