Symptoms of polycystic ovaries

The symptoms of polycystic ovary syndrome are highly variable and often opposite. As E. M. Vikhlyaeva notes, the very definition of polycystic ovary syndrome implies the inclusion of conditions that differ in pathogenesis.

For example, more frequently observed opsomenorrhea or amenorrhea does not exclude the occurrence of menometrorrhagia in these same patients, reflecting the hyperplastic state of the endometrium as a result of relative hyperestrogenism. Hyperplasia and polyposis of the endometrium are also found with significant frequency in patients with amenorrhea or opsomenorrhea. Many authors note an increased incidence of endometrial cancer in polycystic ovary syndrome.

A typical symptom of gonadotropic regulation of ovarian function and steroidogenesis in them is anovulation. However, some patients periodically have ovulatory cycles, mainly with corpus luteum insufficiency. Such ovulatory opsomenorrhea with hypoluteinism occurs at the initial stage of the disease and gradually progresses. With ovulation disorder, infertility is obviously observed. It can be both primary and secondary.

The most common signs of polycystic ovary syndrome, taking into account mild forms, is hirsutism (reaches 95%). It is often accompanied by other androgen-dependent skin symptoms, such as oily seborrhea, acne, and androgenic alopecia.

The latter usually reflects a high degree of hyperandrogenism and is observed mainly in ovarian stromal thecomatosis. This also applies to hypertrophy and virilization of the clitoris, symptoms of defeminization.

Obesity is observed in approximately 40% of patients with polycystic ovary syndrome, and although the reasons for its occurrence remain unknown, it plays a significant role in the pathogenesis of the disease. In adipocytes, peripheral conversion of A to T and to E2 occurs, the pathogenetic role of which has already been discussed. With obesity, the binding capacity of TESG also decreases, which leads to an increase in free T.

Bilateral enlargement of the ovaries is the most pathognomonic symptom of polycystic ovary syndrome. It is caused by hyperplasia and hypertrophy of the ovarian stroma cells, theca interna folliculi, with an increase in the number and persistence of cystically altered follicles. Thickening and sclerosis of the ovarian tunica albuginea depend on the degree of hyperandrogenism, i.e. it is a dependent symptom. However, the absence of macroscopic enlargement of the ovaries does not exclude polycystic ovary syndrome if hyperandrogenism of ovarian genesis is confirmed. In this case, we are talking about polycystic ovary syndrome type II, in contrast to the previously considered typical polycystic ovary syndrome type I (with bilateral enlargement). In Russian literature, this form is known as microcystic ovarian degeneration.

Galactorrhea is rare in polycystic ovary syndrome, despite the fact that hyperprolactinemia is observed in 30-60% of patients.

In some patients, skull X-rays show signs of increased intracranial pressure (hyperpneumatization of the sphenoid sinus, digital impressions), and endocraniosis (calcification of the dura mater in the frontal-parietal region, behind the back of the sella turcica, its diaphragm). In young female patients, X-rays of the hand show advanced bone age.

Such polymorphism of the clinical picture of the disease and the complexity of pathogenetic mechanisms led to the identification of its various clinical forms. As already indicated, in foreign literature, polycystic ovary syndrome type I (typical) and type II (without an increase in the size of the ovaries) are distinguished. In addition, a form of polycystic ovary syndrome with hyperprolactinemia is particularly distinguished.

In domestic literature, the following 3 forms of polycystic ovary syndrome are distinguished.

1. A typical syndrome of sclerocystic ovaries, pathogenetically caused by a primary enzymatic defect of the ovaries (19-hydroxylase and/or 3beta-alpha-dehydrogenase systems).
2. Combined form of sclerocystic ovary syndrome with ovarian and adrenal hyperandrogenism.
3. Syndrome of sclerocystic ovaries of central genesis with pronounced symptoms of disorders of the hypothalamic-pituitary system. This group usually includes patients with the endocrine-metabolic form of hypothalamic syndrome with secondary polycystic ovary disease, occurring with a violation of lipid metabolism, trophic changes in the skin, lability of arterial pressure, signs of increased intracranial pressure, and endocraniosis phenomena. EEG in such patients shows signs of involvement of the hypothalamic structures. However, it should be noted that the division into these clinical groups is conditional. Firstly, the primary enzymatic defect in ovarian tissue has not been confirmed in the works of recent years; secondly, either the triggering role of the adrenal glands or their subsequent involvement in the pathogenesis is known, i.e., the participation of the adrenal glands in the pathogenesis of polycystic ovary syndrome in all cases; thirdly, obesity is described in 40% of patients with polycystic ovary syndrome, and the identification of type III of central genesis sclerocystic ovary syndrome is based on this feature as the main one. In addition, the existence of central and vegetative disorders is possible with typical type I sclerocystic ovary syndrome.

The clinical division into typical sclerocystic ovary syndrome and central sclerocystic ovary syndrome cannot be confirmed at present, since there are no objective criteria due to the lack of a complete, holistic understanding of the pathogenesis of the disease, and only individual pathogenetic links are known. At the same time, there are objective clinical differences in the course of the disease in different patients. They must be taken into account and highlighted, since this is reflected in the treatment tactics, but it is more correct, in these cases, to talk not about the types of central genesis, but about complicated forms of the course of sclerocystic ovary syndrome. As for the allocation of the adrenal form, it should apparently be distinguished not so much as an independent one, but rather to identify the degree of participation of the adrenal cortex in general hyperandrogenism, since this may be important in the choice of therapeutic agents.

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