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*LEVOTHYROXINE
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The Journal of Clinical Endocrinology & Metabolism Vol. 83, No. 10 3545-3549
Copyright © 1998 by The Endocrine Society

Original Studies

Circulating Iodide Concentrations during and after Pregnancy1

Claudio S. Liberman, Salvatore C. Pino2, Shih Lieh Fang2, Lewis E. Braverman2 and Charles H. Emerson

Department of Medicine, Division of Endocrinology and Metabolism, Section of Endocrinology, Hospital Clinico de la Universidad de Chile (C.S.L.), Santos Dumont 999, Santiago, Chile; and the Division of Endocrinology and Metabolism, Department of Medicine, University of Massachusetts Medical Center (S.C.P., S.L.F., L.E.B., C.H.E.), Worcester, Massachusetts 01655

Address all correspondence and requests for reprints to: Charles H. Emerson, M.D., Department of Medicine, Division of Endocrinology and Metabolism, University of Massachusetts Medical Center, 55 Lake Avenue North, Worcester, Massachusetts 01655.


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
Early, indirect studies suggested that an important aspect of thyroid economy during pregnancy was a decline in plasma or serum inorganic iodide (PII) concentrations, but there is little information concerning circulating iodide concentrations as assessed by direct measurement. The present study was undertaken to determine the relationship between gestation and serum iodide concentrations as assessed by direct measurement of PII. PII concentrations, urinary iodide levels, and other parameters of thyroid economy were measured during the first, second, and third trimesters and after delivery in 16 women. Mean serum T4 concentrations were significantly higher in all 3 trimesters than those after delivery. Serum free T4 index concentrations were significantly higher in the first trimester than during later periods of gestation or after delivery, but serum TSH concentrations were not depressed in the first trimester. Serum thyroglobulin concentrations were similar during pregnancy and after delivery. There was wide variability in PII and urinary iodide concentrations during and after pregnancy, but there was no trend for PII concentrations to be depressed during pregnancy. Pregnancy, at least in iodine-sufficient regions, does not have an important influence on circulating concentrations of iodide.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
IT IS WIDELY believed that plasma or serum inorganic iodine (PII) concentrations decline during pregnancy (1, 2). The supporting data for this concept, however, are limited and derived from urinary iodine measurements and the ratio of urinary and plasma 132I after iv injection of 132I (3). In the present study PII concentrations were measured directly in serum obtained during pregnancy and after delivery. The results are not consistent with the concept that there is a significant decline in the plasma iodide concentration during pregnancy.


   Subjects and Methods
Top
 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
The participants in this study were a group of pregnant women from Santiago, Chile who gave their informed consent to participate in the study. The study was approved by the Barros Luco Trudeau Hospital (Santiago, Chile). Blood and 24-h urine samples were collected during the first, second, and third trimesters, as near to the midportion of each trimester as possible. The expected date of conception was used as a guide for sample collection. The relationship of the samples to the time of gestation was calculated from the delivery date. None of the women who participated in the study had a premature delivery. A final blood sample and 24-h urine sample were collected from 1–10 months after delivery (mean, 3.4 months; median, 3.0 months; for the entire group of subjects).

Serum T4, T3 resin uptake ratio (T3RU), thyroglobulin (Tg), hCGß, TSH, and antibodies against thyroid peroxidase (TPO Ab) and Tg (Tg Ab) were measured using commercial assays. The free T4 index (FTI) was calculated as the product of T4 and T3RU measurements. Serum T4 and the T3RU were measured by competitive chemiluminometric immunoassay, and the FTI was automatically calculated (Ciba-Corning Diagnostics, Medfield, MA). Serum Tg was measured by radioimmunoprecipitation (Kronus, San Clemente, CA). Serum hCGß was measured by microparticle enzyme immunoassay (Abbott Laboratories, Abbott Park, IL). Serum TSH was measured by a two-site chemiluminometric immunoassay (Ciba-Corning Diagnostics, Medfield, MA), and serum TPO Ab and Tg Ab were measured by radioimmunoprecipitation (Kronus). Urinary creatinine was determined by the University of Massachusetts Medical Center Laboratory. [125I]T4 (~1200 µCi/µg) was obtained from DuPont-New England Nuclear (Boston, MA).

