Fetal Ultrasound May Effectively Identify Fetal Thyroid Dysfunction

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Fetal Ultrasound May Effectively Identify Fetal Thyroid Dysfunction CME

News Author: Laurie Barclay, MDCME Author: Désirée Lie, MD, MSEd

Complete author affiliations and disclosures, and other CME information, are available at the end of this activity.

Release Date: August 26, 2005; Valid for credit through August 26, 2006

Credits AvailablePhysicians - up to 0.25 AMA PRA Category 1 continuing physician education credits

All other healthcare professionals completing continuing education credit for this activity will be issued a certificate of participation.Participants should claim only the number of hours actually spent in completing the educational activity.

Aug. 26, 2005 — Fetal ultrasound is effective at identifying fetal thyroid dysfunction, according to the results of a study published in the Aug. 23 Rapid Electronic Publications of the Journal of Clinical Endocrinology & Metabolism.

"Foetuses from mothers with Graves' disease may experience hypothyroidism or hyperthyroidism due to transplacental transfer of antithyroid drugs (ATD) or anti-thyrotropin receptor antibodies, respectively," write Dominique Luton, MD, PhD, from Debré Hospital in Paris, France, and colleagues. "Little is known about the foetal consequences. Early diagnosis is essential to successful management."

Monthly from 22 weeks of gestation through birth, a multidisciplinary hospital team monitored 72 mothers with past or present Graves' disease and their fetuses. Ultrasonograms determined fetal thyroid size and fetal bone maturation. Thyroid function and ATD dosage were monitored in the mothers.

Of the 72 fetuses, 31 (43%) had mothers who were anti–thyrotropin-receptor antibody–negative and took no ATDs during late pregnancy; all of these had normal test results. Of the 41 other fetuses, 30 (73%) had normal test results at 32 weeks, including 29 who were euthyroid at birth and one with moderate hypothyroidism on cord blood tests.

Of the remaining 11 fetuses, all had goiter visualized by ultrasonography at 32 weeks, followed by diagnosis and treatment of thyroid dysfunction. One of these patients, who had a late referral, died, and 10 had good outcomes with normal or slightly altered thyroid function at birth. At 32 weeks, the sensitivity of fetal thyroid ultrasound for the diagnosis of clinically relevant fetal thyroid dysfunction was 92%, and specificity was 100%.

"In pregnant women with past or current Graves' disease, ultrasonography of the foetal thyroid gland by an experienced ultrasonographer is an excellent diagnostic tool," the authors write. "This tool, in conjunction with close teamwork among internists, endocrinologists and obstetricians, echographists and paediatrician, can ensure normal foetal thyroid function."

Study limitations include small sample size and lack of standardization of fetal sonograms.

"In that it was a prospective and systematic study of fetal thyroid size, [fetal ultrasound] is a new approach which is not comparable to previous studies," the authors conclude. "Whether this systematic monitoring makes a difference in terms of ultimate psychomotor development of the children compared to more targeted investigations remains to be demonstrated."

The Groupe de Recherche sur la Thyroïde, Brahms, Serono, Bayer, and Merck supported this study.

J Clin Endocrinol Metab. Posted online Aug. 23, 2005.

Learning Objectives for This Educational ActivityUpon completion of this activity, participants will be able to:

Describe the use of thyroid-stimulating hormone (TSH)–receptor antibodies (TRAK) for monitoring neonates at risk for thyroid dysfunction. Describe the use of prenatal screening ultrasonography as a tool for detecting fetal thyroid dysfunction.

Clinical Context

Graves' disease is present in about 0.2% of pregnancies. Neonatal hyperthyroidism seems to occur in only 1% of neonates born to mothers with Graves' disease. The fetal thyroid gland starts secreting thyroid hormones around week 12 of development, and fetal TSH receptors become sensitive around week 20. Fetuses and neonates born to mothers with Graves' disease are at risk for thyroid dysfunction if the mother tests positive for TSH-receptor antibodies (TRAK) and/or takes ATDs during the pregnancy, according to the authors. The role of TRAK tests in following maternal thyroid disease has not been clearly demonstrated, according to the authors. In addition, indications for the use of fetal ultrasonography in pregnant women with thyroid disease are not well defined.

This is a descriptive, prospective cohort study of 72 pregnant women with past or present Graves' disease and their fetuses to examine the utility of TRAK testing and fetal ultrasonography in predicting neonatal thyroid disease.

Study Highlights

72 mothers with past or present Graves' disease and their 72 fetuses were monitored monthly from 22 weeks' gestation. Inclusion criteria were diagnosis by an endocrinologist and laboratory test evidence of hyperthyroidism with goiter, Graves' ophthalmopathy or dermopathy, and at least one positive test for TSH-receptor antibodies. In each woman, thyroid function tests and TRAK assays were done from inclusion to delivery. Treatment of Graves' disease was adjusted by the endocrinologist for free thyroxine (FT4) levels to be maintained at the upper limit of the normal range for pregnant women. Once monthly starting at 22 weeks' gestation, fetal heart rate and fetal ultrasonography were performed for measurement of thyroid size and determination of fetal growth parameters. Fetal thyroid size, Doppler signals, and fetal bone maturation were determined on ultrasonography. Thyroid function was evaluated at birth. ATD dosage and thyroid function were monitored in mothers. Fetal goiter was defined as a thyroid circumference equal or superior to the 95th percentile for gestational age. Bone maturation was obtained at 32 weeks' gestation. Accelerated bone maturation was defined as the presence of the distal femoral ossification center before 31 weeks, and delayed maturation was defined as absence of the center after 33 weeks. Fetal tachycardia was defined as a fetal heart rate persistently more than 160 beats per minute. Hypothyroidism was defined as an FT4 level lower than the 2.5th percentile and a TSH value lower than the 2.5th percentile. Hyperthyroidism was defined as an FT4 level more than the 97.5th percentile. If fetal thyroid dysfunction was diagnosed, the ATD dosage was increased for a diagnosis of hyperthyroidism. When fetal hypothyroidism was diagnosed, intrauterine intra-amniotic levothyroxine was administered by amniocentesis. Mean maternal age was 33 years, and mean gestational age at inclusion was 17 weeks. Of 72 women, 41 were in the high-risk group and 31 in the low-risk group. 45 women received no treatment or only levothyroxine. 27 women received ATD therapy. 31 fetuses whose mothers were TRAK-negative (in the low-risk group) and who took no ATDs during late pregnancy had normal test results. Of 41 other fetuses (in the high-risk group), 11 (27%) had goiters visualized by ultrasonography at 32 weeks, and fetal thyroid dysfunction was diagnosed and treated. There was one death and 10 good outcomes. 30 (73%) of the 41 had normal test results at 32 weeks, 29 (70%) were euthyroid at birth, and 1 (2.4%) had moderate hypothyroidism on cord blood tests. Fetal hypothyroidism was usually associated with low maternal TRAK titers and/or high ATD dosages and/or delayed fetal bone maturation. Fetal hyperthyroidism (n = 4) was usually associated with high maternal TRAK values and/or accelerated fetal bone maturation. The thyroid function did not differ between the low-risk and high-risk groups of mothers. The sensitivity and specificity of fetal thyroid ultrasonography at 32 weeks for diagnosing clinically relevant fetal thyroid dysfunction were 92% and 100%, respectively.

Pearls for Practice

The use of TRAK assays identifies fetuses at risk of thyroid dysfunction in mothers with Graves' disease. Prenatal screening by ultrasonography at 32 weeks is a sensitive and specific method for detecting fetal thyroid dysfunction in maternal Graves' disease.

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