Problem Statement. Thyroid gland in women undergoes functional changes during pregnancy. A few studies have described such changes in pregnant women residing in iodine deficient areas. Objective. To document these changes in pregnant women residing in Lahore, a low iodine intake urban area of Pakistan. Patients and Methods. In 254 pregnant women, data of FT4, FT3, and TSH during the first and subsequent trimesters were obtained and compared with those of 110 nonpregnant women. These hormones were determined in serum by radioimmunoassay (RIA) techniques using commercial kits. Results. Compared to nonpregnant women mean FT4 level was decreased, and FT3 and TSH increased significantly ( ) in pregnant women. A negative correlation of FT4 with TSH was observed in all three trimesters. Serum FT3 was positively correlated with TSH only during the third trimester. As a function of gestation time, FT4 levels progressively decreased, and FT3 and TSH levels increased significantly (one-way ANOVA = 108.2, 17.3, and 44.8, resp.; all ) exhibiting thyroid gland adaptations. Conclusion. Pregnancy is associated with significant alterations in thyroid function due to low iodine intake in women residing in study area. The compensated thyroid function poses a risk of thyroid failure in a number of pregnant women. 1. Introduction Over the past twenty years, there has been a major expansion of our knowledge regarding the relationships between pregnancy and the thyroid hormones. The most important finding in this regard is that maternal thyroid hormones play a vital role in early fetal brain formation, and their deficiency may impair future neuropsychological development of the fetus [1–3]. Pregnancy is associated with certain physiological changes for which the maternal thyroid gland has to adapt accordingly [1, 4]. The first factor is the adjustment of bound to free ratio of T4 and T3 against the marked increase in the circulating levels of thyroxin binding globulin (TBG) levels due to enhanced estrogen production. The second factor is the direct stimulation of the thyroid gland by elevated concentration of human chorionic gonadotropin (hCG). These two factors occur in the first trimester of pregnancy [1]. The third factor is the increased enzymatic activity of type III monodeiodinase. It converts T4 to reverse T3 (rT3) and thus increases the turnover rate of maternal T4 at the placental level. It is operative in later stages of pregnancy [1, 4]. The above mentioned thyroid stimulants during pregnancy enhance maternal iodine requirement which is further exacerbated due to
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