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ORIGINAL ARTICLE
Year : 2012  |  Volume : 9  |  Issue : 1  |  Page : 15-18

Screening for thyroid dysfunction during pregnancy


1 Department of Physiology, NKPSIMS and Lata Mangeshkar Hospital, Nagpur, Maharashtra, India
2 Pitale Diabetes and Hormone Center, Dhantoli, Nagpur, Maharashtra, India

Date of Web Publication28-Jan-2012

Correspondence Address:
Anagha Sahasrabuddhe
5, Charushree Apartments, Khare Town, Dharampeth, Nagpur, 440 010, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-0354.92391

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  Abstract 

Introduction: Thyroid disorders are among the common endocrine disorders in pregnant women. It is now well established that not only overt but subclinical thyroid dysfunction can also have adverse effects on fetal and maternal outcome. Maternal hypothyroidism during pregnancy raises serious concern about long-lasting psycho-neurologic consequences for the progeny, due to the risk of insuf-ficient placental transfer of maternal thyroid hormones to the developing fetus during the first half of gestation. To validate the need of antenatal screening for maternal thyroid dysfunction this study was undertaken to know the prevalence of thyroid dysfunction among pregnant women in Central India. Materials and Methods: In this ongoing study so far 73 patients in the first trimester of pregnancy have been recruited from Matru Seva Sangh Hospital. Detailed history and examination were done. Serum thyroid-stimulating hormone (TSH) estimation was done by the immunoradiometric assay method. Results: Out of 73 patients, 30 (41%) had TSH less than 2 mIU/ml, 35 out of 73 (47.95%) had TSH between 2 mIU/ml and 4 mIU/ml. The TSH value of more than or equal to 4 mIU/ml was seen in 8/73 (10.96%). Two patients also had gestational diabetes. TSH levels were more than 2 in both. Conclusions: Prevalence of hypothyroidism is more than 10%. As per recommendations all patients with TSH levels more than 2 should be evaluated for free T4 and thyroid antibody estimation. Screening for thyroid dysfunction should be done early in pregnancy. Looking at the high percentage of abnormal TSH in pregnancies, universal screening should be considered.

Keywords: Hypothyroidism, thyroid-stimulating hormone, thyroid dysfunction


How to cite this article:
Sahasrabuddhe A, Pitale S. Screening for thyroid dysfunction during pregnancy. Thyroid Res Pract 2012;9:15-8

How to cite this URL:
Sahasrabuddhe A, Pitale S. Screening for thyroid dysfunction during pregnancy. Thyroid Res Pract [serial online] 2012 [cited 2019 Jun 19];9:15-8. Available from: http://www.thetrp.net/text.asp?2012/9/1/15/92391


  Introduction Top


Infants born to hypothyroid mothers appear healthy and without evidence of thyroid dysfunction, provided that there should be no previous severe iodine deficiency in utero. Thyroid disorders are among the common endocrine disorders in pregnant women. It is now well established that not only overt but also subclinical thyroid dysfunction can have adverse effects on fetal and maternal outcome. Maternal hypothyroidism during pregnancy raises serious concern about long-lasting psycho-neurologic consequences for the progeny, due to the risk of insufficient placental transfer of maternal thyroid hormones to the developing fetus during the first half of gestation. To validate the need of antenatal screening for maternal thyroid dysfunction this study was undertaken to know the prevalence of thyroid dysfunction among pregnant women in central India.


  Materials and Methods Top


In this ongoing study so far 73 patients in the first trimester have been recruited from Matru Seva Sangh Hospital. Prior approval of Ethics Committee was sought. The participants consented voluntarily before the procedures were done. Detail history and examination were done. A blood sample was taken and Serum thyroid-stimulating hormone (TSH) estimation was done by the IRMA method using a immunotech kit.


