Comparison of thyroid stimulators and thyroid hormone concentrations in the sera of pregnant women.

To clarify the role of various thyroid stimulators in normal human pregnancy, we measured serum TSH, chorionic TSH (hCT), hCG, bioassayable thyroid-stimulating activity, T4, T3, T3 uptake, free T4 and free T3 indexes, free T4, and free T3 by dialysis in 339 serum samples from pregnant women at various intervals of pregnancy and in 40 normal female controls. Serum T4 and T3 and free T4 and free T3 indexes were significantly elevated throughout pregnancy in comparison with controls. Free T4 concentration was elevated after 10 weeks of pregnancy and free T3 concentration was elevated at 13--20 weeks. Bioassayable thyroid-stimulating activity was elevated from 9--16 weeks when serum hCG concentrations were highest. Serum TSH levels were significantly lower at 9--12 weeks compared with the rest of pregnancy. hCT was detected in only 35% of sera tested; the mean detectable value was 0.60 +/- 0.04 (SE) microU/ml; only 15% of the detectable values exceeded 1 microU/ml. The level of hCG correlated with bioassayable thyroid-stimulating activity (P less than 0.01). The data indicate that hCT is not a significant thyroid stimulator. We propose that hCG, as a weak thyroid stimulator, causes a modest rise in free thyroid hormone levels early in pregnancy which in turn causes a modest reduction in pituitary TSH secretion.     

Maternal thyroid function during pregnancy and puerperal period

It has been noted that hypothyroidism in pregnant women can adversely affect the children's subsequent psychoneurotic development. Also, transient elevation of serum free thyroxine is occasionally seen in the first trimester of normal pregnancy. However, normal thyroid function during pregnancy and the puerperal period has not been clearly defined in Japan. The aim of this study was to assess maternal thyroid function during pregnancy and puerperal period in Japan. The concentrations of thyroid stimulating hormone (TSH), free triiodo-thyronine (free T(3)), free thyroxine (free T(4)) and thyroid binding capacity (TBC) of 522 normal pregnant and puerperal women (119 in the first trimester; 132 in the second trimester; 135 in the third trimester and 136 in the early puerperium) were measured by electrochemiluminescence immunoassay. We compared the measured data with those of healthy nonpregnant control. Twenty-six (21.8%) of 119 women in the first trimester had lower TSH levels and 23 (16.9%) of 136 women in the early puerperium had higher TSH levels than the normal range of healthy nonpregnant controls. Free T(3) gradually decreased during pregnancy, although it remained within the normal control range. Eight (6.7%) of 119 women in the first trimester had high free T(4) levels, which gradually decreased during pregnancy. Sixty (44.4%) of 135 women in the third trimester had low free T(4) levels. The values of TBC in the second trimester increased compared with the first trimester and did not change in the third trimester and decreased after delivery. There were no correlations between maternal TSH and levels of thyroid hormones (free T(3) or free T(4)), except for TSH and free T(4) in the first trimester. In conclusion, we showed that maternal thyroid function, especially TSH and free T(4), changed during the course of pregnancy. In assessing the thyroid function associated with pregnancy, one needs to keep in mind the tendency toward low free T(4) levels in the third trimester and high TSH levels in the early puerperal period.     

