Improvement of diagnostic methods of reproductive health disorders in women of early reproductive age with sexual dysfunction and hypoandrogenism

Abstract

Female sexual dysfunction (FSD) is a global health problem. This is a multifaceted problem that requires the coordinated interaction of many neurotransmitters and hormones, both central and peripheral. In young women with reproductive health problems, the first clinical signs of future imbalances manifest in adolescence. Disruption of adaptation mechanisms at this age leads to the activation of polymorphic genes, resulting in the multifunctional disorders of women’s health in the future. In particular, the role of vitamin D deficiency as a trigger in the formation of many immune‑hormonal imbalances is noted, including formation of methionine metabolism disorders and the accumulation of excess homocysteine in cells. Therefore, improving methods of diagnosing reproductive health disorders in women of early reproductive age with sexual dysfunction and hypoandrogenism can be considered as a method of preventing the formation of conditions in them for future fertility disorders, decreased ovarian reserve, and infertility.
 Objective — to improve methods to diagnose the reproductive health disorders in women of early reproductive age with sexual dysfunction and hypoandrogenism.
 Materials and methods. The research included 20 women of early reproductive age with symptoms of FSD and hypoandrogenism (group I) and 20 healthy women (group II). The hormonal reproductive background was determined on the 5—7th day of the menstrual cycle in all examined women, including levels of thyroid‑stimulating hormone (TSH), antibodies to thyroid peroxidase (TPO‑Ab), vitamin D, homocysteine. IBM SPSS Statistics version 25.0 software was used for statistical processing of the obtained data.
 Results. Vitamin D deficiency significantly raised the probability of decreased levels of luteinizing hormone (LH) (R2=0.705; p<0.001), estradiol (R2=0.320; p=0.022), free testosterone (R2=0.419; p=0.007), dihydroepiandrosterone sulfate (DHEA‑S) (R2=0.697; p<0.001) and increased levels of prolactin (R2=0.691; p<0.001), 17‑OP (R2=0.748; p<0.001). Hyperhomocysteinemia did not significantly affected the changes in the levels of these hormones (p>0.05), but significantly increases the probability of decreased FSH levels (R2=0.376; p=0.012). Moreover, it was established that high TSH levels increased the probability of elevation homocysteine rates (R2=0.561; p=0.001) and decreased levels of reproductive hormones: FSH (R2=0.357; p=0.014), LH (R2=0.626; p<0.001), estradiol (R2=0.451; p=0.004), free testosterone (R2=0.587; p=0.001) and DHEA‑S (R2=0.661; p<0.001). The increased TPO‑Ab levels can serve as a significant predictor of the increased prolactin levels (R2=0.675; p<0.001).
 Conclusions. Optimization of the medical care to women with FSD should include early diagnosis of vitamin D status and evaluation of homocysteine levels. Determination of women’s hormonal background should include assessments of the levels of TSH and antibodies to thyroperoxidase. An endocrinologist’s consultation is required in case of the reveal of thyroid gland disorders. The assessments of polymorphism of folate‑methionine cycle genes and thrombophilia should be performed in case of high levels of homocysteine.