Polycystic ovary syndrome (PCOS). clinic (symptoms), diagnosis and treatment of PCa. Polycystic ovary syndrome Treatment of hyperplastic processes in PCOS

Polycystic ovary syndrome (PCOS) is a pathology of the structure and function of the ovaries, characterized by ovarian hyperandrogenism with impaired menstrual and generative function.

SYNONYMS OF POLYCYSTIC OVARY SYNDROME

Polycystic ovary disease, primary polycystic ovaries, Stein-Leventhal syndrome, scleropolycystic ovaries.

ICD-10 CODE E28.2 Polycystic ovary syndrome.

EPIDEMIOLOGY OF POLYCYSTIC OVARY SYNDROME

The incidence of PCOS is approximately 11% among women of reproductive age, in the structure of endocrine infertility it reaches 70%, and in women with hirsutism, PCOS is detected in 65–70% of cases.

ETIOLOGY AND PATHOGENESIS OF POLYCYSTIC OVARY SYNDROME

The etiopathogenesis of PCOS has not been fully studied, despite the large number of proposed theories. However, most researchers consider PCOS to be a heterogeneous disease, hereditarily determined, characterized by menstrual irregularities, chronic anovulation, hyperandrogenism, an increase in the size of the ovaries and features of their morphological structure: a bilateral increase in the size of the ovaries by 2–6 times, hyperplasia of the stroma and theca cells, many cystic atretic follicles 5–8 mm in diameter, thickening of the ovarian capsule.

Cardinal sign of PCOS- ovarian hyperandrogenism. Summarizing the available scientific work on this problem, the following mechanisms of pathogenesis can be determined.

Violation of gonadotropic function. The era of synthesis and use of GnRH in the 80s. provided not only the opportunity to induce ovulation, but also a more in-depth study of the role of disorders of gonadotropic function in the pathogenesis of PCOS. We hypothesized a primary disturbance in the circhoral rhythm of GnRH release from puberty as the cause of PCOS, possibly genetically determined. An important role is assigned to environmental (stress) factors that disrupt neuroendocrine control in the regulation of GnRH secretion, resulting in an increase in the basal level of LH synthesis and a relative decrease in FSH production. It is known that the period of puberty is critical in a girl’s life, against the background of which genetic and environmental factors contribute to the manifestation of various neuroendocrine syndromes.

As a result of excessive stimulation of LH, the production of androgens in theca cells increases, cystic atresia of the follicles with hyperplasia of theca cells and stroma is formed, selection and development of the dominant follicle does not occur. As a result of the relative deficiency of FSH, necessary for the synthesis of cytochrome P450, which activates enzymes for the metabolism of androgens into estrogens, androgen accumulation and estradiol deficiency occur. By negative feedback mechanisms, a decrease in estradiol levels stimulates LH synthesis, which is the second factor for increasing basal LH levels. In addition, estrogens (mainly estrone), synthesized extragonadally from testosterone in large quantities, increase the sensitivity of pituitary cells to GnRH, which contributes to chronic hypersecretion of LH. Overproduction of androgens leads to atresia of follicles, hyperplasia of theca cell stroma and tunica albuginea. In addition, elevated androgen concentrations are positively correlated with inhibin B levels, which suppress FSH secretion.

On the other hand, the increase in GnRH secretion may not be primary, but secondary in response to overproduction of androgens and a decrease in the synthesis of estradiol in the ovaries. In this case, ovarian hyperandrogenism is the result of a violation of autoparacrine regulation of follicle growth and maturation, as well as dysregulation of cytochrome P450c17. As a result of these disorders, the synthesis of estradiol is reduced, which stimulates the secretion of GnRH through a feedback mechanism. Ovarian hyperandrogenism is observed in patients with normal levels of gonadotropins. In this case, a hyperreaction of theca cells of polycystic ovaries to normal LH levels is shown.

Insulin resistance and hyperinsulinemia. The combination of hyperandrogenism and insulin resistance in PCOS was first reported in 1980, prompting the hypothesis that obesity and hyperinsulinemia must play a major role in the pathogenesis of PCOS in patients with insulin resistance. However, hyperinsulinemia is also observed in patients with normal body weight and PCOS. Therefore, obesity contributes to, but is not among the main factors in the development of insulin resistance in PCOS. The incidence of insulin resistance is 35–60%. The pathogenetic mechanisms of insulin resistance are not fully known; they are multifactorial and in the vast majority of patients with PCOS are caused not by a defect in the insulin receptor, but by disturbances at the receptor and post-receptor level of transduction of the insulin signal into the cell.

Normally, insulin binds to the transmembrane insulin receptor, activating several processes, in particular tyrosine autophosphorylation and sequential reactions of glucose transport into the cell. As a result of the cascade mechanisms that occur, insulin-mediated transport of glucose into the cell is triggered. An important role in the formation of insulin resistance is played by a genetically determined disorder of the tyrosine kinase pathway of phosphorylation of the insulin receptor. Serine phosphorylation of the receptor inhibits insulin receptor tyrosine kinase activity. In patients with PCOS, inhibition of insulin signal transduction into the cell has been proven as a result of the prevalence of serine phosphorylation. The same mechanisms enhance the activity of cytochrome P450c17, which is key in the synthesis of androgens in both the ovaries and adrenal glands.

Hyperandrogenism plays a certain role in peripheral insulin resistance, since androgens change the structure of muscle tissue towards the predominance of type II muscle fibers, which are less sensitive to insulin. Concomitant obesity, often visceral, in approximately 50% of patients aggravates existing insulin sensitivity disorders, producing a synergistic effect.

