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What the Reproductive Specialist Should Know about Detecting Thyroidal Conditions
By Sarah L. Berga, MD, Professor and Chair, Department of Obstetrics and Gynecology, and Vice President for Women's Health Services, Wake Forest Baptist Health, Winston-Salem, NC, is Associate Editor for OB/GYN Clinical Alert.
Dr. Berga reports no financial relationship to this field of study.
Thyroid dysfunction and disease may present as reproductive compromise including oligomenorrhea, infertility, and miscarriage. Thyroid dysfunction and disease may complicate pregnancy and lead to compromised fetal neurodevelopment and preterm labor. Infertility procedures, particularly controlled ovarian hyperstimulation and ovulation induction with gonadotropins, increase the thyroxine requirement before the establishment of pregnancy. As such, the detection of thyroidal conditions may fall to any physician who cares for women, but particularly obstetricians and gynecologists. Although we think of thyroid disease as a simple condition in which thyroxine is given when the thyroid-stimulating hormone (TSH) level is elevated and then TSH levels are monitored to see if the patient is getting the correct amount, it is a bit more complex than that. Indeed, the American Thyroid Association released a 45-page document titled "Guidelines of the American Thyroid Association for the Diagnosis and Management of Thyroid Disease During Pregnancy and Postpartum," which contains 76 separate recommendations.1 The document was endorsed by the American Congress of Obstetricians and Gynecologists among other groups.
The introduction highlights a few key points. During pregnancy, the thyroid gland increases 10%-20% in size and the production of thyroxine (T4) and triiodothyronine (T3) increases by 50% along with a 50% increase in the daily iodine requirement. The range of TSH is decreased throughout pregnancy because of the actions of hCG, and thus the upper and lower limits of TSH must be adjusted to detect and treat thyroidal disease. Approximately 10%-20% of pregnant women have antibodies to the thyroid gland during the first trimester and therefore are at high risk of developing overt hypothyroidism during pregnancy. I would add that it long has been known that symptoms such as fatigue are not a good way to screen for thyroid disease in the non-pregnant state, but fatigue is the sine qua non of pregnancy, so the only way to know if a pregnant patient's fatigue is partly related to subclinical or overt hypothyroidism is to screen.
Some of the recommendations of the report are highlighted below:
It would seem that all but the most straightforward of patients should be considered at risk and therefore screened. I suspect that by recommendation 72, you were already feeling that the detection and treatment of thyroidal conditions had morphed into a complicated topic. However, if recommendations 1 through 75 were not enough to convince you that this is not an entirely straightforward topic, then reading the rather long list of who is considered high risk and therefore eligible for screening probably was the drop that caused the flood. If all women > 30 years are at high risk, then it is starting to look far simpler and less time intensive to screen. TSH, with or without FT4, is inexpensive, particularly when compared to some of the screening tests we already perform universally. Also, as I noted earlier, if symptoms such as fatigue and goiter are used as criteria to determine who should be screened, then we are pushed even closer toward universal screening because which pregnant woman is not fatigued and which does not have an increase in thyroid size?
I remember an adage that a mind is a terrible resource to waste. What we know about fetal neurodevelopment and its dependence on appropriate maternal thyroxine supply shifts us in favor of accurate detection. Although we may lack sufficient evidence from RCTs to make a strong recommendation for universal screening, there is a lot of other evidence from the molecular and cellular investigations and even screening trials2 to suggest that fetal neurodevelopment depends critically on appropriate maternal thyroxine. Let us not forget that the mother is the sole source of fetal thyroxine during the first trimester and the predominant source even in the second and third trimesters. Finally, I would be remiss to not mention another article released in July 2011 showing that the development of fetal goiter in mothers on antithyroid drugs for Grave's hyperthyroidism responds better to intra-amniotic thyroxine than discontinuing the anti-thyroid drugs.3 The authors suggest that centralized care of pregnant women with Grave's disease is urgently needed to maintain optimal fetal development
Screening guidelines are helpful, but they are a work in progress. When routine screening was conducted, 2%-3% of pregnant women had an elevated serum TSH. Also, if subclinical maternal HYPERthyroidism is not associated with adverse maternal or fetal outcomes4 and maternal hypothyroidism is, then it would seem generally better to err on the side of too much thyroxine to the fetus than too little. Not only is TSH a relatively inexpensive test, thyroxine is a relatively inexpensive medication.