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Thyroid Hormone Dysfunction During Pregnancy: a Review Int J Reprod BioMed Vol. 14. No. 11. pp: 677-686, November 2016 Review article Thyroid hormone dysfunction during pregnancy: A review 1 2 2 2 Aynadis AlemuP P M.Sc., Betelihem TerefeP P M.Sc., Molla AbebeP P M.Sc., Belete BiadgoP P M.Sc. 1. Amhara Regional Health Abstract Bureau, Dessie Regional Health Research Laboratory, Dessie, Thyroid dysfunctions such as hypothyroidism, thyrotoxicosis and thyroid nodules Ethiopia may develop during pregnancy leading to abortion, placental abruptions, 2. School of Biomedical and preeclampsia, preterm delivery and reduced intellectual function in the offspring. Laboratory Sciences, College of Epidemiological data have shown the significant role of maternal thyroid hormone Medicine and Health Sciences, University of Gondar, Ethiopia. in fetal neurologic development and maternal health. It has been suggested that the deleterious effects of thyroid dysfunction can also extend beyond pregnancy and delivery to affect neuro-intellectual development in the early life of the child. Pregnancy poses an important challenge to the maternal thyroid gland as hormone requirements are increased during gestation as a result of an increase in thyroid- binding globulin, the stimulatory effect of HCG on TSH receptors, and increased peripheral thyroid hormone requirements. Maternal thyroid dysfunction is associated with increased risk for early abortion, preterm delivery, neonatal morbidity and other obstetrical complications. Early diagnosis for thyroid dysfunction of pregnant Corresponding Author: Belete Biadgo, School of women and treatment of thyroid dysfunction during pregnancy is important and cost Biomedical and Laboratory effective to avoid both fetal and maternal complications secondary to thyroid Sciences, College of Medicine and dysfunction. Therefore the aim of this review was to assess the thyroid function Health Sciences, University of changes occurring during pregnancy, the different disorders with their maternal and Gondar, Ethiopia. P.O.Box: 196. Email: [email protected] 61T fetal implications, the laboratory diagnosis and the best ways of management of Tel: (+25) 1918295071 these conditions. Received: 5 June 2016 Accepted: 22 August 2016 Key words: Thyroid hormone, Pregnancy, Gondar, Ethiopia. Introduction thyrotoxicosis can affect the mother health as well as the child before and after delivery that regnancy is a natural physiological can result in fetal disease; in humans, this changes that is accompanied with includes a high incidence of mental hormonic and metabolic alterations retardation (2). The fetal thyroid gland begins P concentrating iodine and synthesizing THs caused by a variety of conditions that results in many pathophysiologic processes, some of after months of gestation. Although the which have potentially serious outcomes if left requirement for TH before this time is untreated. Thyroid diseases during pregnancy exclusively supplied by the mother which is are related to maternal and fetal most important to fetal brain development, complications. Therefore in this article, we try significant fetal brain development continues to review the thyroid function aberrations considerably beyond the first trimester (1, 2). occurring during pregnancy, the different Evident maternal thyroid failure during the first disorders with their maternal and fetal half of pregnancy has been associated with implications, the laboratory diagnosis and the several pregnancy complications including best ways of management of these conditions. preeclampsia, premature labor, fetal death and low birth weight and intellectual Physiological changes of thyroid function impairment in the offspring (3). in mother and fetus during pregnancy THs have most profound effects on the Thyroid hormones (TH) are very important terminal stages of fetal brain differentiation for growth and development of brain for the and development, including synaptogenesis, fetus and neonate, in addition for many other dendrites growth and axons myelination and aspects of pregnancy, fetal growth and neuronal migration. TH receptors are broadly development (1). The thyroid gland dispersed in the fetal brain, and existing prior dysfunctions like hypothyroidism and to the time the fetus is able to synthesize TH. Alemu et al Evidence has confirmed that it is challenging signaling from the TSH receptor on thyroid to identify the molecular targets for TH action epithelial cells. Closure to the end of the first in the developing brain, but some trimester of pregnancy in humans, when HCG improvement has been made (4, 5). levels reaches at peak, a substantial fraction of the thyroid-stimulating activity is from HCG. Mechanisms of physiological changes of During this time, blood levels of TSH become