Normally, it is not insulin, but rather insulin-like growth factor I that plays an important role in steroidogenesis. But the action of insulin in concentrations above normal is realized not only through insulin receptors, but also through insulin-like growth factor I receptors. Insulin and insulin-like growth factor I enhance LH-dependent synthesis of androgens in theca cells and stroma and stimulate excess LH secretion. Insulin also increases the activity of cytochrome P450c17, thereby increasing the production of ovarian and adrenal androgens. Hyperandrogenism is also promoted by an increase in the concentration of free biologically active testosterone due to a decrease in the formation of SHBG in the liver. Insulin has been shown to regulate SHBG production. With hyperinsulinemia, SHBG synthesis decreases, which leads to increased concentrations of free fractions of both testosterone and estradiol. In addition, insulin suppresses the production of proteins that bind insulin-like growth factor I, increasing their biological activity and, consequently, the synthesis of androgens in the ovaries.

The role of obesity comes down to the extragonadal synthesis of testosterone and estrone. This process is autonomous in nature and does not depend on gonadotropic stimulation. Estrone, synthesized in adipose tissue, closes a “vicious circle” in the pathogenesis of PCOS formation, increasing the sensitivity of the pituitary gland to GnRH.

Ovarian factors. Recent studies explain the hyperproduction of androgens by genetically determined dysregulation of cytochrome P450c17, a key enzyme in the synthesis of androgens in the ovaries and adrenal glands. The activity of this cytochrome is regulated by the same mechanisms that are involved in the activation of the insulin receptor, i.e. There is a genetic determinant of ovarian, adrenal hyperandrogenism and insulin resistance. It has been shown that in patients with PCOS, the concentration of an apoptosis inhibitor is increased in the blood, i.e. the process of atresia of follicles that persist is reduced.

It is known that approximately 50% of patients with PCOS have adrenal hyperandrogenism. The mechanisms of increased DHEAS production in normal and overweight individuals are different. In patients with normal body weight (approximately 30%), there is a genetically determined dysregulation of cytochrome P450c17, which leads to increased production of adrenal and ovarian androgens through a single mechanism. In obese patients, activation of the androgenic function of the adrenal glands is caused by excess production of corticoliberin and, accordingly, ACTH, therefore the synthesis of not only DHEAS, but also cortisol increases.

Based on an analysis of the results of numerous studies, we can propose two options for the pathogenesis of PCOS in patients with normal body weight and in insulin-resistant patients (Fig. 181, 182). The genetic causes of adrenal and ovarian hyperandrogenism in patients with normal body weight are indicated by the data from the anamnesis and clinical picture, since the frequency of past diseases is not higher than in the population, and, except for disorders of menstrual and generative function, nothing bothers the patients. Whereas in obese patients there is an increased incidence of ARVI and many diencephalic symptoms, which indicates a central, hypothalamic genesis of the formation of PCOS - a violation of the neuroendocrine control of GnRH secretion.

The pathogenesis of PCOS in insulin-resistant patients is presented as follows (Fig. 18-2). Puberty is characterized by insulin resistance due to increased production of growth hormone. Insulin is an important mitogenic hormone; it is required in increased concentrations during puberty for normal physical development and maturation of organs and tissues of the reproductive system. As already noted, this is a critical period in life when any genetically determined pathology can manifest itself, especially under the influence of various environmental factors.

Rice. 18-1. Pathogenesis of PCOS in patients with normal body weight.

Fig. 18-2. Pathogenesis of PCOS in insulin-resistant patients.

Thus, the pathogenesis of PCOS is multifactorial, with the involvement of ovarian, adrenal and extraovarian factors in the pathological process and has different mechanisms in patients with normal body weight, obesity, and insulin resistance.

CLINICAL PICTURE OF POLYCYSTIC OVARY SYNDROME

Clinical picture of PCOS characterized by menstrual irregularities, primary infertility, excess hair growth, acne. In recent years, women with normal body weight and mild androgen-dependent dermatopathies, the so-called anhydrous patients, have become increasingly common (about 50%). Menarche is timely - 12–13 years. Disorders of the menstrual cycle from the period of menarche - oligomenorrhea type in the vast majority of women (70%), less often dysfunctional uterine bleeding (7-9%). Secondary amenorrhea (up to 30%) occurs in untreated women over 30 years of age with concomitant obesity, and in patients with normal body weight it is observed at menarche and does not depend on the duration of anovulation.

DIAGNOSIS OF POLYCYSTIC OVARY SYNDROME

Currently, most researchers have accepted the diagnostic criteria proposed at the Rotterdam consensus in 2004: oligomenorrhea and/or anovulation, hyperandrogenism (clinical and/or biochemical manifestations), echographic signs of polycystic ovaries. The presence of two out of three of these signs diagnoses PCOS when other causes of PCOS formation are excluded.

ANAMNESIS

In the history of patients with normal body weight, the frequency of previous diseases is not higher than in the population; with obesity - a high frequency of neuroinfections, extragenital pathology, family history of non-insulin-dependent diabetes mellitus, obesity, arterial hypertension.

PHYSICAL INVESTIGATION

On physical examination, the morphotype is female; with excess body weight, most patients have a visceral type of distribution of adipose tissue; the severity of hirsutism ranges from mild to pronounced. The body mass index is determined: overweight is considered when the body mass index is more than 26 kg/m2, and obesity is considered when the body mass index is over 30 kg/m2. Depending on the nature of the distribution of adipose tissue, obesity can be female type, or gynoid (even distribution of adipose tissue), or male type (central, Cushingoid, android, visceral) with predominant deposition of adipose tissue in the shoulder girdle, anterior abdominal wall and mesentery of internal organs. Visceral obesity is often accompanied by insulin resistance and is observed in 80% of patients with PCOS and overweight. It is recommended to determine not only the body mass index, but also the ratio of waist to hip volume. This index characterizes the type of obesity and the risk of metabolic disorders. A ratio of waist to hip volume of more than 0.85 corresponds to the visceral type, and less than 0.85 corresponds to the female type of obesity.

A clinical manifestation of insulin resistance is the presence of “acanthosis nigroid”: areas of skin hyperpigmentation in areas of friction (groin, axillary area, etc.). When palpating the mammary glands in most patients, signs of fibrocystic mastopathy are determined. During a gynecological examination, enlarged ovaries are detected in patients with normal body weight.

