Study of thyroid function in pregnancy, its feto-maternal outcome; a prospective observational study

Abstract

Background Pregnancy is a stress test of maternal thyroid function. The prevalence of thyroid dysfunction in pregnant women is high. Subclinical hypothyroidism occurs in 10% of all pregnancies. Effects of hypothyroidism in pregnancy are anemia, low birth weight and mental retardation in neonate. This study is aimed to evaluate maternal and fetal outcomes in pregnant women with deranged thyroid profile. The relevance of this study is to document the association of hypothyroidism and its adverse effects on mother and fetus. Methods This prospective observational study was carried out at R.D. Gardi Medical College, Ujjain, India. Subjects of this study were 198 antenatal women in third trimester with singleton pregnancy admitted in the obstetric ward, and informed consent was obtained. Women were chosen irrespective of age, parity, residence and socioeconomic status. Women with multiple pregnancy, a known case of thyroid disorder, or any pre-existing medical disorder were excluded. Routine hematological parameters and estimation of T3, T4 and TSH was conducted. Patients with deranged thyroid profile were subsequently assessed for maternal and fetal complications. History of infertility, family history of thyroid disease, menstrual pattern, recurrent abortion, hemoglobin level and fetal outcome were the main study variables. Data was analysed in SPSS software for statistical co-relation. Results Prevalence of thyroid disorder is 11%; with subclinical hypothyroidism, overt hypothyroidism and subclinical hyperthyroidism occurring in 5.6, 3.5 and 1.5% of subjects respectively. In women with subclinical and overt hypothyroidism, anemia was present in 26.3% being significantly associated with hypothyroidism (p = 0.008). With respect to fetal outcome, LBW 31.6% (p = 0.001), NICU admission 42.1%, (p = 0.000) and low APGAR Score (21.1%, p = 0.042) were statistically associated with hypothyroidism. Risk of anemia, Low Birth weight, NICU admissions, and low APGAR score was 4.8, 6.3, 0.14 and 3.64 times higher respectively in women with hypothyroidism than in women who are euthyroid. Conclusion Prevalence of subclinical hypothyroidism is 5.6% in 3rd trimester of pregnancy. Anemia, pre-eclampsia, high caesarean rates and neonatal morbidities is significantly associated with hypothyroidism.

Study on thyroid function test in pregnancy in a tertiary care hospital

“…In the current study, prevalence of maternal subclinical hyperthyroidism was 1.8 %. Mahadik K et al reported subclinical hyperthyroidism in 1.5 % pregnant women which is almost comparable to our study finding [18]. Subclinical maternal hyperthyroidism is not associated with adverse pregnancy outcome and treatment during pregnancy is unwarranted.…”

Fetal and Maternal Plasma Thyroid Hormone’s Levelsin the Guinea Pigs

“…In present study plasma, T3 hadwasfound to be lower in the fetus than in the mother throughout gestation (Table1). The low fetal T3 concentrations are in agreement with those reported by 13 Increase T4 production and T3is critical for fetal brain development 7 .Fetal development adaptively refers to the process by whichthe fetus is prepared for the environment it is about to enter, this is important for optimal chance of survival and reproductive success for offspringTim 22 . Present results indicated that pituitary and thyroid hormones secretions are important for fetal guinea pig differentiation and development of various organs and neonatal outcome.…”

Differential lipids in pregnant women with subclinical hypothyroidism and their correlation to the pregnancy outcomes

“…Its adverse effects on pregnancy outcomes are becoming apparent. They include spontaneous abortion 1 , preeclampsia 2 , placental abruption, premature rupture of membranes, low birth weight 3 , fetal distress, preterm birth 4 , and abnormal neuropsychological and intellectual development 5 . The pathogenesis of SCH remains unclear, despite being associated with nitric oxide (NO) 6 , Nesfatin-1 7 , gene silencing mediated by microRNAs 8 , inactivation of the thyroid-stimulating hormone receptor gene 9 , and the gut–thyroid axis 10 .…”