Regulation of maternal thyroid during pregnancy

A prospective study was undertaken in 606 healthy women during pregnancy to evaluate the changes occurring in maternal thyroid economy as a result of 1) the increased thyroid hormone-binding capacity of serum, 2) the effects of increased levels of hCG on TSH and on the thyroid, and 3) a marginally low iodine intake in the population (50-75 micrograms/day). Four main features were observed. First, thyroidal activity adjusted to the marked increase in serum T4-binding globulin: pregnancy was accompanied by an overall reduction in the T4/T4-binding globulin ratio, with lower free T4 and T3 levels, although in most cases free hormone levels remained within the normal range. The adjustment of thyroidal output of T4 and T3 did not occur similarly in all subjects. In approximately one third of the women, there was relative hypothyroxinemia, higher T3/T4 ratios (presumably indicating preferential T3 secretion), and higher, although normal, serum TSH concentrations. Second, high hCG levels were associated with thyroid stimulation, both functionally (lower serum TSH) and anatomically (increased thyroid size). The data are consistent with a TSH-like effect of hCG on the thyroid. Hence, regulation of the maternal thyroid is complex, resulting from both elevated hCG (mainly in the first half of gestation) and increasing TSH (mainly in the second half of gestation). Third, a significant increase in serum thyroglobulin levels was observed throughout gestation, especially during the last trimester. Fourth, increased thyroid volume was common, and goiter formation not uncommon (goiter was found in 9% of women at delivery). In conclusion, the alterations in maternal thyroid function during gestation are intricate and far from fully understood. In areas of marginally low iodine intake, gestation is associated in a significant number of women with relative hypothyroxinemia, increased thyroglobulin, and enlarged thyroid.     

Increase in plasma thyrotropin-releasing hormone in normal human pregnancy

Maternal thyroid regulation in pregnancy was examined by measuring the concentrations of TRH, T4, T3, free T4 (by RIA), T4-binding globulin, TSH, PRL, and hCG in the sera of 30 normal pregnant women, 10 puerperally lactating women, and 10 normal pregnant women, 10 puerperally lactating women, and 10 normal nonpregnant female controls. Results showed that serum T4, T3, T4-binding globulin, PRL, and hCG, but not free T4 (by RIA), increased significantly during pregnancy. The plasma level of TRH was significantly higher (P less than 0.01) in the second trimester and significantly lower (P less than 0.05 1 month post partum than those values in nonpregnant controls. No significant correlations, however, were observed between the serum level of TRH and those of the thyroid hormones TSH, PRL, and hCG in pregnancy. The TRH-degrading activity of the plasma in the second trimester was normal. These results indicate that TRH secretion may be increased in the second trimester of pregnancy.     

Components of the total serum thyroid hormone concentrations during pregnancy: high free thyroxine and blunted thyrotropin (TSH) response to TSH-releasing hormone in the first trimester

The distribution of thyroid hormones between free solution and their several protein-binding sites during pregnancy was studied under physiological conditions of temperature and pH. Single serum specimens were obtained from individual women at different stages of pregnancy. During the first 5 weeks of pregnancy, mean serum free T4 and free T3 concentrations were 50% higher than in nonpregnant women or women during the third trimester. Free T4 was increased significantly throughout the first trimester, but because of wide variance, free T3 was significantly above control values only during the first 5 weeks. Free T4 and free T3 concentrations decreased to control levels in the third trimester. These changes in free T4 concentrations are consistent with a weak thyrotropic action of hCG, which attained maximal concentrations early in the first trimester and then decreased markedly in the second and third trimesters. TRH testing of women scheduled for abortion in the first and second trimesters revealed marked inhibition of TSH response to TRH in those first trimester women who had elevated free T4 concentrations. The percent free T4 did not decrease during the first 5 weeks, but then declined progressively to term as T4-binding globulin (TBG) affinity, defined as the product of the capacity and affinity constant, progressively increased. T4 bound to TBG (T4-TBG) increased from early in the first trimester to term, and then decreased in postterm pregnancy and postpartum. T4 bound to prealbumin (T4-PA) and to albumin (T4-Alb) decreased significantly in the third trimester compared with either control or first trimester concentrations. The concentration of free T3 was positively correlated with T4-PA (r = 0.25) and T4-Alb (r = 0.31), but not with free T4 (r = 0.18) or T4-TBG (r = -0.30) concentrations. These results suggest that 1) only the high concentrations of hCG present in the first trimester of pregnancy have a thyrotropic effect in excess of normal levels of TSH, and this can be sufficient to suppress the TSH response to TRH; 2) hepatic TBG secretion continues to respond to the continuously rising estrogen levels throughout pregnancy; and 3) T4-PA and T4-Alb, but not free T4 or T4-TBG, are possible precursors for the extrathyroidal generation of T3.     