LABORATORY RESEARCH

When studying the level of hormones in the blood, most patients are determined to have an increased concentration of LH, testosterone, 17-OP, an increase in the LH/FSH ratio of more than 2.5; in 50–55% of observations - a decrease in the concentration of SHBG, an increase in the concentration of DHEAS, in 25% of patients - an increase in the concentration of prolactin. A sensitive method for diagnosing hyperandrogenism is the determination of the free androgen index, which is calculated using the following formula:

Free Androgen Index = Total T x 100 / SHBG

A significant increase in the levels of 17-OP and DHEAS requires the elimination of CAH first. For this purpose, in modern clinical practice, an ACTH test is used. An increase in the level of 17OP and DHEAS (more than 8–10 times) in response to ACTH administration indicates CAH, which is caused by a genetically determined deficiency of the 21hydroxylase enzyme.

The participation of the ovaries and adrenal glands in the synthesis of testosterone is approximately the same - 30% each. Therefore, increased testosterone concentrations cannot differentiate between adrenal and ovarian hyperandrogenism. In this regard, for the purpose of differential diagnosis, practicing physicians can be recommended to determine in the blood plasma DHEAS, the main marker of adrenal hyperandrogenism, before and after a test with dexamethasone. The study of 17 corticosteroids and the steroid profile of urine is not very informative, since it reflects the metabolism of all androgens and cannot accurately identify their source even after a test with dexamethasone.

Diagnosis of metabolic disorders is primarily aimed at identifying insulin resistance using the oral glucose tolerance test. At the same time, the basal and stimulated intake of 75 g of glucose levels of insulin and glucose are determined in the blood. If after 2 hours the blood glucose level returns to the original values, but there is no insulin, this indicates insulin resistance. If after 2 hours the level of not only insulin, but also glucose is increased, this indicates impaired glucose tolerance. At the same time, there is an increase in basal insulin concentration. At the next stage of metabolic disorders, non-insulin-dependent diabetes mellitus develops, which is diagnosed with increased basal concentrations of both glucose and insulin. However, a glucose tolerance test is not recommended.

The main clinical and biochemical criteria for insulin resistance: visceral obesity, acanthosis nigroid, glucose-stimulated hyperinsulinemia, fasting insulin level 12.2 mIU/l or more, HOMA index more than 2.5 (fasting insulin x fasting glucose / 22.5).

INSTRUMENTAL RESEARCH

The most important method in diagnosing PCOS is the echoscopic picture of polycystic ovaries.

Echoscopic criteria for polycystic ovaries:

  • ovarian volume more than 8 cm3;
  • increase in the area of ​​hyperechoic stroma;
  • the number of anechoic follicles with a diameter of up to 10 mm is at least ten;
  • increased blood flow and abundant vascular network in the stroma (with Dopplerometry).

In contrast to the echoscopic picture of multifollicular ovaries, characteristic of early puberty, hypogonadotropic amenorrhea, resistant ovarian syndrome, a specific manifestation of multifollicular ovaries on ultrasound is a small number of follicles with a diameter of about 10 mm, located throughout the ovary between a small amount of stroma with a weak echo signal, and the volume of the ovaries does not exceed 8 cm3.

According to echographic and endoscopic examinations, two types of polycystic ovaries have been identified depending on the location of the follicles in relation to the stroma: type I polycystic ovaries - diffuse - and type II - peripheral location of the follicles in relation to the hyperechoic stroma. Type I is more often observed in patients with normal body weight, scanty hirsutism, resistant to clomiphene, a high incidence of secondary amenorrhea and OHSS. Type II polycystic ovaries (classic), well known to everyone, is more often detected in obese patients. It was precisely in patients with type I polycystic ovaries that there was a history of pregnancies that ended in spontaneous abortion in the early stages. According to functional diagnostic tests, their ovulatory cycles with NLF are periodically tested, while visual examination during laparoscopy reveals thecal lutein cysts with a diameter of 10–20 mm, similar to the luteinization syndrome of the unovulated follicle. At the same time, the ovaries are large in size, the ovarian capsule is thin, but smooth without stigmas, which indicates anovulation. This clinical and morphological variant of PCOS (normal body weight, scanty hirsutism, high frequency of secondary amenorrhea, type I polycystic ovaries) is becoming more common. Among these patients, “ovulating polycystic ovaries” are observed (approximately 9–11%). Often, laparoscopy reveals OHSS without previous use of ovulation stimulants in the form of thecal lutein cysts, sometimes multi-chamber, with a total size of 5 to 10 cm in diameter. This so-called endogenous hyperstimulation due to the influence of one’s own gonadotropins, the level of which may be normal, occurs in approximately 11–14% of patients with type I polycystic ovaries. This fact indicates a hyperreaction of theca cells to normal LH concentrations.

Endometrial biopsy is indicated for women with acyclic bleeding due to the high prevalence of endometrial hyperplastic processes. There is now no doubt that women with PCOS are at high risk of developing endometrial cancer. Aggravating factors include metabolic disorders and duration of anovulation.

DIFFERENTIAL DIAGNOSIS OF POLYCYSTIC OVARY SYNDROME

Differential diagnosis is carried out in patients with normal body weight with CAH, and in case of obesity - with secondary polycystic ovaries in patients with metabolic syndrome (Table 18-1, 18-2). As can be seen from the presented data, during the formation of secondary polycystic ovaries, the hormonal and echographic picture does not differ from that in PCOS with obesity. Only on the basis of medical history (the presence of a period of regular menstruation, pregnancy, childbirth, secondary disturbances of menstrual and generative function against the background of weight gain) can PCOS with obesity be distinguished from secondary polycystic ovaries. In our opinion, this is important for practicing doctors, since the duration of chronic hyperandrogenic anovulation will be significantly longer in patients with PCOS (with menarche) and obesity, which, first of all, will affect the effectiveness of various methods of stimulating ovulation.

