Abstract
ObjectiveAdverse maternal outcomes and perinatal complications are closely associated with overt maternal hypothyroidism, but whether these complications occur in women with subclinical hypothyroidism (SCH) during pregnancy remains controversial. The aim of this study was to evaluate the effects of SCH on maternal and perinatal outcomes during pregnancy.MethodsA prospective study of data from 8012 pregnant women (371 women with SCH, 7641 euthyroid women) was performed. Maternal serum samples were collected in different trimesters to examine thyroid hormone concentrations. SCH was defined as a thyroid stimulating hormone concentration exceeding the trimester-specific reference value with a normal free thyroxine concentration. The occurrence of maternal outcomes, including gestational hypertension (GH), gestational diabetes mellitus, placenta previa, placental abruption, prelabor rupture of membranes (PROM), and premature delivery; and perinatal outcomes, including intrauterine growth restriction (IUGR), fetal distress, low birth weight (LBW; live birth weight ≤2500 g), stillbirth, and malformation, was recorded. Logistic regression with adjustment for confounding demographic and medical factors was used to determine the risks of adverse outcomes in patients with SCH.ResultsCompared with euthyroid status, SCH was associated with higher rates of GH (1.819% vs. 3.504%, P = 0.020; χ 2 = 7.345; odds ratio (OR), 2.243; 95% confidence interval (CI), 1.251–4.024), PROM (4.973% vs. 8.625%, P = 0.002; χ 2 = 72.102; adjusted OR, 6.014; 95% CI, 3.975–9.099), IUGR (1.008% vs. 2.965%, <0.001; χ 2 = 13.272; adjusted OR, 3.336; 95% CI, 1.745–6.377), and LBW (1.885% vs. 4.582%, P<0.001; χ 2 = 13.558; adjusted OR, 2.919; 95% CI, 1.650–5.163).ConclusionsThe results of this study indicate that pregnant women with SCH had increased risks of GH and PROM, and their fetuses and infants had increased risks of IUGR and LBW. Thus, routine maternal thyroid function testing is necessary to improve maternal and perinatal outcomes.
Highlights
Thyroid hormones are critical for energy production, body temperature regulation, and development modulation [1,2]
Neurological deficits in infants and juveniles, including low intelligence quotient scores, cognitive delay, and psychomotor development impairment, are the main complications induced by maternal hypothyroidism during early pregnancy [5,6,7]
Of the 8012 women, 7641 (95.37%) had TSH and fT4 values within the normal reference ranges in the trimester of testing and were considered to be euthyroid, whereas 371 (4.63%) had high TSH levels coupled with normal fT4 levels and were considered to have subclinical hypothyroidism (SCH)
Summary
Thyroid hormones are critical for energy production, body temperature regulation, and development modulation [1,2]. Because fetal thyroid hormones originate almost exclusively from the maternal system before 12–14 weeks of gestation, maternal thyroid disorders in early pregnancy are closely related to fetal development. Other adverse maternal outcomes and perinatal complications associated with overt maternal hypothyroidism include miscarriage, preeclampsia, preterm labor, and fetal death [9,10,11]. SCH is often missed in pregnant women, its prevalence is about 2–3% [12,13,14,15] This condition has been associated with neurodevelopmental disorders in fetuses and infants and several adverse maternal outcomes, including gestational diabetes mellitus (GDM), preeclampsia, placental abruption, and preterm delivery [3,5,13,14,16,17]. Women who have been previously diagnosed with SCH are at increased risk of stillbirth and GDM in subsequent pregnancies [14]
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