thyroid function in pregnancy suppressed. The thyroid-stimulating activity of Thyroid stimulation starts as early as the HCG actually causes some women to cause first trimester by β-HCG hormone, which transient hyperthyroidism (8, 9). shares some structural homology with thyroid- The potential source of TH for the fetus is stimulating hormone (TSH). There is also an its own thyroid and the thyroid of the mother. estrogen-mediated increase in circulating Human fetuses acquire the ability to levels of thyroid-binding globulin (TBG) during synthesize TH at approximately the first pregnancy by 2-3 times in serum TBG trimester of gestation. Current evidence from concentrations. TBG which is one of the several species indicates that there is numerous protein that transport TH in the significant transfer of maternal THs across the blood with high affinity for thyroxine (T4) placenta and also the placenta contains increases in serum a few weeks after deiodinases that can convert T4 to T3 (10). conception and ranges a plateau during mid- Pregnant mother and infant protection is a gestational period. The mechanism for this priority in the health because these population increase in TBG involves both increased hepatic groups are mostly exposed to the diseases synthesis of TBG and estrogen mediated and death. Thyroid dysfunction is one of the perpetuation in sialylation of TBG that common complications of pregnancy and it increases the half-life from 15 min to 3 days to contributes significantly to the maternal and fully sialylated TBG (6). fetus morbidity and mortality. There is limited Elevated levels of TBG lead to lowered free attention and information related to thyroid T4 concentrations, which results in increased dysfunction and its complication during TSH secretion by the pituitary and, pregnancy. Therefore, the aim of this review subsequently, enhanced production and TH was to assess the magnitude of maternal and secretion. The net effect of elevated TBG fetal thyroid dysfunction and its complication synthesis is to force a new equilibrium in pregnancy secondary to thyroid between free and bound THs and therefore a dysfunction. substantial increase in total T4 and triiodothyronine (T3) levels. The augmented Thyroid hormone abnormalities during demand for THs is reached by about 20 wk of pregnancy gestation and persists until term (6, 7). Reflecting changes in iodine metabolism, Hyperthyroidism which is an essential requirement for TH Hyperthyroidism typically is the disease synthesis, increased demand for iodine results process in which excessive TH is synthesized from a significant pregnancy-associated and excreted, whereas the term thyrotoxicosis increase in iodide clearance by the kidney and refers to increased amounts of TH in the draw off maternal iodide by the fetus. During circulation (11). It can occur in approximately pregnancy there is an increased iodine 1% of the population and up to 0.4% of the excretion in the urine as a result of increased pregnancies (12). Previous study by Wang et glomerular filtration and decreased renal al found that the prevalence of thyroid tubular absorption. In addition, maternal iodine dysfunction was 10.2%, hyperthyroidism, is actively transported to the feto-placental hypothyroidism and hypothyroxinemia were unit, which contributes to a state of relative 1.8, 7.5 and 0.9% respectively (13). iodine deficiency (8, 9). There are 2 causes of hyperthyroidism, like The other factor is the impact of HCG classic causes which is found in the general secreted by the placenta of humans. Thyroid population, and the other causes are specific stimulation in response to the thyrotropic during pregnancy. True hyperthyroidism is activity of HCG overrides the normal action of differentiated from other forms by elevated the hypothalamic pituitary thyroid feedback radioactive iodine uptake (RAIU). The other system. TSH that can bind and transduce forms are differentiated from true 678 International Journal of Reproductive BioMedicine Vol. 14. No. 11. pp: 677-686, November 2016 Thyroid dysfunction hyperthyroidism by decreased RAIU like overstimulation of gland growth. hyperthyroidism caused by factors other than Autoantibodies that react with the orbital thyroid gland over-activity may result from muscle of the eye and fibroblasts of skin are inflammatory thyroid disease, pregnancy- also produced and initiate the extra thyroidal specific associations (like hyperemesis manifestations of GD (22, 23). gravidarum and hydatid form mole) and the Like other autoimmune diseases, the presence of ectopic thyroid tissue or by activity of GD is aggravated during the first exogenous sources of TH (14-17). trimester of gestation and decreased during Tissue effects of hyperthyroidism include the latter half of pregnancy, to be
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