ACOG Committee Opinion
Number 381, October 2007
(Reaffirmed 2012)


Committee on Obstetric Practice

This document reflects emerging clinical and scientific advances as of the date issued and is subject to change. The information should not be construed as dictating an exclusive course of treatment or procedure to be followed. 


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Subclinical Hypothyroidism in Pregnancy

ABSTRACT: Subclinical hypothyroidism is diagnosed in asymptomatic women when the thyroid-stimulating hormone level is elevated and the free thyroxine level is within the reference range. Thyroid hormones, specifically thyroxine, are essential for normal fetal brain development. However, data indicating fetal benefit from thyroxine supplementation in pregnant women with subclinical hypothyroidism currently are not available. Based on current literature, thyroid testing in pregnancy should be performed on symptomatic women and those with a personal history of thyroid disease or other medical conditions associated with thyroid disease (eg, diabetes mellitus). Without evidence that identification and treatment of pregnant women with subclinical hypothyroidism improves maternal or infant outcomes, routine screening for subclinical hypothyroidism currently is not recommended.


Subclinical hypothyroidism is diagnosed in asymptomatic women when the thyroid-stimulating hormone (TSH) level is elevated and the free thyroxine (T4) level is within the reference range. During pregnancy, the diagnosis of thyroid abnormalities is confused by significant but reversible changes in maternal thyroid physiology that lead to alterations in thyroid function tests during gestation. These changes are related to estrogen-mediated increases in maternal thyroid-binding protein, structural homology between TSH and human chorionic gonadotropin, and a relative decrease in availability of iodide during pregnancy (1). There are gestational age-specific normograms and thresholds for evaluating thyroid status during pregnancy (2–4).

Thyroid hormones, specifically T4, are essential for normal fetal brain development (5). Before 12 weeks of gestation, a time when the fetal thyroid begins to concentrate iodine and synthesize T4, the fetus is entirely dependent on maternal transfer of thyroid hormones. Brain development begins during this period of fetal dependency in the first trimester and continues throughout pregnancy and on into infancy. In the case of pregnant women who are iodine-deficient, in which thyroxine production in both mother and fetus is insufficient throughout pregnancy, the impact on neurodevelopment of offspring can be dramatic (6). In women with overt hypothyroidism (elevated TSH and low free T4 levels), T4 supplementation during pregnancy also has been associated with improved pregnancy outcomes. However, data indicating fetal benefit from T4 supplementation in pregnant women with sub-clinical hypothyroidism are not currently available.

Interest in thyroid disease in pregnancy, especially subclinical hypothyroidism, has escalated in part because of reports suggesting that variously defined thyroid deficiency (including both overt and subclinical disease) during pregnancy results in impaired neurodevelopment in offspring (7, 8). Further, other reports have associated subclinical hypothyroidism with preterm delivery (3, 9). These findings have led some national societies as well as public interest groups to recommend routine thyroid screening during pregnancy (10). The rationale for routine screening of pregnant women is tied both to the prevalence of subclinical hypothyroidism and the potential benefits of treatment during pregnancy. The prevalence of subclinical hypothyroidism could be anticipated to be between 2% and 5% of women screened, depending on the TSH and free T4 level thresholds applied, and this represents most women who would be identified with thyroid deficiency through routine screening (3). According to criteria established by The U.S. Preventive Services Task Force, before recommending screening of asymptomatic individuals, there must be demonstrated improvement in important health outcomes of those individuals identified through screening (11, 12). As stated previously, benefit of treatment to either mother or fetus has not yet been demonstrated in pregnant women with subclinical hypothyroidism.

Based on current literature, thyroid testing in pregnancy should be performed on symptomatic women and those with a personal history of thyroid disease or other medical conditions associated with thyroid disease (eg, diabetes mellitus). In these women, it is most appropriate to assess TSH levels first and then evaluate other thyroid functions if the TSH level is abnormal. Women with established overt thyroid disease (hyperthyroidism or hypothyroidism) should be appropriately treated to maintain a euthyroid state throughout pregnancy and during the postpartum period. Without evidence that identification and treatment of pregnant women with subclinical hypothyroidism improves maternal or infant outcomes, routine screening for subclinical hypothyroidism is not currently recommended.

References

  1. Glinoer D, de Nayer P, Bourdoux P, Lemone M, Robyn C, van Steirteghem A, et al. Regulation of maternal thyroid during pregnancy. J Clin Endocrinol Metab 1990;71: 276–87.
  2. Dashe JS, Casey BM, Wells CE, McIntire DD, Byrd EW, Leveno KJ, et al. Thyroid-stimulating hormone in singleton and twin pregnancy: importance of gestational age-specific reference ranges. Obstet Gynecol 2005;106:753–7.
  3. 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.
  4. Casey BM, Dashe JS, Spong CY, McIntire DD, Leveno KJ, Cunningham GF. Perinatal significance of isolated maternal hypothyroxinemia identified in the first half of pregnancy. Obstet Gynecol 2007;109:1129–35.
  5. Morreale de Escobar G, Obregon MJ, Escobar del Rey F. Is neuropsychological development related to maternal hypothyroidism or to maternal hypothyroxinemia? J Clin Endocrinol Metab 2000;85:3975–87.
  6. Glinoer D. Pregnancy and iodine. Thyroid 2001;11:471–81.
  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.
  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 1999;50:149–55.
  9. Stagnaro-Green A, Chen X, Bogden JD, Davies TF, Scholl TO. The thyroid and pregnancy: a novel risk factor for very preterm delivery. Thyroid 2005;15:351–7.
  10. Gharib H, Tuttle RM, Baskin HJ, Fish LH, Singer PA, McDermott MT. Subclinical thyroid dysfunction: a joint statement on management from the American Association of Clinical Endocrinologists, the American Thyroid Association, and The Endocrine Society. Consensus Statement #1. American Association of Clinical Endocrinologists; American Thyroid Association; The Endocrine Society. Thyroid 2005;15:24–8; response 32–3.
  11. Harris RP, Helfand M, Woolf SH, Lohr KN, Mulrow CD, Teutsch SM, et al. Current methods of the US Preventive Services Task Force: a review of the process. Methods Work Group, Third US Preventive Services Task Force. Am J Prev Med 2001;20(suppl):21–35.
  12. Surks MI, Ortiz E, Daniels GH, Sawin CT, Col NF, Cobin RH, et al. Subclinical thyroid disease: scientific review and guidelines for diagnosis and management. JAMA 2004; 291:228–38.

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Subclinical Hypothyroidism in Pregnancy. ACOG Committee Opinion No. 381. American College of Obstetricians and Gynecologists. Obstet Gynecol 2007;110:959–60.