Iodine was measured by the ceric-arsenic redox reaction (4, 5). Whole serum was analyzed to obtain total serum iodine (TI) concentrations, and perchloric acid precipitates of serum were analyzed to determine the protein-bound iodine (PBI) concentration. The formula for calculating the serum PII (6) is as follows: PII = TI - PBI. This method compares favorably with other methods for determining PII values, including estimates derived from salivary iodine concentrations or a value that is a function of the ratio of urinary iodine and the glomerular filtration rate (6). To further refine this method to eliminate contamination by T4, the partition of serum T4 between perchloric acid precipitates and supernates was determined. [125I]T4 was added to aliquots of pooled normal human serum, and perchloric acid supernatants were analyzed by high performance liquid chromatography as previously described (7). The fraction of T4 in serum that was present in perchloric acid supernates was 0.005 ± 0.002 (mean ± SD; n = 6). Accordingly, and in consideration of the fact that iodine composes approximately 65% of T4 by weight, the final formula used to calculate the PII was as follows: PII = TI - PBI - (T4 x 0.65 x 0.005). PII measurements were not corrected for the contribution of T3 because its concentration in serum is typically only 1–3% that of T4. They were also not corrected for any contribution of other iodothyronines because, based on published data for serum concentrations of 10 other iodothyronines (8), they account for only 0.076 µg/dL PII even if they partitioned entirely to the perchloric acid supernatant fraction.

Twenty-two subjects were enrolled in this study, and 16 returned for their postpartum visits. This report describes the data obtained from these 16 women. In addition to returning for their postpartum visits, all of these women also had blood obtained in the first trimester, but samples from the second trimester were not available for 2 subjects and samples from the third trimester were not available for 2 other subjects because they missed their visits during this period. Data for the missing serum T4 and FTI values in these cells were imputed, the assigned value being the previous trimester value in a given subject multiplied by the ratio, in all subjects for whom data was available, of the average value for that trimester to the average value for the previous trimester. Results were analyzed using data for all 16 subjects as well as for the 12 subjects in whom complete datasets were available, and the same results were obtained as far as statistical significance was concerned. Unless otherwise stated, data are presented as the mean ± SEM. The data were analyzed by repeated measures ANOVA, Student-Newman-Keuls multiple comparisons test, and linear regression. Differences were considered significant at P < 0.05.


   Results
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
The women in this study ranged in age from 19–40 yr, with a mean age of 27 yr (Table 1Go). First trimester blood samples were obtained at gestational ages ranging from 5–12 weeks (Table 1Go). Postpartum blood samples were collected, with few exceptions, between 6 weeks and 5 months after delivery. In one patient blood was collected 3 weeks after delivery, and in two patients the postpartum blood was obtained 6 and 12 months after delivery.


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  		Table 1. Age, pariety, and time at which blood samples were obtained

 
Mean serum T4 concentrations and FTI values during pregnancy and after delivery are presented in Fig. 1Go. Mean serum T4 concentrations were significantly higher during the first, second, and third trimesters than after delivery. Serum FTI concentrations, in contrast, were similar in the second and third trimesters to those obtained after delivery, but were significantly higher during the first trimester than later in pregnancy or after delivery (Fig. 2Go).



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  		Figure 1. Mean serum T4 concentrations and FTI values during pregnancy and after delivery.

 


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  		Figure 2. The relationship between serum FTI and serum hCGß concentrations during pregnancy.

 
The mean serum hCGß concentration was 108 ± 16 IU/mL in the first trimester and was significantly lower (18 ± 5 and 24 ± 9 IU/mL, respectively) in the second and third trimesters. Serum FTI values during pregnancy were positively correlated with serum hCGß concentrations or the log of serum hCGß concentrations, but the correlation coefficient for either of these was only between 0.40–0.45. To compensate for the fact that basal FTI values are variable among normal individuals, the FTI for each subject was assigned a value that reflected the difference in the FTI between the first and the third trimesters. These adjusted FTI values also significantly correlated with the serum hCGß concentrations, but the correlation was similar to that noted when absolute FTI values were used in the analysis.

