Purpose of the study~Evaluation of ovarian reserve indices in women with normogonadotropic anovulation with SCH and without thyroid disease.~Detailed objectives~i) Assessment of AMH, FSH, LH, estradiol, astral follicle count (AFC)/ovarian volume in the subpopulation of women with PCOS and SCH compared to women with PCOS without thyroid disease ii) Assessment of AMH, FSH, LH, estradiol, AFC/ovarian volume in the subpopulation of women with HPOD (other than PCOS) with SCH compared to women with HPOD without thyroid disease iii) Comparison of AMH, FSH, LH, estradiol, AFC/ovarian volume in women with PCOS and HPOD with and without thyroid disease and evaluation of correlation with US ovarian morphology iv) Calculation of the cut-off point of AMH concentration correlating with a high probability of PCOS diagnosis and TSH correlating with unfavorable parameters of ovarian function/HPO axis.
Thyroid hormones (TH) can modify the functioning of the hypothalamic-pituitary-ovarian axis, affecting the functions of granulosa cells and the development and apoptosis of preantral follicles. TH receptors are present within the oocytes, and TH and anti-thyroid antibodies (ATA) are present in the follicular fluid. Improper thyroid function can cause ovulation disorders, luteal phase failure, impaired endometrial receptivity and result in implantation failures and recurrent miscarriages. While overt hypothyroidism is treated to improve fertility, the effect of subclinical hypothyroidism (SCH) and the presence of circulating ATAs on fertility and obstetric outcomes is uncertain and data on ovarian reserve rates are conflicting. Among the causes of ovulation disorders (group II according to the WHO classification), polycystic ovary syndrome (PCOS) dominates, found in 3-15% of women of reproductive age, and the remaining group of causes is the so-called Hypothalamic-Pituitary-Ovarian Axis Dysfunction (HPOD). The exact etiology of both entities is unknown.