Normal values of thyroid-stimulating hormone and free thyroxin in pregnant women

Einstein 01/2007;
Source: DOAJ

ABSTRACT Objective: To prepare a chart for normal values of thyroid-stimulatinghormone (TSH) and free thyroxin (free T4) and to verify the correlationbetween them, in pregnant women. Methods: A prospective crosssectionalstudy was performed on 850 pregnant women of thePrenatal Outpatient Clinic of the Hospital do Servidor Público Estadual– Francisco Morato de Oliveira (HSPE – FMO), from August 2003 toAugust 2005. Serum TSH and free T4 levels were determined usingmicroparticle enzyme immunoassay (MEIA). Maternal age ranged from18 to 47 years, mean of 32.5 ± 6.9 years. Mean gestational age was19.1 ± 8.5 weeks. With linear regression analysis, the 50th and 97.5thpercentiles for TSH and the 2.5th, 50th and 97.5th percentiles for free T4,at weeks 6 to 42 were calculated. The possible correlation betweenthese two indicators was analyzed. Results: Mean TSH and free T4values were 2.14 ± 1.51 μIU/ml and 0.98 ± 0.30 ng/dl, respectively.The correlation between free T4 and TSH levels was positive andstatistically significant according to the Pearson’s correlation coefficient(r = 0.069, p = 0.044). Conclusion: Identifying the normal TSH andfree T4 limits during pregnancy is the first step to safely determine thereal need for thyroid dysfunction treatment.

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    ABSTRACT: Iodine deficiency is well known as the cause of several disorders such as endemic goitre and cretinism, along with a wide spectrum of psychoneurological development disorders including endemic mental deficiency and endemic cognitive deficiency, which are generally correlated to damage to the fetus. Such damage is, by inference, deemed a consequence either directly of iodine deficiency or of insufficient availability of thyroxine at the feto-placental unit level. Early pregnancy represents the crucial period for neurogenesis in the embryo. Several experimental studies have emphasized the direct role of maternal T4 in neurological embryogenesis, before the onset of fetal thyroid function and, therefore, its protective role in fetal thyroid failure. The objective of this study was to evaluate whether iodine deficiency may influence thyroid status of pregnant women throughout the first half of pregnancy. Thyroid function tests including total and free T4 and T3, TBG and TSH along with urinary iodine excretion were measured in the serum of pregnant women from an iodine deficient endemic goitre area in north-eastern Sicily, at 8, 13 and 20 weeks of gestation. The times of sampling were chosen to correspond approximately to a period prior to, coincident with and after the onset of fetal thyroid function, respectively. The longitudinal study was undertaken in 16 euthyroid pregnant women from the iodine deficient area in which major iodine deficiency disorders such as endemic cretinism and endemic cognitive deficiency in schoolchildren still persist (area A) and in 7 age matched volunteer pregnant women from a marginally iodine sufficient area (area B). Hormones and TBG were measured using commercial kits. Urinary iodine was measured by an automated method. The divergent changes in serum T4 and TBG with pregnancy progression induced a progressive TBG desaturation by T4 during the whole study period (from 22 to 17% in area A, ANOVA two-way F = 18.9, P < 0.0001; from 33 to 20% in area B, F = 20.7, P < 0.0005) in both areas. At 20 weeks, average FT4 levels were lower in area A than in area B (11.5 +/- 2.5 vs 14.3 +/- 2.4 pmol/l, t = 2.7 P < 0.01) and were below the normal range in 2/16 and borderline-low in 6/16 pregnant women. FT4 serum levels were inversely related to TSH concentrations (r = -0.54, P < 0.0001) which progressively increased, in area A, during the whole study period (F = 6.0, P < 0.01) and were abnormally high in the two women with low FT4, but not in area B. Also in area A (F = 3.4, P < 0.05) a significant T3/T4 molar ratio increase was observed. Iodine deficiency induces in early pregnancy a series of events (reduced synthesis of maternal T4, TBG desaturation by T4, critical decrease of FT4 levels with consequent TSH increase) responsible for overt or marginal biochemical hypothyroidism in about 50% of pregnant women. It is hypothesized that the imbalance of maternal thyroid hormone homeostasis during pregnancy as a consequence of endemic iodine deficiency may be responsible for the impaired psychoneurological development observed in children from that area so appropriate iodine and/or thyroxine prophylaxis to women in that region may prevent the neurobehavioural, cognitive and motor compromise of the population.
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