Mean serum TSH concentrations were similar in samples collected during the first, second, and third trimesters and postpartum (Fig. 3Go). In the first trimester, none of the 16 subjects had serum TSH concentrations below the normal range (<0.35 µU/mL). One of the 6 other patients who did not return postpartum had a low serum TSH of 0.20 µU/mL. The distribution of values in samples collected during the postpartum period was skewed by patient 11, whose serum TSH rose to 13.4 µU/mL after delivery (Fig. 3Go). This subject was 1 of 3 women who had positive Tg and TPO Ab, but was the only subject whose antibody tests were consistently positive throughout pregnancy and after delivery. One of the 3 subjects had positive thyroid antibodies only in the first trimester, and the other was positive only in the second trimester and after delivery. No patient had a serum TSH value after delivery that was below the normal range (<0.35 µU/mL).



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  		Figure 3. Mean serum TSH and Tg concentrations during pregnancy and after delivery.

 
Figure 3Go also presents data for serum Tg concentrations in subjects in whom tests for Tg antibodies were negative. Serum Tg concentrations varied widely at all gestational periods as well as after delivery. There was no apparent relationship between the level of serum Tg and the time of gestation or the duration between delivery and postpartum blood samples.

Figure 4Go and Table 2Go presents data for PII concentrations during and after pregnancy. There was marked variation in PII concentrations, even within the same individuals. Mean PII concentrations were similar throughout pregnancy and were actually slightly higher during pregnancy than after delivery, but this small difference was not significant. As was the case for PII, urinary iodine excretion was markedly variable among different subjects and in the same subjects at different sampling times. Mean urinary iodine excretion ranged from 477 ± 74 µg/g creatinine in the second trimester to 809 ± 139 µg/g creatinine in the first trimester, but none of the differences in values during pregnancy or after delivery were significant (Table 2Go).



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  		Figure 4. PII concentrations during pregnancy and after delivery.

 

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  		Table 2. Urinary iodine and serum inorganic iodine concentrations during pregnancy and after delivery

 

   Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
The effects of pregnancy on maternal thyroid economy have been widely studied (1, 2, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28). There is universal agreement, also noted in the present study, that maternal serum T4 concentrations are elevated throughout gestation. This is due to increases in serum T4-binding globulin concentrations (2, 10, 25). The influence of pregnancy on serum free T4 concentrations is more complex. Serum FTI values are relatively high during the first trimester and decline thereafter. In most reports, including the present study, the FTI or a related index declined to a level at term similar to that in nonpregnant women (9, 10, 12, 18, 23, 29).

The present study is consistent with other reports in that there was a significant correlation between serum hCGß or related proteins and the FTI (26, 30, 31, 32, 33, 34, 35). Although the correlation was not strong, it was similar to that noted by Foulk et al. (35) for the correlation between serum concentrations of intact hCG and free T4. High serum FTI values in the first trimester are sometimes attended by suppressed serum TSH concentrations, supporting the concept of first trimester thyroid activation (12, 15, 18, 36). The best example of this is seen in patients with hyperemesis gravidarum and the related syndrome of gestational thyrotoxicosis (32). Interestingly, in the present study, serum FTI concentrations were elevated in the first trimester, but none of the women had serum TSH concentrations below the normal range. Moreover, there was no significant relationship between relatively high FTI values and low serum TSH levels in the first trimester, even when the two subjects whose first trimester TSH was greater than 3.5 µU/mL were eliminated from the analysis. This was the case not only if absolute FTI values were employed but also if, to eliminate individual variation in basal FTI values, the value for the difference between the FTI during the first trimester and the FTI after delivery was employed to analyze the correlation. Kimura et al. (19) did observe a significant negative correlation between serum FTI concentrations in the first trimester and serum TSH values, but the correlation coefficient was only 0.47, and the correlation was particularly poor in subjects with the highest serum FTI concentrations. The results of the present study as well as that by Kimura et al. (19) raise the question of whether relatively high serum FTI concentrations noted in the first trimester always reflect thyroid stimulation. One way to assess this question would be to compare serum free T4 concentrations as determined by equilibrium dialysis with serum TSH concentrations. Such data are limited at this time. Yamamoto et al. (9) reported serum TSH and free T4 concentrations as determined by equilibrium dialysis in eight women. Serum free T4 concentrations were relatively high in the first trimester, and serum TSH concentrations were relatively low, but the overall correlation between mean T4 and mean TSH concentrations at different times of gestation was poor and not significant. In this study, serum free T4 concentrations declined only slightly during gestation and were elevated compared to nonpregnant control values at term. Another study (12) of serum free T4 concentrations during gestation did not provide data regarding basal serum TSH concentrations, but did report that the TSH response to TRH administration was blunted in a subset of women with high serum T4 concentrations who were scheduled for abortion in the first trimester. In this report (12), serum free T4 concentrations were elevated in the first trimester and declined to levels seen in nonpregnant women at term.