Table 18-1. Differential diagnostic criteria for CDN and PCOS with normal body weight

Table 18-2. Differential diagnostic criteria for secondary PCOS against the background of MS and PCOS with obesity

TREATMENT OF POLYCYSTIC OVARY SYNDROME

TREATMENT GOALS

Treatment of patients with PCOS is aimed at:

  • normalization of body weight and metabolic disorders;
  • restoration of ovulatory menstrual cycles;
  • restoration of generative function;
  • elimination of endometrial hyperplastic processes;
  • elimination of clinical manifestations of hyperandrogenism - hirsutism, acne.

DRUG TREATMENT OF POLYCYSTIC OVARY SYNDROME

Regardless of the final goal of treatment, the first stage requires normalization of body weight and correction of metabolic disorders. Complex metabolic therapy, including the principles of rational nutrition and medications, is described in detail in the “Metabolic syndrome” section.

In insulin-resistant patients with normal body weight, treatment with metformin, a drug from the biguanide class, is recommended at stage I. Metformin leads to a decrease in peripheral insulin resistance, improving glucose utilization in the liver, muscles and adipose tissue. The drug is prescribed at 1000–1500 mg per day under the control of a glucose tolerance test. The duration of therapy is 3–6 months, including against the background of ovulation stimulation.

Stimulation of ovulation is carried out in patients planning pregnancy after normalization of metabolic disorders. At the first stage of ovulation induction, clomiphene citrate is used. It should be noted that the long-used method of stimulating ovulation by prescribing estrogen progestogen drugs, based on the rebound effect after their withdrawal, has not lost its popularity. Clomiphene citrate belongs to synthetic antiestrogens - a class of selective ER modulators. Its mechanism of action is based on blockade of the ER at all levels of the reproductive system. After discontinuation of clomiphene citrate, the secretion of GnRH increases via a feedback mechanism, which normalizes the release of LH and FSH and, accordingly, ovarian folliculogenesis. Clomiphene citrate is prescribed from the 5th to the 9th day of the menstrual cycle, 50–100 mg per day. If there is no effect when prescribing 100 mg, then further increasing the dose of clomiphene citrate is inappropriate. If there is no ovulation at the maximum dose for 3 months, the patient can be considered resistant to clomiphene citrate. The criterion for assessing the effectiveness of ovulation stimulation is the restoration of regular menstrual cycles with hyperthermic basal temperature for 12–14 days, the level of progesterone in the middle of the second phase of the cycle is 15 ng/ml or more, as well as confirmation of ovulation by an individual test that determines the preovulatory peak of LH in the urine.

Hyperinsulinemia reduces the effectiveness of ovulation stimulation, so for insulin-resistant patients with PCOS, clomiphene citrate is prescribed while taking metformin, which increases the frequency of ovulation and pregnancy compared to clomiphene citrate monotherapy. The duration of hyperandrogenic anovulation (more than 10 years), age over 28 years can also contribute to resistance to clomiphene citrate. The following criteria for clomiphene resistance can be distinguished: age over 30 years, body mass index >25, ovarian volume >10 cm3, LH level >15 IU/l, estradiol level<150 пмоль/л.

Combined treatment regimens with clomiphene citrate. Prescribing an ovulatory dose of 10,000 IU of hCG may increase the likelihood of pregnancy in the absence of a response to clomiphene citrate alone. In this case, ultrasound monitoring of the growing follicle is necessary; hCG is administered when the diameter of the dominant follicle is at least 18 mm, after which ovulation is noted after 34–36 hours. Ultrasound monitoring is also carried out to assess the condition of the endometrium, the thickness of which must be at least 6 mm, otherwise it is impaired implantation process. Due to the antiestrogenic effect of clomiphene citrate, there may be insufficient tension of the cervical mucus in the preovulatory period and a decrease in proliferative processes in the endometrium. Therefore, the effect of clomiphene citrate in relation to the induction of ovulation is higher than in the onset of pregnancy. In order to treat these undesirable effects, it is recommended to prescribe natural estrogens - estradiol at a dose of 2-4 mg from the 9th to the 14th day of the cycle. For NLF, you can increase the dose of clomiphene citrate or prescribe gestagens in the second phase of the cycle from the 16th to the 25th day. In this case, natural progesterone preparations are preferable (dydrogesterone 20 mg per day or progesterone 200 mg per day).

Combination therapy with clomiphene citrate and gonadotropins is more effective. Clomiphene citrate is prescribed 100 mg from the 2nd-3rd to the 6th-7th day of the cycle, then on the 5th, 7th, 9th, 11th, 13th day recombinant FSH is administered at 50-150 IU per day under ultrasound control of folliculogenesis. If the diameter of the preovulatory follicle is at least 18 mm, 10,000 IU of hCG is administered. The second phase can be supported by the administration of gestagens (dydrogesterone, progesterone). In the absence of pregnancy against the background of ovulatory cycles, laparoscopy is indicated to exclude peritoneal factors of infertility. In recent years, GnRH antagonists have been used to obtain a rebound effect after their withdrawal (by analogy with estrogen progestogen drugs). But against the background of GnRH antagonists, a more pronounced suppression of gonadotropic function occurs, therefore the effect in stimulating ovulation after discontinuation is higher than after estrogen progestogen drugs. 4–6 injections of GnRH antagonists are recommended. This method of stimulating ovulation is preferable to recommend in young patients with normal body weight with type I polycystic ovaries in order to avoid the development of OHSS.