Human fetal and cord serum thyroid hormones: developmental trends and interrelationships

Thyroid hormone is essential for fetal and neonatal development in particular of the brain, but little is known about regulation of fetal thyroid hormone levels throughout human gestation. The purpose of this study was to clarify developmental trends and interrelationships among T(4), free T(4) (FT4), thyroxine-binding globulin (TBG), TSH, T(3), rT(3), and T(4) sulfate (T4S) levels in cord and fetal blood sera (n = 639, 15-42 wk gestation) and correlate infant levels (23-42 wk gestation) to maternal values (n = 428, 16-45 yr) and those of nonpregnant women (n = 233, 16-46 yr). In cord and fetal serum, T(4), T(3), and TBG levels increase with gestation until term; TSH, FT4, T4S, and rT(3) levels increase and peak in the late second/early third trimester and then decline to term; T(4)/TBG ratios increase until late second trimester and plateau to term. Term cord sera TSH, TBG, and all iodothyronine levels, except T(3), are higher than nonpregnant women. In the third trimester, cord serum FT4, TSH, rT(3), and T4S levels are also higher than corresponding maternal levels, but T(4), T(3), and TBG levels are lower than maternal values. The late second/early third trimester is a critical transition period in fetal thyroid hormone metabolism, which may be interrupted by preterm birth and contribute to postnatal thyroid dysfunction.     

Secretion of thyroxine, 3,5,3'-triiodothyronine and 3,3'5'-triiodothyronine in euthyroid man

The secretion of iodothyronines from the normal human thyroid gland was assessed by radioimmunoassay analyses of the concentrations of thyroxine (T4), 3,5,3'-triiodothyronine (T3) and 3,3',5'-triiodothyronine (reverse T3, rT3) in thyroid venous and peripheral venous blood. The subjects studied were euthyroid patients undergoing parathyroid surgery. Measurements were carried out both under apparently normal conditions, following peroral T3 pre-treatment, and before and after acute administration of TSH into a thyroid artery. In the control subjects, significant gradients between thyroid venous and peripheral venous concentrations were recorded both for T4, T3 and rT3, suggesting that all three iodothyronines are secreted by the normal human thyroid. T3 pre-treatment seemed to reduce this secretion, and acute administration of TSH promoted rapid, marked, and concomitant increments in the thyroid venous concentrations of all three iodothyronines. Hence, it appears that not only T4 but also T3 and rT3 are secreted by the normal human thyroid gland, and that TSH stimulates the secretion of all three iodothyronines. On the other hand, calculations of the relative secretion rates uielded the relation T4:T3:rT3 as 85:9:1. This indicates that, in euthyroid subjects, most of T3, and almost all of rT3, is produced by extrathyroidal conversion of T4 and not by direct thyroidal secretion.     

Resistance to thyroid hormone does not abrogate the transient thyrotoxicosis associated with gestation: report of a case

We report the occurrence of transient thyrotoxicosis during pregnancy in a subject with resistance to thyroid hormone. Before pregnancy, the subject was euthyroid, with normal serum TSH and elevated levels of free T(3) and free T(4) caused by a mutation in the TRbeta gene (R243Q). Beginning at the fourth week of gestation serum levels of free T(3) and T(4) increased in parallel with an increase in hCG. At 6-7 wk gestation she manifested hypermetabolic features, with mild nausea and vomiting. Peak levels of serum hCG and thyroid hormone concentrations were attained at 12 wk gestation, when serum TSH was fully suppressed. In the following weeks of gestation, thyroid hormone levels declined, with amelioration of the symptoms. A baby boy also affected with resistance to thyroid hormone harboring the same TRbeta gene mutation was born by normal vaginal delivery.     