  Results Top


Mean age of the patients was 23 ± 2.6 years (19-33 years). Out of 73 patients, 30 (41%) had TSH less than or equal to 2 mIU/ml, 35 out of 73 (47.95%) had TSH between 2 mIU/ml and 4 mIU/ml. A TSH value of more than or equal to 4 mIU/ml was seen in 8/73 (10.96%) [Figure 1]. Two patients also had gestational diabetes. TSH levels were more than 2 in both. Pregnancy-induced hypertension was seen in four patients. Family history of thyroid dysfunction was present in 6 out of 73 patients; 2 of these subjects had TSH less than 2 mIU/ml, 1 had TSH between 2-4 mIU/ml, and 3 had TSH above 4 mIU/ml.
Figure 1: Thyroid-stimulating hormone distribution. 1st qtr - 41% TSH less than 2 mIU/ml, 2nd qtr - 47.95% TSH between 2-4 mIU/ml, 3rd qtr - 10.96% TSH more than or equal to 4 mIU/ml was seen in (10.96%)

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  Discussion Top


Development of fetal brain (with neuronal multiplication, migration and architectural organization) during the second trimester corresponds to a phase during which the supply of thyroid hormones to the growing fetus is almost exclusively of maternal origin. During later phases of fetal development (with glial cell multiplication, migration, and myelination) from the third trimester onward, the supply of thyroid hormone to the fetus is essentially of fetal origin. [1] The euthyroid status is important during the first and second trimesters of pregnancy for optimal fetal neuronal development. Suboptimal maternal thyroid functioning indicated by high levels of TSH may have detrimental effects on the fetal brain development and IQ. Thyroid disease has multiple deleterious impacts on pregnancy, the postpartum, and the developing fetus. Complications include miscarriage, [2],[3],[4],[5],[6] decreased intelligence quotient, [7],[8] visual-motor deficiencies in the offspring, [9] preterm delivery, [10],[11] and postpartum thyroiditis [12],[13],[14] Hence prenatal screening TSH in early pregnancy is important for good pregnancy outcome.

In our ongoing study (73 patients recruited till now) we found that49% of the patients have TSH levels above the recommended guidelines in the first trimester. In our study antibody status of the pregnant subjects was not done. Positive thyroid antibodies during pregnancy warrants treatment at a lower TSH level (2-4 mIU/ml) [1]

Studies have reported adverse perinatal outcomes, maternal complications, and caesserian section as an indication for fetal distress is significantly high among women with subclinical hypothyroidism which reinforces the importance of detecting subclinical thyroid disorders in pregnancy. [15]

A study has reported 43% of the TSH values at or above the recently recommended guidelines in the first trimester (2.5 mU/l), as opposed to 33% of the values in the second trimester (3.0 mU/l). Twenty percent of the TSH values at or above a less restrictive 98th percentile of normal in the first trimester, as opposed to 23% of the values in the second trimester. Mean TSH levels are higher in women with antibodies. [16] The findings of our study match with this study. However, antibody status was not looked at in our study.

Women with otherwise unexplained previous pregnancy losses probably should be treated if their TSH level is above 2.5 mIU/l and/or they have a positive test for antibodies. During pregnancy, a 30-40% increased need for thyroid hormones is the result of increased placental uptake, higher thyroid-binding globulin levels, and greater blood volume. Those with subclinical hypothyroidism and/or high-normal TSH levels at the beginning of pregnancy may not be able to meet these needs and may show signs of thyroid insufficiency during pregnancy. The pregnancy loss rate was 3.6% in women with a TSH level of < 2.5 mIU/l, and 6.1% in women with TSH levels between 2.5 mIU/l and 5.0 mIU/l. This difference was statistically significant. The risk for miscarriage increased by 15% for each 1 mIU/l elevation of the TSH level on the basis of logistic regression analysis. [17]

Screening recommendations suggest that screening should be done with TSH only and fT3 and fT4 if required. Whether universal screening or screening high risk women should be practiced is not yet settled. A message from the study of Vaidya et al. commented that 30% women with thyroid dysfunction remain undiagnosed. [18] High risk women who should be definitely screened are those with history of hypo/hyperthyroidism or thyroid lobectomy or postpartal thyroiditis, family history of thyroiditis, goiter, thyroid autoantibodies, symptoms, signs or biochemical markers suggestive of thyroid disease, type-1 diabetes, other autoimmune disorders, infertility, previous head or neck irradiation, history of miscarriage or preterm delivery. [18]