At the second stage of ovulation stimulation in clomiphene-resistant patients with PCOS planning pregnancy, gonadotropins are prescribed. The latest generation of drugs are created using fundamentally new technologies. One of the first was a recombinant preparation of pure FSH - Puregon ©, its analogue - GonalF ©, with the use of which there is a lower risk of developing OHSS. When prescribing gonadotropins, the patient should be informed about the risk of multiple pregnancy, the possible development of OHSS, as well as the high cost of treatment. In this regard, treatment should be carried out only after excluding pathology of the uterus and tubes, male factor infertility. There are many treatment regimens with gonadotropins (they are described in detail in the relevant manuals). The main principle of treatment with gonadotropins is strict transvaginal ultrasound monitoring to promptly stop stimulation in order to prevent the development of OHSS. The use of GnRH antagonists in ovulation stimulation protocols in patients with PCOS is increasingly used because it suppresses peaks of excess LH secretion, which improves the quality of oocytes and reduces the risk of developing OHSS.

SURGICAL TREATMENT OF POLYCYSTIC OVARY SYNDROME

The surgical method of stimulating ovulation using laparoscopic access is most popular among clomiphene-resistant women with PCOS due to the affordable cost of treatment. In addition, the advantages of laparoscopy include the absence of the risk of OHSS, the occurrence of multiple pregnancies and the possibility of eliminating the often associated peritoneal factor of infertility. In addition to wedge resection, laparoscopy offers cauterization of the ovaries using various energies (thermal, electrical, laser), which is based on the destruction of the stroma. The absence of ovulation for 2–3 cycles requires additional administration of clomiphene citrate, and in insulin-resistant patients, metformin, which increases the pregnancy rate. As a rule, pregnancy occurs within 6–12 months, and then the frequency of pregnancy decreases.

The choice of surgical stimulation of ovulation depends on the type and volume of polycystic ovaries and the duration of anovulation. If there is a significant increase in the volume of polycystic ovaries, regardless of the type, wedge resection is recommended. With a slight increase in the volume of polycystic ovaries, endocoagulation of the stroma can be performed using the type of demedulation. This tactic is based on the pathogenetic mechanisms of surgical stimulation of ovulation - maximum removal (or destruction) of the androgen-secreting stroma of polycystic ovaries is carried out, as a result, extragonadal synthesis of estrone from testosterone is reduced, and the sensitivity of the pituitary gland to GnRH is normalized.

FOLLOW-UP

Despite the fairly high overall effectiveness of various methods of ovulation stimulation (75–80%) in restoring ovulation and fertility in PCOS patients, most practitioners note a relapse of symptoms. Mostly, relapse is observed in patients who have achieved their generative function using conservative treatment methods, as well as after cauterization of polycystic ovaries. Therefore, after childbirth, it is necessary to prevent the relapse of PCOS, as well as the risk of developing endometrial hyperplastic processes and long-term consequences of insulin resistance - cardiovascular diseases, non-insulin-dependent diabetes mellitus. For this purpose, it is most advisable to prescribe COCs, preferably monophasic ones (Yarina ©, Zhanin ©, Marvelon ©, Diane ©, etc.), and in obese patients it is recommended to introduce the intravaginal hormonal releasing system NuvaRing ©, with the use of which there is no weight gain. If COCs are poorly tolerated, gestagens can be recommended in the second phase of the cycle.

Treatment of endometrial hyperplastic processes. When endometrial hyperplasia is detected, confirmed by histological examination, at the first stage, therapy with estrogenstagens, progestogens or GnRH antagonists is carried out; in case of obesity, progestogens are preferable. Hormone therapy for endometrial hyperplastic processes provides for a central and local mechanism of action of the drug, which consists in suppressing the gonadotropic function of the pituitary gland, which inhibits folliculogenesis and, as a consequence, reduces the endogenous synthesis of steroids; The local effect of hormonal drugs contributes to the atrophic processes of the endometrium. Hormonal treatment of endometrial hyperplasia in insulin-resistant patients with PCOS is carried out against the background of metabolic therapy. Without correction of metabolic disorders (hyperinsulinemia, hyperglycemia, dyslipidemia), relapse is natural, which is associated with the role of adipose tissue in steroidogenesis, as well as hyperinsulinemia in aggravating existing endocrine disorders in PCOS.

To regulate the menstrual cycle and treat androgen-dependent dermatopathies, COCs with antiandrogenic action are recommended. A prolonged regimen of taking COCs is more effective in reducing hirsutism, since during a seven-day break the gonadotropic function of the pituitary gland is restored, and therefore the synthesis of androgens.

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Polycystic ovaries (ICD-10 code: E28.2) is one of the main causes of female infertility. This common disease contributes to the formation of disorders in a woman’s body: ovulation does not occur, the chances of conceiving a child are reduced to almost zero. With polycystic disease, the ovaries are enlarged and small growths (cysts) form in them, which are filled with fluid.

The disease is often found in women with an excess of male sex hormones. The egg does not mature and there is no ovulation. The follicle does not rupture, but fills with fluid and becomes a cyst. For this reason, the ovaries enlarge.

Symptoms

The disease can be identified by symptoms only in 10% of women of reproductive age. Quite often, this disease is discovered during puberty. The most reliable symptom is an irregular monthly cycle, its absence, long delays, up to several months, infertility (female infertility according to ICD-10). The disease often accompanies diabetes mellitus and candidiasis. Combined with disorders of the thyroid gland and adrenal glands. Polycystic ovary syndrome is characterized by a sharp increase in weight (10 kg or more). According to research, fat deposits in the center of the torso indicate increased levels of androgens, lipids and sugar. Excess weight is a common problem for women with this disease. With polycystic disease, many women cannot conceive for a long time. But not all patients report the presence of such symptoms.

Causes

There are several theories about the causes of the disease.

According to one theory, the disease occurs due to the body's inability to process insulin. Increased levels of insulin produced by the pancreas promote the production of androgens. Hormonal imbalance interferes with the ovulation process.

According to another theory, thickening of the protein membrane of the ovary leads to intensive formation of androgens.

Also, doctors do not exclude the importance of heredity and genetic factors.

Another cause of polycystic ovary syndrome may be pregnancy, which occurs with severe toxicosis, threat of miscarriage and other pathologies.

The disease can also appear after using hormonal drugs during pregnancy.