妊娠一过性甲状腺毒症的临床研究

目的 调查沈阳地区既往健康的妇女妊娠早期妊娠一过性甲状腺毒症(GTT)的患病率及其病因.方法 对来自沈阳地区10家医院的534例妊娠早期妇女进行问卷调查、体格检查、血清促甲状腺素(TSH)、游离T4(FT4)、游离T3(FT3)、甲状腺过氧化物酶抗体(TPOAb)、促甲状腺素受体抗体(TRAb)和人绒毛膜促性腺激素(hCG)水平的检测.结果 (1)妊娠早期甲状腺毒症总患病率为9.75%,GTT的患病率为7.86%,占甲状腺毒症的80.77%;88.89%临床GTT表现为单纯FT3升高.(2)妊娠6、8～10和12周孕妇血清hCG水平逐渐升高,中位数分别为25300、85220和81780IU/L(P=0.000).血清TSH中位数依次降低(P＜0.01),分别为1.45、1.10和0.84mIU/L.(3)当妊娠妇女血清hCG水平＞50 000 IU/L时,GTT的比例明显升高;当血清hCG水平在80 000～110000IU/L时发生亚临床GTT的比例明显升高;当血清hCG水平＞110 000IU/L时发生临床CTT的比例明显升高.相关分析结果 显示,妊娠早期血清hCG与TSH显著负相关(r=-0.402,P=0.000),与FT3正相关(r=0.165,P=0.000),而与FT4无相关.结论 GTT是妊娠早期甲状腺功能亢进症的首要病因,占妊娠早期甲状腺毒症的80.77%,其血清学特点主要表现为血清FTT升高.妊娠早期血清hCG水平与GTT严重程度相关.     

EVIDENCE FOR THYROIDAL SECRETION OF 3,3'',5''-TRIIODOTHYRONINE IN MAN AND ITS CONTROL BY TSH

Thyroidal secretion of 3,3',5'-triiodothyronine (reverse T3, rT3) and its control by TSH was assessed by measuring (1) arterio-venous hormone gradients in patients undergoing surgery, (2) changes of hormone concentrations after induction of anaesthesia, and (3) changes induced by TRH administration. In ten patients in whom thyroid activity was under TSH control (parathyroidectomy and non-toxic goitre) increased thyroid vein/carotid artery ratios (TV/CA) for rT3 (mean TV/CA ratio 2.53) were found when compared to six patients with non-toxic goitre on suppressive doses of T4 (mean TV/CA ratio, 1.27) (P less than 0.05). The mean calculated operative secretion rate of rT3 was 12.5 microgram/day but only 2.4 microgram/day in patients receiving T4. In thirteen patients undergoing elective surgery induction of anaesthesia significantly increased rT3 levels. In nine euthyroid adults intravenous TRH (200 microgram) increased peripheral venous rT3 levels between 3 h (P less than 0.005) and 8 h (P less than 0.05) after the injection. It is concluded that significant amounts of rT3 are secreted by the thyroid gland at operation and this is, in part, under TSH control.     

Lack of Association Between Peripheral Activity of Thyroid Hormones and Elevated TSH Levels in Childhood Obesity

Ob­jec­ti­ve: An elevated thyroid stimulating hormone (TSH) level is a frequent finding in obese children, but its association with peripheral hormone metabolism is not fully understood. We hypothesized that in obesity, the changes in thyroid hormone metabolism in peripheral tissues might lead to dysregulation in the thyroid axis. The purpose of this study was to investigate the association of TSH with thyroid hormones in a group of obese children as compared to normal-weight controls.Methods: Serum TSH, free thyroxine (fT4) and free triiodothyronine (fT3) levels were measured in 101 obese children and in 40 controls. Serum reverse T3 (rT3) levels were also measured in a subgroup of 51 obese children and in 15 controls. Results: Serum TSH level was significantly higher in obese children compared to controls (2.78 vs. 1.99 mIU/L, p<0.001), while no difference was found in fT4, fT3, rT3 levels and in fT3/rT3 ratio. In the obese group, fT3 level positively correlated with fT4 (r=0.217, p=0.033) and inversely with rT3 (r=-0.288, p=0.045). However, thyroid hormone levels and TSH levels were not correlated. Conclusion: In obese children, normal fT4, fT3 and rT3 levels suggest an undisturbed peripheral hormone metabolism. These levels show no correlation with elevated TSH levels.     

