Diagnosis of polycystic ovaries

In the presence of a classic symptom complex, the clinical diagnosis of polycystic ovaries is not difficult and is based on a combination of symptoms such as opso- or amenorrhea, primary or secondary infertility, bilateral enlargement of the ovaries, hirsutism, and obesity in almost half of the patients. The results of the study (TFD) confirm the anovulatory nature of the menstrual dysfunction; in some cases, colpocytology can reveal an androgenic type of smear.

Objectively, an increase in the size of the ovaries can be determined by pneumopelvigraphy, which takes into account the Borghi index (normally, the sagittal size of the ovaries is less than the sagittal size of the uterus, in polycystic ovary syndrome - greater than or equal to 1). Ultrasound determines the size of the ovaries, their volume (normal - 8.8 cm ³ ) and echostructure, which allows identifying cystic degeneration of the follicles.

Laparoscopy is also widely used, allowing, in addition to visual assessment of the ovaries and their size, to perform a biopsy and confirm the diagnosis morphologically.

The main place in the diagnosis of polycystic ovary syndrome is occupied by hormonal research methods aimed at identifying hyperandrogenism, its source and determining the level of gonadotropic hormones (GH) - LH and FSH.

The level of urinary excretion of total 17-KS in polycystic ovary syndrome fluctuates widely, often being at the upper limit of normal or slightly exceeding it. The basal level of 17-KS does not indicate the source of hyperandrogenism. Determination of 17-KS fractions (DHEA, 11-oxidized ketosteroids, androsterone and etiocholanolone) also does not localize the source of hyperandrogenism, although DHEA excretion mainly reflects the adrenal genesis of hyperandrogenism. It is known that a reliable indication of the adrenal origin of androgens is the determination of DHEA sulfate in the blood. In recent years, radioimmunological methods for determining androgens in blood plasma, such as T, A, DHEA and DHEA sulfate, have been widely used. Polycystic ovary syndrome is characterized by a moderate increase in the blood plasma level of T and a more pronounced increase in A, while a high content of DHEA sulfate indicates the adrenal genesis of hyperandrogenism. To clarify the localization of the source of hyperandrogenism, various functional tests have been proposed, the most widespread of which are the dexamethasone (DM) test and its combination with human chorionic gonadotropin (hCG).

The DM test is based on the suppression of the adrenal cortex function due to the administration of DM at 2 mg/day for two days with the determination of the excretion of 17-KS in the urine. It is believed that a decrease in this indicator by 50% or more indicates adrenal hyperandrogenism, while an insignificant decrease (less than 50%) indicates the ovarian genesis of hyperandrogenism, since the ovarian function is not regulated by ACTH and, therefore, does not change under the influence of DM. The test can be informative in the case of a sufficiently pronounced initial increase in the excretion of 17-KS, which is usually not observed in polycystic ovary syndrome. With a normal level of this indicator in patients with polycystic ovary syndrome, as well as in healthy women, the introduction of DM should lead to its decrease according to the feedback principle. In addition, it is known that DM, in addition to suppressing ACTH, inhibits the secretion of LH through the hypothalamus. It should also be emphasized that the excretion of 17-KS does not reflect the level of increase in T, the main androgen in polycystic ovary syndrome. Considering all of the above, we believe that the DM test is of little informational value for differential diagnosis of the source of hyperandrogenism in polycystic ovary syndrome.

A more accurate test is one with suppression of the adrenal cortex function by DM and stimulation of the ovarian function by hCG against this background with determination of T in the blood plasma. DM is prescribed at 2-4 mg per day for 4 days, during the last 2 days hCG is additionally administered at 1500 IU intramuscularly at 8 a.m. Blood is taken before the test, on the 3rd day, before the administration of hCG, and on the 5th day of the test in the morning. According to research data, this test has proven informative in diagnosing the source of hyperandrogenism and its functional or tumor nature. The test results for various genesis of hyperandrogenism are presented in Fig. 77. Against the background of DM, a moderate decrease in the T level is observed, which, however, remains slightly above the norm, and stimulation of the ovaries by hCG leads to a significant increase in the T level, despite the continued use of DM. In congenital adrenal cortex dysfunction (CACD), DM leads to a decrease in the T level to normal values, and additional stimulation with hCG does not change it. In virilizing ovarian tumors, the significantly increased initial T content in the blood does not change reliably under the conditions of the test.