Polycystic ovary syndrome is possible with an infectious disease or regular colds in childhood. Frequent tonsillitis (ICD-10:J35.0) affects the formation of the disease: the ovaries and tonsils are interconnected.

Stress and excessive physical activity may well contribute to the development of polycystic disease.

Diagnostics

If characteristic symptoms are present, doctors can immediately make a diagnosis, which is confirmed after examination. During the examination, the specialist pays attention to the condition of the skin, the presence of excess weight, the nature of hair growth and the general condition of the body.

Clinical and laboratory examination is prescribed to determine the condition of the genital organs. A pelvic ultrasound can reveal changes in the ovarian tissues, how much they are enlarged in size. There is a proliferation of connective tissue. An ultrasound examination can also show the presence of small cysts in one or two ovaries at once and a decrease in the size of the uterus.


Image by jk1991 at FreeDigitalPhotos.net

A biochemical blood test reveals metabolic disorders. This disease is usually characterized by elevated cholesterol or glucose levels. The blood is also examined for lipid and insulin levels.

A blood test to determine hormones helps determine how elevated the level of male sex hormones is. With polycystic disease, testosterone and insulin levels are usually increased, and progesterone levels are decreased.

Sometimes doctors resort to a biopsy. The endometrium is scraped and then examined under a microscope. The procedure is often prescribed to patients with dysfunctional bleeding.

Basal temperature readings can also indicate pathology. If the woman is healthy, the temperature will increase in the second half of the cycle. Remains unchanged during illness. It is also necessary to identify the likelihood of the influence of a genetic factor, examine the flora of vaginal smears, and use tomography to exclude the possibility of a tumor.

The laparoscopic method is used for diagnosis and treatment. It reveals subcapsular cysts, ovarian size, and capsule thickening.

Treatment

Along with getting rid of polycystic disease, treatment will help reduce the manifestation of other symptoms: hirsutism, acne, pain and others. Polycystic ovary syndrome is treated with conservative and surgical methods.

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Hormonal medications are often prescribed. Their action is aimed at normalizing the functioning of hormones. The patient can also get rid of acne, alopecia, hair growth and other unwanted symptoms. Oral contraceptives are usually prescribed. They will help regulate your cycle and normalize ovulation. They also stimulate the growth of follicles in the ovaries and cause ovulation.

If a woman's main goal is pregnancy, but oral contraceptives have not helped, she should make sure that there are no other causes of infertility. To do this, you should check for obstruction of the fallopian tubes, your husband needs to donate sperm for analysis. If the results are good, the doctor will prescribe ovulation stimulation.

Endovaginal vibration massage can also be effective. Exposure to low-frequency vibration helps dilate blood vessels in the genital organs and stimulate ovulation. Access of drugs to the ovaries will improve, metabolic processes will accelerate. Vibromassage is contraindicated during pregnancy, menstruation, tumors, inflammation of the pelvic organs, thrombophlebitis.

Surgical treatment for polycystic ovary syndrome is considered in the following cases:

  • if the medication method did not bring positive results;
  • the disease occurs with long-term disruption of the cycle;
  • The woman is over thirty years old.

During surgery, they destroy the part of the ovaries that synthesizes androgens. But the ovary is able to recover quickly, so the effect is short-lived. If the patient is seeking to become pregnant, she should try to conceive several months after the operation.

Many operations for polycystic ovary syndrome are performed laparoscopically. All tests before laparoscopy should be normal. The presence of violations will lead to complications after surgery. Laparoscopy can be performed on any day of the cycle, except for the days of menstruation: there is a risk of large blood loss. Typically, doctors use the following laparoscopy methods: wedge resection and electrocoagulation.

Wedge resection

This method of surgery helps reduce testosterone and androstenedione levels. If polycystic ovary syndrome is the main obstacle to conception, most women become pregnant after resection.

Afterwards, the patient must take a course of hormonal medications to restore menstruation. Ovulation often appears two weeks after resection. The patient can return home on the third day if complications do not occur. After this type of operation, there is a high probability of pregnancy in the first month and first six months.

Gradually, cysts may appear again. Some patients experience cessation of stable menstruation 3 years after resection. Therefore, you should carefully monitor your cycles and see a doctor.

Possible negative consequences of wedge resection:

  • adhesions;
  • ectopic pregnancy;
  • infertility.

The main contraindication to surgery is ovarian cancer.

Laparoscopic electrocoagulation

During laparoscopic electrocoagulation, incisions are made on the ovary with an electrode, and blood vessels are cauterized to avoid bleeding. This is a more gentle way. With this procedure, the chance of forming an egg increases. Laparoscopy usually lasts 15 minutes. The patient is prescribed hospitalization for several days.

Patients are advised to move more within a few hours after laparoscopy. Women rarely need pain medication because there is virtually no trauma to the tissue. Electrocoagulation has a number of advantages over wedge resection:

  • minimal risk of adhesions;
  • slight blood loss;
  • no stitches on the stomach.

The rehabilitation period includes restrictions: sexual rest for up to one month, sports are contraindicated. Hormonal medications will help avoid relapse. Laparoscopy can regulate the monthly cycle and ovarian function.

Diet

If a woman is overweight, she will need to lose weight. She should monitor the amount of carbohydrates and calories in her diet and exercise regularly. Weight loss alone can lower androgen and insulin levels and restore ovulation. With a loss of even 10% of the initial weight, it is possible to restore the normal menstrual cycle and reduce dangerous consequences in the future. But too strict diets and fasting are contraindicated.

You should exclude soda and packaged fruit juices from your diet. They contain too much sugar. Preference should be given to freshly squeezed grapefruit juice diluted with water. It is worth excluding sweets, chocolate, and sweet pastries. It is better to replace them with dried fruits, nuts, and berries. Sweeteners are also harmful. They are almost completely calorie-free, but contain easily digestible carbohydrates. Steamed meat is much healthier than fried meat. White flour foods should be replaced with whole grains. Whole grains are a source of fiber, minerals, and vitamins. Intestinal function improves and skin structure is restored. Whole grain products include unbroken buckwheat, whole grain oatmeal, unprocessed wheat and barley flakes, brown and wild rice.