Thyroid function tests are rarely abnormal in patients with severe hyperemesis gravidarum

OBJECTIVES: There is considerable controversy in the literature as to the cause of hyperemesis gravidarum. The aim of this project was to measure a range of thyroid hormone levels in a group of hyperemetic pregnant women. PATIENTS: The study was carried out in 10 first trimester pregnant women with hyperemesis gravidarum. All had been admitted to hospital due to the severity of their symptoms. Fifty age matched, healthy first trimester pregnant women were used as controls. MEASUREMENTS: Blood samples from the women were analysed for total T3 (TT3), total T4 (TT4), free T4 (FT4), TSH, thyrotrophin receptor antibodies (TRAb), thyroid stimulating antibodies (TSAb) and thyroid microsomal and thyroglobulin antibodies. Human chorionic gonadotrophin (hCG) levels were also measured. RESULTS: While individual patients were found to have some abnormal thyroid function tests the group as a whole showed no consistent pattern of abnormality and did not differ significantly from a group of healthy first trimester pregnant women. hCG levels were also within the normal range in the hyperemetic patients. DISCUSSION: None of the women in this study received any antithyroid medication and their symptoms improved as the pregnancy progressed. These results would suggest that there is no underlying thyroid abnormality in patients with hyperemesis gravidarum. It would appear that neither thyroid hormones, nor hCG contribute to the pathogenesis of the condition.     

Thyroid-pituitary function in eight anencephalic infants

The function of the thyroid pituitary axis was investigated in 8 anencephalic infants with no hypothalamus. Thyrotrophin (TSH), thyroxine (T4), 3,5,3'-triiodothyronine (T3) and 3,3',5'-triiodothyrone (reverse T3 and rT3) were measured in the cord blood in 5 cases and during the first 4 h of life in 3 cases. TSH response to synthetic thyrotrophin-releasing hormone (TRH) (200 microgram iv) was carried out in two cases and thyroid hormone response to bovine TSH (5 IU iv) was evaluated in 3 cases. The following results wre obtained: 1) The pituitary gland was found in all infants and the thyroid was normal both grossly and by microscopic sections. 2) TSH levels at birth were normal but there was no spontaneous post-delivery surge. 3) T4 and T3 values at delivery were within normal range, but no T3 increase was present after birth. rT3 levels at birth were higher than normal in 3 cases. 4) Administration of TRH caused a marked and rapid TSH release. 5) Thyroid hormone response to TSH was normal. The present findings suggest that in the anencephalic foetus both pituitary TSH-secreting cells and the thyroid gland do develop despite the absence of the hypothalamus and are able to function if adequately stimulated.     

Human chorionic gonadotropin may not be responsible for thyroid-stimulating activity in normal pregnancy serum.

Although hCG can activate thyroid cells in culture there is considerable doubt as to whether it is responsible for the changes in thyroid function which occur during normal pregnancy. Thyroid-stimulating activity (TSA), measured using iodide uptake into FRTL-5 cells, was demonstrated in 32/51 (63%) first and 15/29 (52%) third trimester sera. Free T3 was increased (P less than 0.001) and TSH decreased (P less than 0.01) in first trimester. In the early pregnancy group there was a positive correlation between hCG and TSA (r = 0.594, P less than 0.001) and a negative correlation between hCG and TSH (r = -0.329, P less than 0.02). In third trimester hCG concentration was often below that required to produce TSA in vitro and TSA could not be neutralized by antibodies to hCG. There was no correlation between hCG and TSH or thyroid hormones in the third trimester. In 26 women TSA decreased in parallel with serum hCG concentration after termination of pregnancy (P less than 0.001). Free T3 also decreased (P less than 0.01) and TSH increased (P less than 0.05) after termination. TSA persisted in many patients even after hCG was either very low or undetectable. Purified hCG stimulated iodide uptake in a concentration-dependent manner. Stimulation of iodide uptake by TSH was inhibited by the simultaneous presence of low concentrations of hCG while activity was restored with high concentrations. hCG may contribute to the thyroid changes in early pregnancy. However the poor correlation between TSA and thyroid tests suggests that other factors may be involved. The partial agonist activity of hCG may account for some of the inconsistencies observed but TSA in serum from late pregnancy or after termination of pregnancy is almost certainly due to another hormone or growth factor.     