There is no consensus whether universal screening should be done; however one more study has pointed out that over half (55%) of pregnant women with abnormalities suggestive of autoimmune thyroiditis and/or hypothyroidism would be missed if only those with high-risk criteria were examined. A more extensive screening of thyroid autoimmunity and dysfunction seems warranted. [19] This study was carried out in 400 pregnant females between 9 and 11 weeks of gestation. Twenty-seven cases of child loss were observed. The mean TSH and FT 4 levels in the women with child loss were 1.48 mU/l and 9.82 pmol/l compared with 1.11 mU/l and 9.58 pmol/l in women without child loss. The incidence of child loss increased by 60% (OR=1.60 (95% confidence interval (CI): 1.04-2.47)) for every doubling in TSH concentration. This association remained after adjustment for smoking, age, parity, diabetes mellitus, hypertension, previous preterm deliveries, and previous preterm stillbirth/miscarriage (adjusted odds ratio=1.80 (95% CI: 1.07-3.03)). This was not true for FT 4 concentrations (OR=1.41 (95% CI: 0.21-9.40); P=0.724). [19]

Few studies have also pointed that no significant differences were seen in adverse outcomes between the case-finding and universal screening groups. Adverse outcomes were less likely to occur among low-risk women in the screening group than those in the case-finding group. [20]

One more prospective randomized trial of case-finding versus universal screening for thyroid dysfunction in pregnancy was performed. Universal screening compared with case finding did not result in a decrease in adverse outcomes. Low-risk women in the universal screening group had fewer overall adverse outcomes than low-risk women in the case-finding group; moreover, more low-risk women in the universal screening group with abnormal thyroid function (who were treated) avoided any adverse outcome more often than low-risk women in the case-finding group with abnormal thyroid function (who were not detected and therefore not treated). The study demonstrated that whereas universal screening did not result in a decrease in adverse outcomes, treatment of identified thyroid hormonal abnormalities during pregnancy results in a significant decrease in adverse outcomes. Our study confirms that case finding fails to detect the majority of pregnant women with thyroid disease. A comprehensive cost-effectiveness analysis is required to resolve the debate of universal screening for thyroid disease in pregnancy. [21]


  Conclusions Top


TSH levels more than trimester-specified normal values were observed in more than 10% of our patients. Even though universal TSH screening is not yet a recommendation, it should be considered in view of results shown by different studies. Screening for thyroid dysfunction should be done early in pregnancy. Looking at the high percentage of abnormal TSH in pregnancies, universal screening should be considered.

 
  References Top

1.Glinoer D. Thyroid disease during pregnancy in Werner and Ingbar's The Thyroid A Fundamental and Clinical Text. In: Braverman L, Utiger R, editors. 9 th ed. Philadelphia: Lippincott Williams and Wilkins; 2004.   Back to cited text no. 1
    
2.Stagnaro-Green A, Roman SH, Cobin RH, el-Harazy E, Alvarez-Marfany M, Davies TF. Detection of at-risk pregnancy by means of highly sensitive assays for thyroid autoantibodies. JAMA 1990;264:1422-5.   Back to cited text no. 2
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3.Glinoer D, Soto MF, Bourdoux P, Lejeune B, Delange F, Lemone M, et al. Pregnancy in patients with mild thyroid abnormalities: Maternal and neonatal repercussions. J Clin Endocrinol Metab 1991:73:421-7.  Back to cited text no. 3
    
4.Prummel MF, Wiersinga WM, Thyroid autoimmunity and miscarriage. Eur J Endocrinol 2004;150:751-5.   Back to cited text no. 4
    