You should avoid high-fat dairy products. You need to consume about a kilogram of dairy products per week. You should also reduce your intake of caffeinated products.

Folk remedies

Some folk remedies can improve the functioning of the hormonal system. But you should not use the products without a doctor’s permission.

For polycystic disease, it is recommended to take an infusion of boron uterus. Pour 2 tablespoons of herb into two glasses of boiling water, cover, and leave to steep for 2 hours. When boiled, the plant loses its beneficial properties. Afterwards, the liquid must be filtered and taken one spoon per day. Licorice root has antiviral and antibacterial effects. The infusion can lower blood pressure and cholesterol levels. May reduce testosterone production. Should not be used continuously for longer than 6 weeks. Pour one tablespoon of root into a glass of boiling water, let it brew for an hour and drink once a day.

Folk remedies are useless outside the complex of drug treatment, and their haphazard or excessive use can be harmful to health.

Consequences

Why is polycystic ovary syndrome dangerous? It often develops into serious and dangerous diseases. Women with this diagnosis are predisposed to diabetes, strokes, other heart diseases and oncology. The main complication of polycystic disease is endometrial cancer (endometrial cancer according to ICD-10). With an irregular cycle and lack of ovulation, only estrogen affects the uterus. Therefore, monthly shedding of the uterine layer does not occur, and it grows. Without progesterone, the endometrium becomes thick, which can lead to cell changes and cancer.

Polycystic ovary syndrome cannot always be cured once and for all, and it should be constantly monitored. Women with this disease should immediately contact a gynecologist-endocrinologist. Polycystic ovary syndrome contributes to the development of very serious ailments: diabetes, oncology and infertility. Women with symptoms should be tested. Once the diagnosis is confirmed, it is necessary to start hormonal therapy or turn to other treatment methods under the supervision of a specialist.

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What is polycystic ovary syndrome and how to treat a gynecological disease combined with dysfunction of the endocrine system

Polycystic ovary syndrome is a gynecological disease combined with dysfunction of the endocrine system. The absence of a full-fledged dominant follicle provokes problems with conception. Against the background of PCOS, obesity often develops; women complain of irregular menstruation, the appearance of acne, and excessive hair growth.

What to do if polycystic ovary syndrome is diagnosed? What treatments are effective? What measures help you get pregnant with PCOS? The answers are in the article.

Polycystic ovary syndrome: what is it?

With polycystic ovary syndrome, many small, underdeveloped follicles appear. The number of bubbles can reach a dozen or more. In the absence of a full-fledged dominant follicle, there are disruptions in the ovulation process, the egg does not mature, and the regularity of the cycle is disrupted.

In patients with PCOS due to anovulation, doctors diagnose primary infertility. Carrying out full hormonal therapy and stimulating ovulation in many cases allows you to restore the level of fertility, increasing the chance of full conception and gestation.

Amenorrhea (lack of monthly bleeding) or oligomenorrhea (scanty, infrequent menstruation) often develops. Sometimes bleeding due to endometrial tissue rejection is accompanied by severe pain, and the blood volume is significantly higher than normal.

Causes of disturbances and discomfort: long-term influence of estrogens on the inner layer of the uterus and anovulation. In combination with a decrease in progesterone levels, the development of hyperplastic processes is possible, which sometimes leads to pathological uterine bleeding. In the absence of treatment and inattention to the symptoms of PCOS, a negative effect on the uterus and appendages occurs over a long period, which can cause a malignant process.

Polycystic ovary syndrome ICD code – 10 – E28.2.

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Reasons for the development of pathology

PCOS develops with severe disruption of the endocrine system. The pathological process develops when there is a malfunction in the functioning of the ovaries, pituitary gland, and adrenal glands.

With the progression of chronic autoimmune pathology, the levels of female sex hormones noticeably decrease: estradiol and progesterone, testosterone production is higher than normal. Hormonal imbalance occurs against the background of excessive synthesis of luteinizing hormone and prolactin, which is produced by the pituitary gland.

Note! Autoimmune pathology is congenital; hormonal disorders during fetal development are often associated with poor nutrition of the mother. With a meager diet, the growing body lacks many important substances, without which the full formation of the endocrine and reproductive systems in a female embryo is impossible.

First signs and symptoms

The first menstruation in girls occurs at the prescribed time - from 12 to 13 years, but the cycle is not established for a long time. Scanty periods or absence of bleeding for six months indicates ovulation. During puberty, excessive hair growth is noticeable, acne often appears, and examination shows a bilateral increase in the size of the ovaries. A characteristic symptom is the uniform accumulation of fat in different parts of the body, which leads to an increase in body weight, sometimes 10–20% above normal.

Dyshormonal disorders can be identified not only during a gynecological ultrasound and the results of a blood test for hormones, but also by external manifestations. With PCOS, a woman often gains extra pounds, and hirsutism increases psycho-emotional discomfort. As you get older, acne often disappears, but obesity and hair growth due to excess testosterone remain. Sometimes the male hormone levels are not much higher than normal, and the manifestations of hirsutism are minimal.

Specific symptoms of polycystic ovary syndrome:

  • menstrual irregularities;
  • absence or rare occurrence of ovulation;
  • primary infertility;
  • obesity, development of prediabetes;
  • increased cholesterol levels in the blood;
  • hair thinning or active growth on the body;
  • acne;
  • During the examination, the doctor notes the appearance of multiple cysts and enlarged ovaries.

Diagnostics

The presence of PCOS in a woman can be confirmed based on a comprehensive examination, based on a combination of echoscopic and clinical symptoms. When making a diagnosis, the basis is a prolonged absence of ovulation in combination with high testosterone levels and hyperandrogenism syndromes.