There are numerous studies of serum Tg concentrations in pregnant women (11, 13, 17, 18, 20, 21, 24, 29, 37, 38, 39). Tg concentrations have been reported to increase (17, 18, 21, 37, 38, 39), remain unchanged (24), or even decrease (13) during pregnancy. Increases in serum Tg during pregnancy are the rule in iodine-deficient regions. The present study was performed in individuals whose mean iodine intake was almost 600 µg/day. This is relatively high, even for regions that are considered iodine sufficient. The present study is consistent with that of Berghout et al. (24), who noted no change in serum Tg in women living in an iodine-sufficient area. The concept that iodine deficiency causes serum Tg concentrations to increase during pregnancy is supported by reports demonstrating that iodine supplementation during pregnancy ameliorates the increase in serum Tg (38, 39).

There are at least two influences of pregnancy on serum TSH concentrations. Insofar as serum TSH concentrations are suppressed by thyroid hypersecretion in the first trimester, this should result in serum TSH concentrations being higher in the third trimester that in the first trimester. In addition, reports from iodine-deficient regions indicate that maternal thyroid hormone deficiency is aggravated as gestation proceeds. In this setting, the gradual increase that occurs in serum TSH during gestation can, for the most part, be rectified by iodine supplementation (29, 39). The lack of an effect of pregnancy on serum TSH concentrations that was noted in the present study is consistent with the concept that maternal thyroid status is relatively stable during gestation unless iodine supplies are limited. Although increases in serum TSH and Tg occur together during pregnancy (29, 39), one study reported a decline in serum Tg in late pregnancy (13).

Early studies of PII concentrations in pregnancy relied on an indirect method that used urinary iodine measurements and the ratio of urinary and plasma 132I after iv injection of 132I (3). The present report is the first in which direct measurements of PII concentrations have been made during pregnancy and after delivery. Importantly, women in the present study did not receive iodine supplementation during pregnancy and, as noted above, their iodine intake was more than adequate. None of the differences in urinary iodine excretion was significant, and there was no relationship between mean urinary iodine excretion and mean PII concentrations. There was a marked variation in iodine intake and PII during pregnancy. This probably occurs on a day to day basis as well as from trimester to trimester. Given that variability, it was not unexpected that no significant differences among mean PII values during gestation or after delivery could be demonstrated. The fact that mean PII concentrations during pregnancy were actually slightly higher that those after delivery, however, suggests that pregnancy in regions of iodine sufficiency does not have an important influence on circulating iodide concentrations. Whether similar data for PII would be obtained in iodine-deficient regions is not clear, but this might occur more as a consequence of increases in TSH that, in turn, would augment thyroid iodide uptake than as an effect of pregnancy on renal iodide clearance. It should be noted that there are other mechanisms besides a decline in PII that could explain the propensity of goiter and thyroid insufficiency to develop in iodine-deficient regions. Thus, thyroid hormone requirements are increased during pregnancy (40, 41), and studies in rats indicate that iodine deficiency potentates the goitrogenic effect of TSH (42).

In conclusion, the present study is the first to report direct measurements of PII concentrations during pregnancy and after delivery. Pregnancy does not have an important influence on PII concentrations or thyroid status in iodine-sufficient regions. These studies, however, in no way negate the concept that adequate iodine during pregnancy is critical for optimal fetal thyroid function and development. The finding of elevated serum FTI but normal serum TSH concentrations in the first trimester is of interest but requires further study.


   Footnotes
 
1 This work was supported in part by Grant DK-18919 from the NIDDK, NIH (Bethesda, MD). Back

2 Current address: Brigham and Women’s Hospital, Genetics Division, Richardson-Fuller Building, Room 157, 221 Longwood Avenue, Boston, Massachusetts 02115 Back

Received April 17, 1998.

Revised June 12, 1998.

Accepted June 22, 1998.


   References
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

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Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals