Iodine Deficiency In Pregnant Women Research Articles

Thyroglobulin as a biomarker of iodine deficiency: a review.

Thyroglobulin, produced exclusively by the thyroid gland, has been proposed to be a more sensitive biomarker of iodine status than thyrotropin or the thyroid hormones triiodothyronine and thyroxine. However, evidence on the usefulness of thyroglobulin (Tg) to assess iodine status has not been extensively reviewed, particularly in pregnant women and adults. An electronic literature search was conducted using the Cochrane CENTRAL, Web of Science, PubMed, and Medline to locate relevant studies on Tg as a biomarker of iodine status. Since urinary iodine concentration (UIC) is the recommended method to assess iodine status in populations, only studies that clearly reported both Tg and UIC were included. For the purpose of this review, a median Tg <13 μg/L and a median UIC ≥100 μg/L (UIC ≥150 μg/L for pregnant women) were used to indicate adequate iodine status. We excluded studies conducted in subjects with either known thyroid disease or those with thyroglobulin antibodies. The search strategy and selection criteria yielded 34 articles of which nine were intervention studies. The majority of studies (six of eight) reported that iodine-deficient pregnant women had a median Tg ≥13 μg/L. However, large observational studies of pregnant women, including women with adequate and inadequate iodine status, as well as well-designed intervention trials that include both Tg and UIC, are needed. In adults, the results were equivocal because iodine-deficient adults were reported to have median Tg values of either <13 or ≥13 μg/L. Only studies in school-aged children showed that iodine-sufficient children typically had a median Tg <13 μg/L. Some of the inconsistent results may be partially explained by the use of different methodological assays and failure to assess assay accuracy using a certified reference material. These data suggest that Tg does hold promise as a biomarker of iodine deficiency. However, it is associated with limitations. A median Tg cutoff of 13 μg/L warrants further investigation, particularly in adults or pregnant women, as there is a lack of both observational and intervention studies in these groups.

Iodine insufficiency in pregnant women from the State of São Paulo.

The intake of adequate amounts of iodine during pregnancy is essential for the neurological development of the fetus. The aim of this study was to assess iodine nutrition status in pregnant women from the state of São Paulo, Brazil. We analyzed urinary iodine concentration (UIC) in 191 pregnant and 58 non-pregnant women matched by age. We used the World Health Organization criteria to define sufficient iodine supply (median UIC: 150-249 µg/L among pregnant women, and 100-199 µg/L for non-pregnant women). Median UIC of the pregnant women studied was lower than the recommended value (median = 137.7 µg/L, 95% CI = 132.9 - 155.9), while non-pregnant women had UIC levels within the appropriate range (median = 190 μg/L; 95% IC = 159.3-200.1). UIC was below 150 µg/L in 57% of the pregnant women. Although a larger sample is needed to consolidate these findings, these results raise concerns about the adequacy of the iodine supply of pregnant women in Brazil, especially considering the new determinations of the Brazilian government, which have recently reduced the concentrations of iodine in table salt to 15-45 mg/kg of salt.

Iodine deficiency in pregnant women living in the South East of the UK: the influence of diet and nutritional supplements on iodine status

Iodine is a key component of the thyroid hormones which are crucial for brain development. Adequate intake of iodine in pregnancy is important as in utero deficiency may have lifelong consequences for the offspring. Data on the iodine status of UK pregnant women are sparse, and there are no such data for pregnant women in the South East of the UK. A total of 100 pregnant women were recruited to a cross-sectional study carried out at the Royal Surrey County Hospital, Guildford, at their first-trimester visit for an ultrasound scan. The participants provided a spot-urine sample (for the measurement of urinary iodine concentration (UIC) and creatinine concentration) and 24h iodine excretion was estimated from the urinary iodine:creatinine ratio. Women completed a general questionnaire and a FFQ. The median UIC (85·3μg/l) indicated that the group was iodine deficient by World Health Organisation criteria. The median values of the iodine:creatinine ratio (122·9μg/g) and of the estimated 24h iodine excretion (151·2μg/d) were also suggestive of iodine deficiency. UIC was significantly higher in women taking an iodine-containing prenatal supplement (n 42) than in those not taking such a supplement (P<0·001). In the adjusted analyses, milk intake, maternal age and iodine-containing prenatal supplement use were positively associated with the estimated 24h urinary iodine excretion. Our finding of iodine deficiency in these women gives cause for concern. We suggest that women of childbearing age and pregnant women should be given advice on how to improve their iodine status through dietary means. A national survey of iodine status in UK pregnant women is required.

Iodine status as indited by neonatal thyroid stimulating hormone screening in Mitre Keluarga Hospital in Surabaya at 2005-2010

Iodine Deficiency Disorders (IDD) is a significant public health problem in the world. One of the consequences of iodine deficiency is subclinical hypothyroidism during pregnancy and early infancy. Neonatal thyroid screening using serum thyrotropin (TSH) to detect hypothyroidism may also be used to monitor the prevalence of IDD. We aim to evaluate iodine status by neonatal TSH screening in Mitra Keluarga Surabaya Hospital (RSMKS) from year 2005 to 2010. The study was a cross sectional, hospital-based, and non-interventional in RSMKS conducted from January 2005 to December 2010. Out of the 5619 babies born, 3354 (59.7%) healthy babies with parent’s agreement took part in this study. Blood specimens for TSH measurement were collected between 2 to 6 days after birth and sent to a reference laboraratory. The neonatal TSH values were analysed for iodine deficiency on the basis of WHO/UNICEF/International Council for the Control of IDD criteria. A total of 3349 newborn babies undergone neonatal TSH screening in RSMKS. The mean of TSH concentration was 5.14 mIU/L. About 1270 (37.9%) had TSH concentration >5mIU/L. There were 166 (27.6%) in 2005, 252 (44.0%) in 2006, 331 (47%) in 2007, 356 (57.5%) in 2008, 114 (20.7%) in 2009 and 51 (16.7%) in 2010 respectively. 22 neonates had TSH >20 mIU/L. Only 2 babies were confirmed positive for hypothyroidism. Newborn babies in RSMKS from January 2005 to December 2010 is categorised as IDD ranging from mild to severe.This research can be developed further to allow plans for screening of iodine deficiency in pregnant women as well as their newborn babies.

Effect of iodine supplementation during pregnancy on neonatal thyroid stimulating hormone

Background Thyroid hormone is essential for neurological development, particularly in the developing brain. Iodine is the important constituent of thyroid hormone. Its requirement during pregnancy is increased. Elevated neonatal thyroid stimulating hormone (TSH) is a sensitive indicator of iodine insufficiency in pregnant women. Our previous study in the year 2000 demonstrated that median urine iodine (UI) concentration in pregnant women was 85 μg/ L, a level of which indicates mild iodine deficiency. Since October 2010, Thai national universal iodine supplementation program has been started by prescribing a 150 μgiodine tablet daily to all pregnant women throughout their gestation. We, therefore, aimed to determine the effect of maternal iodine supplementation on neonatal TSH.

Overweight increases risk of first trimester hypothyroxinaemia in iodine‐deficient pregnant women

Hypothyroxinaemia early in pregnancy may impair fetal brain development. Increased body weight has been associated with low thyroxine concentrations in non-pregnant women. In pregnant women, morbid maternal obesity is a risk factor for thyroid dysfunction. But whether lesser degrees of overweight that are much more common could be a risk factor for hypothyroxinaemia in pregnancy is unclear. The objective of this study was to investigate if overweight increases risk for thyroid dysfunction, and specifically hypothyroxinaemia, in iodine-deficient pregnant women. We performed a cross-sectional study at first hospital visit among healthy Thai pregnant women. We measured weight and height, urinary iodine concentration (UIC), serum thyroid hormones and thyroglobulin. Pre-pregnancy weight and relevant dietary factors were determined by questionnaire, and body mass index (BMI) was used to classify weight status. Among 514 women (mean gestational age, 11 weeks) with a median UIC of 111 μg dL(-1) , indicating mild iodine deficiency, 12% had low free thyroxine (fT4) concentrations: 3% had overt hypothyroidism; 7% had subclinical hypothyroidism; and 8% had isolated hypothyroxinaemia. Based on pre-pregnancy BMI, 26% of women were overweight or obese. In a multiple regression model, BMI was a negative predictor of fT4 (β = -0.20, P < 0.001). Compared to normal weight women, the prevalence ratio (95% CI) of a low fT4 in overweight women was 3.64 (2.08-6.37) (P < 0.01). Iodine-deficient pregnant Thai women who are overweight have a 3.6-fold higher risk of hypothyroxinaemia in the first trimester compared to normal weight women. Targeted screening should consider overweight a potential risk factor for thyroid dysfunction in pregnant women in iodine-deficient areas.

A Unique Child: Health - A guide to … iodine deficiency

Research shows that iodine deficiency in pregnant women can impair a child's cognitive development. Ruth Thomson examines the impacts of the deficiency and outlines what can be done to prevent it.

Iodine Supplementation throughout Pregnancy Does Not Prevent the Drop in FT4 in the Second and Third Trimesters in Women with Normal Initial Thyroid Function

Objectives: The aim of the study was to determine the evolution of thyroid tests throughout pregnancy and postpartum in healthy women with and without iodine supplementation. Methods: This was a prospective, randomized, interventional study of iodine supplementation (150 μg/day) from the first trimester until 3 months postpartum versus controls. 111 pregnant women with normal initial thyroid tests were enrolled, undergoing comprehensive thyroid assessment at each trimester. We present results of longitudinal and cross-sectional analyses. Results: Initial ioduria suggested mild iodine deficiency in both groups, while third-trimester ioduria rose to levels of iodine sufficiency in the iodine-supplemented group. In the longitudinal study, free T4 (FT4) levels decreased in the second and third trimesters compared to the first trimester in both groups, with no change in TSH, and rose postpartum, though lower than the first trimester. FT3 levels and the total T4 (TT4)/thyroxine-binding globulin (TBG) ratio followed the same evolution as FT4. TT4 levels rose due to TBG increase. Thyroglobulin (Tg) of iodine group remained stable, contrasting with the rise in the control group. In the cross-sectional study, there was no difference between the two groups in thyroid tests at any time-point, except for lower Tg in the second trimester and postpartum visits in the iodine group. Conclusions: In healthy, mildly iodine-deficient pregnant women, a ‘drop' of FT4 and TT4/TBG without TSH increase occurs between the first and second trimesters, and is not prevented by iodine supplementation, suggesting physiology. Therefore, FT4 is valuable to assess thyroid function in pregnancy in clinical practice with appropriate trimester-specific reference range. It brings up reflection on threshold for diagnosis and treatment of hypothyroxinemia.

Effect of inadequate iodine status in UK pregnant women on cognitive outcomes in their children: results from the Avon Longitudinal Study of Parents and Children (ALSPAC)

As a component of thyroid hormones, iodine is essential for fetal brain development. Although the UK has long been considered iodine replete, increasing evidence suggests that it might now be mildly iodine deficient. We assessed whether mild iodine deficiency during early pregnancy was associated with an adverse effect on child cognitive development. We analysed mother-child pairs from the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort by measuring urinary iodine concentration (and creatinine to correct for urine volume) in stored samples from 1040 first-trimester pregnant women. We selected women on the basis of a singleton pregnancy and availability of both a urine sample from the first trimester (defined as ≤13 weeks' gestation; median 10 weeks [IQR 9-12]) and a measure of intelligence quotient (IQ) in the offspring at age 8 years. Women's results for iodine-to-creatinine ratio were dichotomised to less than 150 μg/g or 150 μg/g or more on the basis of WHO criteria for iodine deficiency or sufficiency in pregnancy. We assessed the association between maternal iodine status and child IQ at age 8 years and reading ability at age 9 years. We included 21 socioeconomic, parental, and child factors as confounders. The group was classified as having mild-to-moderate iodine deficiency on the basis of a median urinary iodine concentration of 91·1 μg/L (IQR 53·8-143; iodine-to-creatinine ratio 110 μg/g, IQR 74-170). After adjustment for confounders, children of women with an iodine-to-creatinine ratio of less than 150 μg/g were more likely to have scores in the lowest quartile for verbal IQ (odds ratio 1·58, 95% CI 1·09-2·30; p=0·02), reading accuracy (1·69, 1·15-2·49; p=0·007), and reading comprehension (1·54, 1·06-2·23; p=0·02) than were those of mothers with ratios of 150 μg/g or more. When the less than 150 μg/g group was subdivided, scores worsened ongoing from 150 μg/g or more, to 50-150 μg/g, to less than 50 μg/g. Our results show the importance of adequate iodine status during early gestation and emphasise the risk that iodine deficiency can pose to the developing infant, even in a country classified as only mildly iodine deficient. Iodine deficiency in pregnant women in the UK should be treated as an important public health issue that needs attention. None.

Iodine deficiency in the UK: an overlooked cause of impaired neurodevelopment?

This review describes historical iodine deficiency in the U.K., gives current information on dietary sources of iodine and summarises recent evidence of iodine deficiency and its association with child neurodevelopment. Iodine is required for the production of thyroid hormones that are needed for brain development, particularly during pregnancy. Iodine deficiency is a leading cause of preventable brain damage worldwide and is associated with impaired cognitive function. Despite a global focus on the elimination of iodine deficiency, iodine is a largely overlooked nutrient in the U.K., a situation we have endeavoured to address through a series of studies. Although the U.K. has been considered iodine-sufficient for many years, there is now concern that iodine deficiency may be prevalent, particularly in pregnant women and women of childbearing age; indeed we found mild-to-moderate iodine deficiency in pregnant women in Surrey. As the major dietary source of iodine in the U.K. is milk and dairy produce, it is relevant to note that we have found the iodine concentration of organic milk to be over 40% lower than that of conventional milk. In contrast to many countries, iodised table salt is unlikely to contribute to U.K. iodine intake as we have shown that its availability is low in grocery stores. This situation is of concern as the level of U.K. iodine deficiency is such that it is associated with adverse effects on offspring neurological development; we demonstrated a higher risk of low IQ and poorer reading-accuracy scores in U.K. children born to mothers who were iodine-deficient during pregnancy. Given our findings and those of others, iodine status in the U.K. population should be monitored, particularly in vulnerable subgroups such as pregnant women and children.

Monitoring and effects of iodine deficiency in pregnancy: still an unsolved problem?

Iodine is required for the production of thyroid hormone. Thyroid hormone affects many metabolic processes in the body, including maturation of the central nervous system. In early pregnancy, the fetus is dependent on maternal thyroid hormone for normal brain development. If iodine deficiency leads to inadequate production of thyroid hormone during pregnancy, irreversible brain damage can result in the fetus. Therefore, achieving adequate iodine nutrition during pregnancy is an important public health objective. Although there have been tremendous gains over the last several decades in our understanding of the effects of iodine deficiency in pregnancy and how to combat them, a number of questions remain about how best to monitor the iodine status of pregnant populations, the effects of mild to moderate iodine deficiency on maternal and child outcomes, the safe upper limit of daily iodine intake in pregnant women and the risks and benefits of iodine supplementation for mildly iodine-deficient pregnant women.

Iodine deficiency among Belgian pregnant women not fully corrected by iodine-containing multivitamins: a national cross-sectional survey

Low iodine intake during pregnancy may cause thyroid dysfunction in pregnant women and their newborn. In the present study, iodine status among a nation-wide representative sample of Belgian pregnant women in the first and third trimester of pregnancy was determined, and determinants of iodine status were assessed 1 year after the introduction of bread fortified with iodised salt. The women were selected according to a multistage proportionate-to-size sampling design. Urine samples were collected and a general questionnaire was completed face to face with the study nurse. The median urinary iodine concentration (UIC) among pregnant women (n 1311) was 124.1mg/l and 122.6 mg/g creatinine when corrected for urinary creatinine. The median UIC in the first trimester (118.3 mg/l) was significantly lower than that in the third trimester (131.0 mg/l) but significantly higher than among non-pregnant women (84.8 mg/l). Iodine-containing supplement intake was reported by 60.8% of the women and 57.4% of the women took this supplement daily. The risk of iodine deficiency was significantly higher in younger women, in women not taking iodine-containing supplements, with low consumption of milk and dairy drinks and during autumn. Women with a higher BMI had a higher risk of iodine deficiency but the risk was lower in women who reported alcohol consumption. The median UIC during pregnancy indicates iodine deficiency in Belgium and some women are at a higher risk of deficiency. The current low iodine intake in women of childbearing age precludes the correction of iodine deficiency in pregnant women supplemented with multivitamins containing 150 mg iodine as recommended.

Iodine deficiency in pregnant women in the apparently iodine‐sufficient capital city of Turkey

Previous studies of the current iodine status in Turkey have yielded contradictory results. Although urinary iodine concentration (UIC) in school age children (SAC) suggests sufficient iodine status, studies on neonatal thyroid-stimulating hormone (TSH) indicate that iodine deficiency is a continuing problem. We aimed to assess the iodine nutritional status of pregnant women living in Ankara, an area that has appeared to be iodine sufficient in earlier studies. Hospital-based, noninterventional, prospective, cross-sectional study. A total of 162 pregnant women in their second trimester were examined regarding iodized salt use, UIC, presence or absence of goitre and thyroid function. Goitre status was determined by palpation. UIC was measured using colorimetric method based on Sandell-Kolthoff reaction. Thyroid hormones and TSH were measured by chemiluminescence immunoassays. While the proportion of iodized salt use was 80·2%, UIC was below 150 μg/l in 72·8% of the women. The median UIC was 80·5 (8·9-340·3) μg/l, indicating insufficient iodine intake. Total goitre rate was 15·4%. Preferential T3 secretion reflected by elevated molar ratios of FT3/FT4 was present in 89·5% of the women. 12·4% had subclinical hypothyroidism or isolated hypothyroxinaemia based on serum TSH and FT4 levels. Our study shows that iodine deficiency is a serious problem among pregnant women in Ankara. These data confirm that iodine nutritional status among SAC does not reflect the iodine supply for pregnant women. We propose that nationwide surveillance studies should urgently be performed to directly assess and monitor the iodine status of pregnant women. We also consider that pregnant women in Turkey should be supplemented by iodine-containing preparations in addition to iodized salt.

Prenatal iodine deficiency results in structurally and functionally immature lungs in neonatal rats

Maternal hypothyroidism affects postnatal lung structure. High prevalence of hypothyroxinemia (low T4, normal T3) in iodine-deficient pregnant women and associated risk for neuropsychological development along with high infant/neonatal mortality ascribed to respiratory distress prompted us to study the effects of maternal hypothyroxinemia on postnatal lung development. Female Sprague Dawley rats were given a low-iodine diet (LID) with 1% KClO(4) in drinking water for 10 days, to minimize thyroid hormone differences. Half of these rats were continued on iodine-deficient diet; ID (LID with 0.005% KClO(4)) for 3 mo, whereas the rest were switched to an iodine-sufficient diet; IS [LID + potassium iodide (10 μg iodine/20 g of diet + normal drinking water)]. Pups born to ID mothers were compared with age-matched pups from IS mothers at postnatal days 8 (P8) and 16 (P16) (n = 6-8/group). ID pups had normal circulating T3 but significantly low T4 levels (P < 0.05) and concomitantly approximately sixfold higher thyroid hormone receptor-β mRNA in alveolar epithelium. Lung histology revealed larger and irregularly shaped alveoli in ID pups relative to controls. Lung function was assessed at P16 using a double-chambered plethysmograph and observed reduced tidal volume, peak inspiratory and expiratory flow, and dynamic lung compliance in ID pups compared with IS pups. Significant lowering of surfactant protein (SP)-B and SP-C mRNA and protein found in ID pups at P16. ID pups had 16-fold lower matrix metalloproteinase-9 mRNA levels in their alveolar epithelium. In addition, mRNA levels of thyroid transcription factor-1 and SP-D were significantly higher (3-fold) compared with IS pups. At P16, significantly lower levels of SP-B and SP-C found in ID pups may be responsible for immature lung development and reduced lung compliance. Our data suggest that maternal hypothyroxinemia may result in the development of immature lungs that, through respiratory distress, could contribute to the observed high infant mortality in ID neonates.

Iodine Deficiency in Northern Paris Area: Impact on Fetal Thyroid Mensuration

IntroductionIodine is essential for normal fetal and neonatal development. We studied the prevalence and impact on fetal thyroid development of iodine deficiency in pregnant women in the northern part of the Paris conurbation.Materials and Methods110 patients underwent several determinations of urinary iodine excretion (UIE) and of serum FT4, FT3, and TSH. Fetal thyroid gland size was assessed using ultrasonography.ResultsWe found evidence of widespread iodine deficiency (mean UIE, 49.8 µg/L [standard deviation, 2.11]). Iodine deficiency did not correlate significantly with maternal thyroid parameters but showed a significant negative correlation with fetal thyroid gland size (rho = 0.25, P = 0.02).ConclusionIodine deficiency during pregnancy is still a problem in our geographical area and affects the fetal thyroid gland.Clinical Trials.gov NCT00162539

Iodine intakes of 100–300 μg/d do not modify thyroid function and have modest anti-inflammatory effects

Little information is available as to whether doses of iodide similar to those recommended in clinical practice for the prevention of iodine deficiency in pregnant women affect thyroid function. The aim of the present study was to analyse whether doses of iodide can affect thyroid function in adults, and evaluate its effect on plasma markers of oxidative stress, inflammation and acute-phase proteins. A total of thirty healthy volunteers (ten men and twenty women) with normal thyroid function were randomly assigned to three groups (n 10). Each group received a daily dose of 100, 200 or 300μg of iodide in the form of KI for 6 months. Free tetraiodothyronine (FT4) levels at day 60 of the study were higher in the groups treated with 200 and 300μg (P=0·01), and correlated with the increase in urinary iodine (r 0·50, P=0·007). This correlation lost its significance after adjustment for the baseline FT4. The baseline urinary iodine and FT4 correlated positively with the baseline glutathione peroxidase. On day 60, urinary iodine correlated with C-reactive protein (r 0·461, P=0·018), and free triiodothyronine correlated with IL-6 (r -0·429, P=0·025). On day 60, the changes produced in urinary iodine correlated significantly with the changes produced in α1-antitrypsin (r 0·475, P=0·014) and ceruloplasmin (r 0·599, P=0·001). The changes in thyroid-stimulating hormone correlated significantly with the changes in α1-antitrypsin (r -0·521, P=0·005) and ceruloplasmin (r -0·459, P=0·016). In conclusion, the administration of an iodide supplement between 100 and 300μg/d did not modify thyroid function in a population with adequate iodine intake. The results also showed a slight anti-inflammatory and antioxidative action of iodide.

Iodine deficiency in pregnant women in the ACT

In response to growing concern of an iodine deficiency emergence in Australia, this study was conducted to document the iodine status of pregnant women in the ACT. One hundred women presenting to the antenatal clinic at The Canberra Hospital answered a brief dietary questionnaire and provided a spot urine sample for the measurement of urine iodine excretion. The results revealed that the majority of women were consuming a diet low in iodine, confirmed by suboptimal concentrations of iodine in their urine.

Perchlorate and Thiocyanate Exposure and Thyroid Function in First-Trimester Pregnant Women

Thyroid hormone, requiring adequate maternal iodine intake, is critical for fetal neurodevelopment. Perchlorate decreases thyroidal iodine uptake by competitively inhibiting the sodium/iodide symporter. It is unclear whether environmental perchlorate exposure adversely affects thyroid function in pregnant women. Thiocyanate, derived from foods and cigarette smoke, is a less potent competitive sodium/iodide symporter inhibitor than perchlorate. Our objective was to determine whether environmental perchlorate and/or thiocyanate exposure is associated with alterations in thyroid function in pregnancy. We conducted a cross-sectional study at health centers in Cardiff, Wales, and Turin, Italy. During 2002-2006, 22,000 women at less than 16 wk gestation were enrolled in the Controlled Antenatal Thyroid Screening Study. Subsets of 261 hypothyroid/hypothyroxinemic and 526 euthyroid women from Turin and 374 hypothyroid/hypothyroxinemic and 480 euthyroid women from Cardiff were selected based on availability of stored urine samples and thyroid function data. Urinary iodine, thiocyanate, and perchlorate and serum TSH, free T(4) (FT(4)), and thyroperoxidase antibody were measured. Urinary iodine was low: median 98 microg/liter in Cardiff and 52 microg/liter in Turin. Urine perchlorate was detectable in all women. The median (range) urinary perchlorate concentration was 5 microg/liter (0.04-168 microg/liter) in Turin and 2 microg/liter (0.02-368 microg/liter) in Cardiff. There were no associations between urine perchlorate concentrations and serum TSH or FT(4) in the individual euthyroid or hypothyroid/hypothyroxinemic cohorts. In multivariable linear analyses, log perchlorate was not a predictor of serum FT(4) or TSH. Low-level perchlorate exposure is ubiquitous but did not affect thyroid function in this cohort of iodine-deficient pregnant women.

Iodine deficiency in pregnant women living in the South-East of the UK

Iodine deficiency in pregnant women living in the South-East of the UK

Prévention des désordres thyroïdiens au cours de la grossesse

Iodine is essential for biosynthesis of thyroid hormones and daily iodine intake needs are increased during pregnancy. Thyroid dysfunctions (hypothyroidism, hyperthyroidism) are due to autoimmune diseases (Hashimoto's disease, Graves' disease) in most women of childbearing age. During pregnancy they are associated with maternal and fetal complications: maternal hypothyroxinemia during the first trimester of gestation can be associated with abnormal cognitive development and intellectual outcomes in the newborn and the children. In patients with Graves' disease, TSH-receptor antibodies cross the placenta and can induce fetal and neonatal dysfunctions. In order to prevent maternal and fetal complications and ameliorate the pronostic of thyroid disorders in pregnant women, the prevention should be: a systematic prophylaxis of iodine deficiency in pregnant women; an adjustment of the preconception levothyroxine treatment in women with hypothyroidism diagnosed before the pregnancy; a targeted screening for maternal hypothyroidism in high-risk women; a rational measurement for TSH-receptor and anti-thyroperoxydase antibodies in some women with autoimmune thyroid diseases.