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Thyroid HT decreases pregnancy-loss risk in subclinical hypothyroidism
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The risk for pregnancy loss may be decreased among women with subclinical hypothyroidism who are treated with thyroid hormone therapy, particularly when thyroid-stimulating hormone levels are between 4.1 mIU/L and 10 mIU/L, according to researchers.
“A recent analysis of 18 studies showed that pregnant women with untreated subclinical hypothyroidism are at higher risk for pregnancy loss, placental abruption, premature rupture of membranes and neonatal death,” Spyridoula Maraka, MD, of the Knowledge and Evaluation Research Unit in the division of endocrinology, diabetes, metabolism and nutrition at the Mayo Clinic in Rochester, Minnesota, said in a press release. “It seemed likely that treating subclinical hypothyroidism would reduce the chance of these deadly occurrences. But we know that treatment brings other risks, so we wanted to find the point at which benefits outweighed the risks.”
Maraka and colleagues evaluated data from the OptumLabs Data Warehouse on 5,405 pregnant women with subclinical hypothyroidism between 2010 and 2014 to determine the efficacy and safety of thyroid HT among them. Subclinical hypothyroidism was defined as TSH levels from 2.5 mIU/L to 10 mIU/L.
Overall, 15.6% of participants started thyroid HT, 98.7% with levothyroxine, 0.8% with a thyroid extraction formulation, and 0.5% with a combination of levothyroxine and liothyronine. Higher mean TSH concentration and pre-existing thyroid disease were more common in treated participants compared with untreated participants (P < .01). Prevalence of past recurrent pregnancy loss and hypertension were higher among treated participants compared with untreated participants (P < .01).
Compared with untreated participants, pregnancy loss was less common among treated participants (P < .01) with a 38% lower odds for pregnancy loss after adjustment for age, TSH concentration, ethnicity, income, Charlson index, hypertension, obesity, history of thyroid disease and history of pregnancy loss (OR = 0.62; 95% CI, 0.48-0.82). The risks for preterm delivery (OR = 1.6; 95% CI, 1.14-2.24), gestational diabetes (OR = 1.37; 95% CI, 1.05-1.79) and preeclampsia (OR = 1.61; 95% CI, 1.1-2.37) were significantly higher among treated participants compared with untreated participants.
Compared with untreated participants, the risk for pregnancy loss was significantly lower among treated participants with pretreatment TSH levels of 4.1 mIU/L to 10 mIU/L (OR = 0.45; 95% CI, 0.3-0.65) but not those with pretreatment TSH levels of 2.5 mIU/L to 4 mIU/L (P for interaction < .01).
“ On the basis of our findings, continuing to offer thyroid hormone treatment to decrease the risk of pregnancy loss in pregnant women with TSH concentrations of 4.1-10 mIU /L is reasonable,” Maraka told Endocrine Today. “However, overtreatment could be possible in the group with lower TSH levels. Given the smaller magnitude f effect in the group with lower RSH levels of 2.5-4 mIU /L, and in light of the possible increased risk of other adverse events, treatment may need to be withheld in this group.”
Maraka added that further research is need to “understand whether a causal mechanism exists behind the association of thyroid hormone treatment and decreased risk for pregnancy loss.”
“The association of thyroid hormone treatment with increased risk for gestational diabetes, preeclampsia, and preterm delivery should be seen as preliminary findings and calls for additional studies evaluating its safety,” she told Endocrine Today. – by Amber Cox
For more information:
Spyridoula Maraka, MD, can be reached at Division of Endocrinology-UAMS, 4301 W. Markham St., #587, Little Rock, AR 72205; email: maraka.spyridoula@mayo.edu..
Disclosure: The study was funded by AcademyHealth and the Agency for Healthcare Research and Quality.
Perspective
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These data address a clinically important question for which definitive answers are currently lacking. Thyroid hormone treatment for pregnant women with baseline TSH values 4.0-10 mIU/L was associated with decreased risk for pregnancy loss, but there was no observed treatment benefit if baseline TSH was 2.5-4.0 mIU/L. Treatment was associated with increased risks for preeclampsia, gestational diabetes and preterm delivery. Strengths of the study include the large, ethnically and geographically diverse sample. Limitations are those inherent to retrospective observational data; residual confounding and incomplete outcome ascertainment cannot be ruled out.
Previous observational studies strongly suggest that the adverse gestational outcomes associated with mild TSH elevations may occur at lower TSH thresholds in women with positive thyroperoxidase (TPO) antibodies. Unfortunately, TPO antibody status was not ascertained in this study. Randomized clinical trials are needed to truly understand whether initiation of levothyroxine in subclinically hypothyroid women in early gestation improves obstetric outcomes. However, these data strengthen the evidence base for recently published guidelines by the American Thyroid Association, which recommend consideration of levothyroxine for TPO antibody-negative pregnant women with TSH 4-10 mIU/L as well as for TPO-positive women with TSH 2.5-4.0 mIU/L, and definitely recommend levothyroxine for TPO-positive pregnant women with TSH > 4.0 mIU/L.
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