Symptoms of polycystic ovaries

Symptoms of the syndrome of polycystic ovaries differ significantly in variability, and are often opposite. As E. Vikhlyaeva notes, the very definition of the polycystic ovary syndrome suggests the inclusion of various pathogenesis states in it.

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

Anomaly is a typical symptom of gonadotropic regulation of ovarian function and steroidogenesis in them. However, in some patients, ovulatory cycles are observed periodically, mainly with a deficiency in the function of the yellow body. This ovulatory hypoxemia occurs in the initial stage of the disease and gradually progresses. In violation of ovulation, apparently observed infertility. It can be both primary and secondary.

The most common signs of polycystic ovary syndrome with light forms are hirsutism (up to 95%). It is often accompanied by other androgen-dependent skin symptoms, such as oily seborrhea, acne, androgenic alopecia.

The latter, as a rule, reflects a high degree of hyperandrogenism and is observed mainly in stromal ovary tecomatosis. This also applies to hypertrophy and virilization of the clitoris, symptoms of defemination.

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

Bilateral enlargement of the ovaries is the most pathognomonic symptom of the polycystic ovary syndrome. It is caused by hyperplasia and hypertrophy of ovarian stroma cells, theca interna folliculi, with an increase in the number and persistence of cystically altered follicles. Thickening and sclerosing of the ovary's white coat depends on the degree of hyperandrogenia, ie, it is a dependent symptom. However, the absence of macroscopic enlargement of the ovaries does not exclude the syndrome of polycystic ovaries with confirmation of the ovarian genesis of hyperandrogenism. In this case we are talking about the syndrome of polycystic ovaries of type II, in contrast to the previously considered typical syndrome of polycystic ovary type I (with bilateral increase). In the domestic literature this form is known as small-cystic ovarian degeneration.

Galactorrhea occurs in the syndrome of polycystic ovaries rarely, despite the fact that hyperprolactinemia occurs in 30-60% of patients.

In a number of patients, signs of an increase in intracranial pressure (hyperplasticization of the sinus of the basal bone, finger impressions), phenomena of endocranium (calcification of the dura mater in the frontotemporal area, behind the back of the Turkish saddle, its diaphragm) are revealed on a radiograph of the skull. In young patients on the roentgenogram of the brush, the precognition of bone age is revealed.

This polymorphism of the clinical picture of the disease and the complexity of the pathogenetic mechanisms led to the isolation of its various clinical forms. As already mentioned, ovarian polycystic ovary syndrome (typical) and type II polycystic ovary syndrome (without ovarian enlargement) are isolated in foreign literature. In addition, the form of the polycystic ovary syndrome with hyperprolactinemia is highlighted.

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

1. A typical syndrome of sclerokistoznyh ovaries, pathogenetically due to the primary enzymatic defect of the ovaries (19-hydroxylase and / or Zbeta-alpha dehydrogenase systems).
2. Combined form of the syndrome of sclerocystic ovaries with ovarian and adrenal hyperandrogenism.
3. Syndrome of sclerocystic ovaries of the central genesis with severe symptoms of disorders of the hypothalamic-pituitary system. This group usually includes patients with endocrine-exchange form of the hypothalamic syndrome with secondary polycystic ovary, which occurs with a violation of fat metabolism, trophic skin changes, lability of blood pressure, signs of increased intracranial pressure, phenomena of endocranosis. On EEG in such patients there are signs of interest in hypothalamic structures. However, it should be noted that the division into the indicated clinical groups is conditional. First, in the works of recent years, the primary enzymatic defect in ovarian tissue is not confirmed; Secondly, either the triggering role of the adrenal glands or their involvement in pathogenesis is known, that is, the involvement of the adrenal glands in the pathogenesis of the polycystic ovary syndrome in all cases; thirdly, obesity is described in 40% of patients with polycystic ovary syndrome, and the isolation of type III syndrome of sclerocystosis ovaries of the central genesis is based on this sign as the main one. In addition, the existence of central and autonomic disorders with a typical syndrome of type I sclerostestic ovaries is possible.

The clinical division into a typical syndrome of sclerocystic ovaries and the syndrome of sclerocystosis ovaries of the central genesis can not now be confirmed, since there are no objective criteria due to the lack of a complete, holistic view of the pathogenesis of the disease, and only certain 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 allocated, as this is reflected in the treatment tactics, but more correctly, in these cases, it is not talking about the types of central genesis, but about the complicated forms of the flow of the syndrome of sclerocystic ovaries. As for the allocation of the adrenal form, it should apparently not be isolated as an independent one, but rather to reveal the degree of involvement of the adrenal cortex in general hyperandrogenism, since this can have a significance in the choice of therapeutic agents.

[1], [2], [3], [4]