Euthyroid hyperthyroxinemia due to a generalized 5'-deiodinase defect

We studied an 11-yr-old girl with asymptomatic hyperthyroxinemia, who remained euthyroid and healthy for 5 yr of follow-up. Besides having elevated serum T4 concentrations, her serum free T4 concentrations were consistently elevated, as measured by three different methods, including equilibrium dialysis and ultrafiltration. Serum total and free T3 concentrations were in the low normal range, and serum 3,5-diiodothyronine (3,5-T2) levels were low, suggesting reduced 5'-deiodination of both T4 and T3. Serum total and free rT3 and total and free 3', 5'-T2 concentrations were all markedly elevated, whereas serum total and free 3,3'-T2 were low, suggesting unaltered 5-deiodination of T4 to rT3 and of rT3 to 3',5'-T2 in combination with reduced 5'-deiodination of rT3 and 3',5'-T2. The girl had a small diffuse goiter, her serum TSH response to TRH was exaggerated, and thyroid radioiodine uptake was elevated, suggesting slightly increased TSH secretion and, consequently, increased thyroid secretion. Both T3 and T4 administration resulted in suppressed basal as well as TRH-stimulated serum TSH concentrations, and radioiodine uptake was suppressed during T3 administration. Our data suggest reduced activity of several (all?) peripheral 5'-deiodination pathways, including possibly also thyrotroph T4 5'-deiodination. Thus, this girl seems to have a previously unrecognized syndrome of generalized 5'-deiodinase deficiency.     

Human chorionic gonadotropin (hCG) and thyroid function in early human pregnancy: circadian variation and evidence for intrinsic thyrotropic activity of hCG

To explore the diurnal variation and the relationship between serum hCG levels and thyroid function during pregnancy, 26 women with an uncomplicated early pregnancy were studied before and after interruption of pregnancy. The high serum hCG levels in early pregnancy were accompanied by an increase in serum thyroid hormone and a decrease in serum TSH levels. Nevertheless, serum TSH exhibited diurnal variation similar to that in nonpregnant women. The nocturnal surge of TSH exceeded the daytime nadir by 112% and was distinctly different from the normal serum cortisol variation. The diurnal serum T4 and hCG variations were similar to the variation in serum protein concentrations. After pregnancy interruption, serum hCG levels decreased by 95% within 10 days, and TSH levels rose concomitantly from 0.80 to 1.48 mIU/L (P less than 0.001). In individual women serum hCG correlated negatively with TSH (r = 0.322; P = 0.005) and positively with free T3 (r = 0.388; P less than 0.001). These results suggest that hCG has thyrotropic activity, which, through rises in thyroid hormone levels, suppresses TSH secretion. In this regard, 27,000-128,000 IU hCG correspond to 1 mIU TSH. Pregnancy-induced changes in thyroid function, however, do not affect the circadian TSH rhythm.     

Thyroid and adrenomedullary reactions during sleep deprivation.

The possible influence of a 48 h period of sleep deprivation on the serum concentrations of total and unbound 3,5,3',5'-thyroxine (T4) and 3,5,3'-triiodothyronine (T3), and of total 3,3',5'-triiodothyronine (reverse T3, rT3) was studied in 12 young male volunteers. In addition, plasma concentrations of TSH and the urinary excretion of noradrenaline and adrenaline were examined. Both total S-T4, S-T3 and S-rT3, and unbound S-T4 and S-T3 (unbound rT3 was not calculated) were significantly enhanced following sleep deprivation. P-TSH showed a numerical but statistically not significant increase, while the catecholamines remained unaltered. The results suggest that sleep deprivation provokes enhanced secretion of thyroid hormone(s), supposedly via increased secretion of TSH.     

