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 opsono- or amenorrhea, primary or secondary infertility, bilateral ovarian enlargement, hirsutism, obesity in almost half of patients. The results of the study (TFD) confirm the anovulatory nature of menstrual dysfunction; in colpositis, in a number of cases, an androgenic type of smear can be detected.

Objectively, an increase in the size of the ovaries can be determined with pneumopylicography, which takes into account the Borghi index (normally the sagittal size of the ovaries is less than the sagittal size of the uterus, with polycystic ovary syndrome - greater than or equal to 1). With ultrasound determine the size of the ovaries, their volume (the norm is 8.8 cm ³ ) and the echostructure, which allows to reveal cystic degeneration of the follicles.

A wide application is also found in laparoscopy, which allows, in addition to visual assessment of the ovaries and their dimensions, to make a biopsy and to confirm the diagnosis morphologically.

The main place in the diagnosis of the syndrome of polycystic ovaries occupy hormonal methods of research aimed at detecting hyperandrogenism, its source and determining the level of gonadotropic hormones (HG) - LH and FSH.

The urinary excretion level of total 17-KC in polycystic ovary syndrome varies widely, more often at or near the upper limit of the norm. The basal level of 17-CS does not indicate a source of hyperandrogenism. The determination of 17-CS fractions (DHEA, 11-oxidized ketosteroids, androsterone and etiocholanolone) also does not provide localization of the hyperandrogenic source, although DHEA excretion predominantly 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, radioimmunoassays for the determination of androgens, such as T, A, DHEA and DHEA-sulfate, have been widely used in the blood plasma. The syndrome of polycystic ovaries is characterized by a moderate increase in the blood plasma level of T and more pronounced - A, while a high content of DHEA sulfate indicates an adrenal genesis of hyperandrogenism. To clarify the localization of the source of hyperandrogenia, various functional tests were proposed, the most common of which was a sample with dexamethasone (DM) and its combination with chorionic gonadotropin (HG).

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

A more accurate sample is the suppression of the function of the DM adrenal cortex and stimulation of the function of the ovary CG with the T in the blood plasma against this background. DM is prescribed for 2-4 mg per day for 4 days, in the last 2 days, an additional HG is added at 1500 units IM at 8 o'clock in the morning. Blood sampling is performed before the test, on the third day, before the administration of HG, and on the 5th day of the test in the morning. According to research, this study was informative in diagnosing the source of hyperandrogenia and its functional or tumor character. The results of the test for different genesis of hyperandrogenism are shown in Fig. 77. Against the background of DM, there is a moderate decrease in the T level, remaining, however, slightly above the norm, and stimulation of the ovarian CG leads to a significant increase in the T level, despite the continued use of DM. With congenital adrenal cortex dysfunction (DMC), DM leads to a decrease in the T level to normal values, and additional stimulation of HCG does not change it. With virilizing tumors of the ovaries, the significantly elevated baseline T in the blood under the conditions of the sample does not change significantly.

In addition to the sample with DM and HG, a sample with DM and estrogen-gestagenic preparations (such as bisekurin) is known, in which the stimulation of the ovary CG is replaced by their suppression of progestins. This sample has a number of shortcomings (longer, the effect of progestins on the function of the adrenal cortex and their inclusion in metabolism is not excluded), which make interpretation of the results difficult.

There is also a sample with DM and clomiphene, in which direct stimulation of the function of the ovary CG is replaced by indirect stimulation through endogenous gonadotropins. In addition to androgens, this reaction takes into account the reaction of E2 and gonadotropic hormones. The use of the sample is limited by its longer duration and a larger spectrum of hormones under study.

In recent years, the literature affirms the view that all functional tests to identify the source of hyperandrogenism are of little informative. It is believed that the influence of an increased level of DHEA sulfate is pathognomonic for the detection of adrenal genesis of hyperandrogenism.

The hopes placed on the method of direct catheterization of the adrenal and ovarian veins also failed because of the pulsating nature of the secretion of hormones, not only by the adrenal glands, but also by the ovaries, and by the complexity of the technique.

In addition to determining the total T, it is very important to determine its free level, which is always increased in the case of polycystic ovary syndrome.

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

When determining the GH level in patients with polycystic ovary syndrome, an increase in the level of LH and a normal or slightly decreased FSH level is characteristic. In this case, the ratio of LH / FSH is always increased (greater than 1). With a sample of luliberin (100 mcg iv), patients with polycystic ovary syndrome have a hyperergic response to LH and a normal FSH response. In central forms of the disease, the levels of GH may be different, as well as the ratio of LH / FSH, which is associated with both the form of hypothalamic-pituitary disorders and the duration of the disease.

In the syndrome of polycystic ovaries, an increased level of prolactin is detected in 20-70% of cases. Its role in the pathogenesis of the polycystic ovary syndrome is not fully understood.

When determining the syndrome, one should remember the possibility of hyperplastic processes in the endometrium. Therefore, in the complex of studies should include diagnostic scraping of the uterine cavity. It is also possible to develop diffuse fibrocystic mastopathy.

Differential diagnosis of the polycystic ovary syndrome should be conducted with all diseases in which symptoms caused by hyperandrogenic symptoms can occur clinically. These include:

• adrenal forms of hyperandrogenism:
  • congenital dysfunction of the adrenal cortex and its post-pubertal form;
  • virilizing adrenal tumors (androsteromas), Itenko-Cushing syndrome;
  • hyperplasia of the adrenal glands ( Isenko-Cushing's disease );
• virilizing tumors of the ovaries;
• acromegaly (elevated levels of hyperthyroidism cause hyperandrogenism, there are enlarged ovaries);
• hypothyroidism [increased TSH leads to an increase in prolactin (PRL), resulting in increased DHEA due to 3beta-ol dehydrogenase blockade, which leads to the development of hirsutism; in addition, a high level of PRL can disrupt the ratio of LH / FSH, which leads to a violation of ovulation, the development of polycystic ovaries];
• idiopathic and constitutional forms of hirsutism;
• hyperprolactinemic dysfunction of ovaries with hirsutism;
• liver disease, accompanied by a decrease in the synthesis of testosterone-estrogen-binding globulin (TESG);
• hypothalamic-pituitary syndromes, including tumors of various parts of it. Hypothalamic syndromes with impaired fat metabolism;
• dysgenesis of ovaries with hirsutism (except for increased LH, FSH level is also increased).
• The so-called stromal ovarian tecomatosis (L. Frenkel's tecomatosis) is distinguished into a special clinical group, which is clinically characterized by:
• pronounced virilization;
• obesity and other signs of the hypothalamic-pituitary syndrome;
• hyperpigmentation of the skin, sometimes with hyperkeratosis in the inguinal and axillary folds, on the neck and elbows;
• a violation of carbohydrate metabolism;
• the size of the ovaries can range from normal to significantly enlarged;
• often the family character of the disease is revealed;
• resistance to conservative therapy, including clomiphene;
• The lower efficiency of wedge resection of the ovaries in comparison with the polycystic ovary syndrome.

[1], [2], [3], [4], [5], [6], [7]