5.Abalovich M, Gutierrez S, Alcaraz G, Maccallini G, Garcia A, Levalle O. Overt and subclinical hypothyroidism complicating pregnancy. Thyroid 2002;12:63-8.  Back to cited text no. 5
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6.Allan WC, Haddow JE, Palomaki GE, Williams JR, Mitchell ML, Hermos RJ, et al. Maternal thyroid deficiency and pregnancy complications: implications for population screening. J Med Screen 2000;7:127-30.   Back to cited text no. 6
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7.Haddow JE, Palomaki GE, Allan WC, Williams JR, Knight GJ, Gagnon J, et al. Maternal thyroid deficiency during pregnancy and subsequent neuropsychological development of the child. N Engl J Med 1999;341:549-55.  Back to cited text no. 7
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8.Pop VJ, Kuijpens JL, van Baar AL, Verkerk G, van Son MM, de Vijlder JJ, et al. Low maternal free thyroxine concentrations during early pregnancy are associated with impaired psychomotor development in infancy. Clin Endocrinol (Oxf) 1999;50:149-55.  Back to cited text no. 8
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9.Zoeller RT, Rovet J. Timing of thyroid hormone action in the developing brain: Clinical observations and experimental findings. J Neuroendocrinol 2004;16:809-18.  Back to cited text no. 9
    
10.Casey BM, Dashe JS, Wells CE, McIntire DD, Byrd W, Leveno KJ, et al. Subclinical hypothyroidism and pregnancy outcomes. Obstet Gynecol 2005;105:239-45.   Back to cited text no. 10
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11.Stagnaro-Green A, Chen X, Bodgen JD, Davies TF, Scholl TO. The thyroid and pregnancy: a novel risk factor for very preterm delivery. Thyroid 2005;15:351-7.  Back to cited text no. 11
    
12.Stagnaro-Green A, Roman SH, Cobin RH, el-Harazy E, Wallenstein S, Davies TF. A prospective study of lymphocyte-initiated immunosuppression in normal pregnancy: Evidence of a T-cell etiology for postpartum thyroid dysfunction. J Clin Endocrinol Metab 1992;74:645-53.   Back to cited text no. 12
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13.Alvarez-Marfany M, Roman SH, Drexler AJ, Robertson C, Stagnaro-Green A. Long-term prospective study of postpartum thyroid dysfunction in women with insulin dependent diabetes mellitus. J Clin Endocrinol Metab 1994;79:10-6.  Back to cited text no. 13
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14.Nicholson WK, Robinson KA, Smallridge RC, Ladenson PW, Powe NR. Prevalence of postpartum thyroid dysfunction: A quantitative review. Thyroid 2006;16:573-82.   Back to cited text no. 14
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15.Sahu MT, Das V, Mittal S, Agarwal A, Sahu M. Overt and subclinical thyroid dysfunction among Indian pregnant women and its effecton maternal and fetal outcome. Arch Gynaecol Obstet 2010;281:215-20.   Back to cited text no. 15
    
16.McClain MR, Lambert-Messerlian G, Haddow JE, Palomaki GE, Canick JA, Cleary-Goldman J, et al. Sequential first- and second-trimester TSH, free thyroxine, and thyroid antibody measurements in women with known hypothyroidism: A FASTER trial study. Am J Obstet Gynecol 2008;199;129.e1-6.  Back to cited text no. 16
    
17.Negro R, Schwartz A, Gismondi R, Tinelli A, Mangieri T, Stagnaro-Green A. Increased Pregnancy Loss Rate in Thyroid Antibody Negative Women With TSH Levels Between 2.5 and 5.0 in the First Trimester of Pregnancy. J Clin Endocrinol Metab 2010;95:E44-48  Back to cited text no. 17
    
18.Banerjee S. Thyroid disorders in pregnancy. J Assoc Physicians India 2011;59 Suppl:32-4.  Back to cited text no. 18
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19.Horacek J, Spitalnikova S, Dlabalova B, Malirova E, Vizda J, Svilias I, et al. Universal screening detects two-times more thyroid disorders in early pregnancy than targeted high-risk case finding. Eur J Endocrinol 2010;163;645-50.  Back to cited text no. 19
    
20.Benhadi N, Wiersinga WM, Reitsma JB, Vrijkotte TG, Bonsel GJ. Higher maternal TSH levels in pregnancy are associated with increased risk for miscarriage, fetal or neonatal death . Eur J Endocrinol 2009;160:985-91.  Back to cited text no. 20
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21.Negro R, Schwartz A, Gismondi R, Tinelli A, Mangieri T, Stagnaro-Green A. Universal screening versus case finding for detection and treatment of thyroid hormonal dysfunction during pregnancy. J Clin Endocrinol Metab 2010;95:1699-07.  Back to cited text no. 21
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