Change in serum thyroid hormone levels in patients with acute myocardial infarction

It has been reported that there is a decrease in the serum concentration of thyroid hormones in non-thyroidal illness. In the present study we made serial measurements of serum concentration of thyroid hormones [triiodothyronine (T3), thyroxine (T4), free triiodothyronine (FT3), free thyroxine (FT4), reverse triiodothyronine (rT3)], thyroid stimulating hormone (TSH) and thyroxine binding globulin (TBG) in 10 patients with acute myocardial infarction (AMI, Grade I, according to the classification of Killip & Forrester) during 14 days after onset. In the early phase of AMI, serum T3, T4, FT3 and FT4 levels decreased while rT3 increased. TSH and TBG levels, however, were unchanged. In the patients with a high peak creatine phosphokinase activity (greater than or equal to 400 mU/ml), the decrease in thyroid hormone and increase in serum rT3 levels were greater than in patients with a low peak value (less than 400 mU/ml), suggesting a correlation between severity of AMI and changes in serum thyroid hormone levels. Especially, serum FT3 levels fell below the lower limit of controls within 14 days, with the lowest levels and the rT3 peak on the third day after onset. These data suggest that in AMI peripheral conversion of T4 favours rT3 production and that low levels of serum FT3 and T3 protect the infarcted heart muscle against thyroid hormone action.     

Cord blood iodothyronine and thyrotropin concentrations in newborns of mothers exposed to povidone iodine in the last trimester

In the present study, we have evaluated thyroid function in neonates at delivery and in their mothers who used vaginal povidone-iodine (PVP-I) during the last trimester of pregnancy. Newborns and their mothers without a history of iodine exposure, admitted to the same department and residing in the same geographical area served as controls. Maternal serum thyroxine (T4), triiodothyronine (T3), reverse triiodothyronine (rT3) and thyrotropin (TSH) concentrations at delivery were not significantly different between the two groups of pregnant women. Cord blood thyroid hormone concentrations in the newborns of iodine exposed mothers were not significantly different from those in control newborns. In contrast, cord blood TSH concentrations in the neonates of mothers exposed to PVP-I during the last trimester of pregnancy were significantly higher than values in control neonates (p less than 0.05). These data confirm that the fetal thyroid gland, even in the last trimester of pregnancy, does not adapt completely to the inhibitory action of iodine on thyroid hormone synthesis and/or release.     

The effect of growth hormone on the plasma levels of T4, free-T4, T3, reverse T3 an TBG in hypopituitary patients

The plasma concentrations of thyroxine (T4), free thyroxine (free-T4), triiodothyronine (T3), reverse triiodothyronine (rT3), TSH and thyroxine-binding globulin (TBG) were measured in 19 children suffering from idiopathic growth hormone deficiency. Blood was taken before and one month after growth hormone treatment. Ten patients were hypothyroid (group 1) and 9 were euthyroid (group 2). The basal T3 and rT3 levels correlated well with the T4 concentrations. Free-T4 levels were very low in all the hypothyroid patients and proved to be the most reliable index of TSH deficiency. TBG concentration was high in th hypopituitary patients regardless of their thyroid function. Following growth hormone treatment T4, free-T4 and rT3 levels fell in both groups. The T3 concentration rose in group 1 but no change was seen in group 2. There was a significant correlation between the changes of T4 and T3, such that the increase in T3 level was greatest in those with only a slight reduction of T4 concentration and no T3 increase was seen with more marked T4 decreases. The plasma TBG concentration is enhanced in growth hormone deficiency causing relatively high T4 values. Growth hormone treatment reduces T4 secretion and affects the peripheral metabolism of thyroid hormones resulting in an increase of T3 and a reduction of rT3 concentration.