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Objective:Objective was to evaluate reproductive hormones levels in hypothyroid women and impact of treatment on their levels.Materials and Methods:A total of 59 women with untreated primary hypothyroidism were included in this prospective study. Venous blood was taken at baseline and after euthyroidism was achieved for measuring serum free thyroxine, free triiodothyronine (FT3), thyroid stimulating hormone (TSH), prolactin (PRL), follicular stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E2), testosterone (T), and thyroid peroxidase antibody. Thirty-nine healthy women with regular menstrual cycles without any hormonal disturbances served as controls. The statistical analysis was performed using the Statistical Package for the Social Sciences Version 20 ([SPSS] IBM Corporation, Armonk, NY, USA). P < 0.05 was considered statistically significant.Results:On an average at diagnosis cases have more serum TSH (mean [M] = 77.85; standard error [SE] = 11.72), PRL (M = 39.65; SE = 4.13) and less serum E2 (M = 50.00; SE = 2.25) and T (M = 35.40; SE = 2.31) than after achieving euthyroidism (M = 1.74; SE = 0.73), (M = 16.04; SE = 0.84), (M = 76.25; SE = 2.60), and (M = 40.29; SE = 2.27), respectively. This difference was statistically significant t (58) = 6.48, P <0.05; t (58) = 6.49, P < 0.05; t (58) = 12.47; P < 0.05; and t (58) = 2.04, P < 0.05; respectively. Although average serum FSH (M = 12.14; SE = 0.40) and LH (M = 5.89; SE = 0.27) were lower in cases at diagnosis than after achieving euthyroidism (M = 12.70; SE = 0.40), (M = 6.22; SE = 0.25), respectively, but these differences were statistically insignificant t (58) = 1.61, P = 0.11; t (58) = 1.11, P = 0.27, respectively.Conclusion:The study has demonstrated low E2 and T levels in hypothyroid women which were increased after achieving euthyroidism. Although average serum FSH and LH were increased in hypothyroid women after achieving euthyroidism but this difference was statistically insignificant.

Congenital hypothyroidism (CH) is the one of the most common preventable cause of mental retardation. In the majority of patients, CH is caused by an abnormal development of the thyroid gland (thyroid dysgenesis) that is a sporadic disorder and accounts for 85% of cases and the remaining 15% of cases are caused by dyshormonogenesis. The clinical features of congenital hypothyroidism are so subtle that many newborn infants remain undiagnosed at birth and delayed diagnosis leads to the most severe outcome of CH, mental retardation, emphasizing the importance of neonatal screening. Dried capillary blood is used for screening and it is taken from heel prick optimally between 2 and 5 days of age. Blood spot TSH or thyroxine (T4) or both are being used for CH screening in different programs around the world. Neonates with abnormal thyroid screening tests should be recalled immediately for examination and a venipuncture blood sample should be drawn for confirmatory serum testing. Confirmatory serum should be tested for TSH and free T4, or total T4. Serum TSH and T4 undergo dynamic changes in the first weeks of life; it is important to compare serum results with age-normal reference ranges. Treatment should be started promptly and infant should be rendered euthyroid as early as possible, as there is an inverse relationship between intelligence quotient (IQ) and the age at diagnosis. Levothyroxine (l-thyroxine) is the treatment of choice and American academy of pediatrics and European society of pediatric endocrinology recommend 10-15μgm/kg/day as initial dose. The immediate goal of therapy is to normalize T4 within 2 weeks and TSH within one month. The overall goal of treatment is to ensure growth and neurodevelopmental outcomes as close as possible to their genetic potential.