In addition to the test with DM and hCG, there is a test with DM and estrogen-gestagen drugs (such as bisecurin), in which the stimulation of the ovaries with hCG is replaced by their suppression with progestins. This test has a number of disadvantages (it is longer, the effect of progestins on the function of the adrenal cortex and their inclusion in metabolism cannot be ruled out), which complicates the interpretation of the results obtained.

There is also a test with DM and clomiphene, in which direct stimulation of the ovarian function by hCG is replaced by indirect stimulation through endogenous gonadotropins. In addition to androgens, this test takes into account the reaction of E2 and gonadotropic hormones. The use of the test is limited by its longer duration and a wider range of hormones studied.

In recent years, the literature has been arguing that all functional tests for identifying the source of hyperandrogenism are uninformative. It is believed that the effect of elevated DHEA sulfate levels is pathognomonic for identifying the adrenal genesis of hyperandrogenism.

The hopes placed on the method of direct catheterization of the veins of the adrenal glands and ovaries were also not justified due to the pulsating nature of hormone secretion not only by the adrenal glands, but also by the ovaries, as well as the complexity of the technique.

In addition to determining total T, determining its free level, which is always elevated in polycystic ovary syndrome, is of great importance.

The level of E2 in patients with polycystic ovary syndrome usually corresponds to this indicator in healthy women in the early follicular phase or is reduced. The content of E2 is increased.

When determining the HG content in patients with polycystic ovary syndrome, an increase in the LH level and a normal or slightly reduced FSH level are characteristic. In this case, the LH/FSH ratio is always increased (more than 1). When testing with luliberin (100 mcg intravenously), a hyperergic LH response and a normal FSH reaction are observed in patients with polycystic ovary syndrome. In central forms of the disease, the HG levels may vary, as well as the LH/FSH ratio, which is associated with both the form of hypothalamic-pituitary disorders and the duration of the disease.

In polycystic ovary syndrome, elevated prolactin levels are detected in 20-70% of cases. Its role in the pathogenesis of polycystic ovary syndrome has not been fully elucidated.

When determining the syndrome, one should remember about the possibility of hyperplastic processes in the endometrium. Therefore, diagnostic curettage of the uterine cavity should be included in the complex of studies. The development of diffuse fibrocystic mastopathy is also possible.

The differential diagnosis of polycystic ovary syndrome should be made with all diseases in which clinical symptoms caused by hyperandrogenism may occur. These include:

• adrenal forms of hyperandrogenism:
  • congenital dysfunction of the adrenal cortex and its postpubertal form;
  • virilizing tumors of the adrenal glands (androsteromas), Itsenko-Cushing syndrome;
  • adrenal hyperplasia ( Itsenko-Cushing's disease );
• virilizing ovarian tumors;
• acromegaly (elevated levels of STH cause hyperandrogenism, there are enlarged ovaries);
• hypothyroidism [an increase in TSH leads to an increase in prolactin (PRL), which can result in an increase in DHEA due to the blockade of 3beta-ol dehydrogenase, which leads to the development of hirsutism; in addition, a high level of PRL can disrupt the LH/FSH ratio, which leads to ovulation disorders and the development of polycystic ovary syndrome];
• idiopathic and constitutional forms of hirsutism;
• hyperprolactinemic ovarian dysfunction with hirsutism;
• liver diseases accompanied by a decrease in the synthesis of testosterone-estrogen-binding globulin (TEBG);
• hypothalamic-pituitary syndromes, including tumors of its various parts. Hypothalamic syndromes with impaired lipid metabolism;
• ovarian dysgenesis with hirsutism (in addition to elevated LH, the FSH level is also elevated).
• A special clinical group is the so-called stromal ovarian thecomatosis (L. Frenkel's thecomatosis), which is clinically characterized by:
• pronounced virilization;
• obesity and other signs of hypothalamic-pituitary syndrome;
• hyperpigmentation of the skin, sometimes with hyperkeratosis in the groin and axillary folds, on the neck and elbows;
• carbohydrate metabolism disorder;
• the size of the ovaries can vary from normal to significantly enlarged;
• a familial nature of the disease is often revealed;
• resistance to conservative therapy, including clomiphene;
• lower efficiency of wedge resection of the ovaries compared to polycystic ovary syndrome.

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