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Thyroid disorders are often ubiquitous and insidious in their presentation (Redmond G.P., 2004). In a nationwide study, hypothyroidism was found to be a common form of thyroid dysfunction affecting approximately 11% of the study population. The older population (above the age of 35 years) seemed to be at higher risk of hypothyroidism than the younger population. Almost one-third of the hypothyroid patients were not aware of the condition and were diagnosed for the first time during the course of study related screening (Chandrakant, Pandav, Yadav et al., 2013).
Thyroid disorders are 10 times more common in women than men and have unique consequences related to menstrual cycle and reproduction. Thyroid dysfunction is associated with menstrual abnormalities in females of all age groups (Pahwa, Kaur & Gupta, 2013). Menarche, pubertal growth and development, menstrual cycles, fertility and fetal development, post- partum period, menopausal years are profoundly influenced by the thyroid status of the women (Bhavani, Sathineedi, Giri et al., 2015).
The menstrual pattern is influenced by thyroid hormones directly through impact on the ovaries and indirectly through impact on sex hormone binding globulin, prolactin and gonadotropin-releasing hormone, and coagulation factors (Poppe, Velkeniers & Glinoer, 2007). Severe hypothyroidism is commonly associated with ovulatory dysfunction due to numerous interactions of thyroid hormones with the female reproductive system. Both hyperprolactinaemia, due to increased TRH production, and altered GnRH pulsatile secretion, leading to a delay in LH response and inadequate corpus luteum, have been reported (Longcope, Abend, Braverman & Emerson, 1990; Scanlon, Chan, Heath et al., 1981; Thomas & Reid, 1987). Thyroid responsivity by the ovaries could be explained by the presence of thyroid hormone receptors in human oocytes (Wakim, Polizotto, Buffo et al., 1993). Thyroid hormones also synergize with the FSH-mediated LH/hCG receptor to exert direct stimulatory effects on granulosa cell function (progesterone production) (Cecconi, Rucci, Scaldaferri et al., 1999) and in in vitro studies effects on differentiation of the trophoblast have been shown (Maruo, Matsuo & Mochizuki, 1991). Another pathway through which hypothyroidism may impact on fertility is by altering the peripheral metabolism of estrogen and by decreasing Sex Hormone Binding Globulin (SHBG) production. Both pathways may result in an abnormal feedback at the pituitary level. Independently of hormonal changes, hypothyroidism can also lead to menorrhagia by altered production of coagulation factors (decreased levels of factors VII, VIII, IX and XI) (Ansell, 1996).
SHBG production increases in hyperthyroid women, the metabolism of estrogen is altered and the conversion of androgens to estrogens is increased. Hyperthyroxinemia increases the gonadotrophin response to GnRH and baseline gonadotrophin concentrations are also frequently elevated. The decrease in menstrual flow may also relate to effects on haemostatic factors, including the synthesis of factor VIII (Goldsmith, Sturgis, Leiman et al., 1952). Despite these metabolic changes, hyperthyroid women usually maintain ovulation, according to endometrial biopsies (Krassas, Poppe & Glinoer, 2010).