On bimanual examination, the paired organs are dense and larger than usual in size. Multiple cysts in the body of the ovaries in the absence of a mature dominant follicle are a characteristic sign of polycystic disease (“poly” means “many”).

Be sure to conduct hormone tests: it is important to know the level of progesterone, estrogen, FSH, testosterone, LH. Often, estrogens are practically normal, androgen values ​​are slightly increased, which reduces the diagnostic value of a blood test if PCOS is suspected. You cannot refuse tests: when selecting hormonal drugs, you need to see the indicators of the main regulators that affect the state of the reproductive and reproductive systems.

In difficult cases, ovarian laparoscopy is prescribed for an in-depth examination of the affected organs. If necessary, the doctor performs a tissue biopsy for research.

Objectives and main directions of therapy

Treatment goals for polycystic ovary syndrome:

  • restore the menstrual cycle;
  • reduce negative symptoms that worsen a woman’s appearance and health;
  • achieve ovulation if a woman is planning a pregnancy;
  • protect the walls of the uterus from excessive accumulation of endometrial cells that were not rejected during menstruation, which did not occur on time;
  • stabilize weight;
  • prevent long-term complications due to PCOS.

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Main methods of therapy:

  • taking combined oral contraceptives to stabilize menstrual function. Depending on the testosterone level, the gynecologist selects the optimal type of COC: Jazz, Janine, Diane 35, Yarina, Marvelon;
  • To achieve pregnancy, ovulation is stimulated. There are several schemes, but the most effective and in demand is the combination of Clomiphene in the first phase of the cycle and Duphaston tablets for 10 days in the luteal (second) phase. Ovarian hyperstimulation requires strict adherence to the medication regimen, timely testing, and an ovulation test as recommended by a doctor;
  • diet correction is a mandatory element of treatment. If you have polycystic ovaries, you need to stabilize your weight at levels that are optimal for your height, age, and body type. You cannot starve, adhere to strict diets, or eat only vegetables or buckwheat. An unbalanced diet increases hormonal fluctuations, which interferes with the treatment process. You should not eat sugar, smoked meats, baked goods, fatty foods, you need to limit salt and spices. It is useful to eat five to six times throughout the day, drink up to one and a half to two liters of water to maintain water balance;
  • baths with pine elixir, herbal infusions, sea salt are useful;
  • As prescribed by your doctor, you need to take a complex of vitamins: tocopherol, ascorbic acid, riboflavin, biotin, cyanocobalamin. Vitamin therapy is needed to stimulate metabolic processes, normalize progesterone synthesis, strengthen the immune system, and improve the condition of blood vessels;
  • Surgical treatment with removal of multiple cysts is carried out when the effectiveness of conservative therapy is low. Endoscopic surgery is low-traumatic, the result after the procedure is positive in most cases - the likelihood of pregnancy against the backdrop of maturation of a full-fledged follicle increases several times.

Possible consequences

Against the background of long-term malfunctions of the reproductive and endocrine systems, an increased risk of negative processes in various parts of the body has been confirmed. The more attention a woman pays to her health, the lower the likelihood of complications, but the development of pathologies cannot be completely excluded: diabetes mellitus, arterial hypertension, endometrial hyperplasia, oncopathology of the uterus and appendages.

Polycystic ovary syndrome and pregnancy

Is it possible to get pregnant with polycystic ovary syndrome? Some “specialists” provide inaccurate information in their materials: with PCOS, infertility inevitably develops, and the likelihood of getting pregnant is extremely low. After reading such articles, women diagnosed with polycystic ovary syndrome panic, despair, and become depressed. Nervous overload, taking tranquilizers, and depressed mood cause even more active hormonal fluctuations, which does not help restore the ability to conceive.

Reproduction doctors recommend that women with PCOS do not despair and go to a clinic with modern diagnostic equipment and qualified personnel. To achieve the long-awaited pregnancy, you will have to undergo a course of drug therapy or undergo endoscopic surgery to remove multiple cysts. To achieve a positive result, time must pass: most often, conception occurs six months to a year after the start of treatment, sometimes therapy lasts longer. In some cases, it is possible to stabilize the menstrual cycle in a shorter period of time if ovulation occurs periodically.

A woman will need patience and accuracy in plotting her basal temperature chart. It is important to take antiandrogenic COCs strictly on schedule.

To stimulate the ovaries, in which a full-fledged egg must mature, on certain days the woman receives hormonal injections (hCG - human chorionic gonadotropin). Under the influence of regulators, a healthy follicle is formed in the ovary, which bursts and allows the prepared egg to be released. It is during this period that you need to do an ovulation test to confirm the optimal period for conception. Sexual intercourse is required (also the next day) for sperm to penetrate the mature egg.

Before ovarian stimulation, you need to pass a test for tubal patency (the procedure is called hysterosalpinography); free passage into the uterine cavity from the ovaries is important. A man must have a spermogram to confirm a sufficient number of motile and healthy sperm. If the conditions are met and there are no obstacles or pathological changes in the ejaculate and fallopian tubes, ovarian hyperstimulation can be performed.

If the ovaries are unresponsive to the standard dose, the reproductologist increases the rate of Clomiphene or, when the level reaches 200 mg, prescribes drugs from another group. It is important to monitor with ultrasound to ensure there is no overstimulation of the ovaries.

A positive result in the treatment of infertility due to PCOS is provided by “drilling” the ovaries - a laparoscopic operation during which the surgeon removes part of the thickened capsule with multiple cysts, freeing the passage for the follicle. After surgery, the production of testosterone decreases, an excess of which often makes it difficult to get pregnant. After ovarian laparoscopy, pregnancy can occur as early as the next full menstrual cycle. In most cases, conception occurs within a year after ovarian surgery.

After pregnancy, a woman with PCOS is under medical supervision. It is important to monitor hormonal levels to avoid spontaneous abortion, gestational diabetes, and other complications.

Prevention

Damage to the endocrine system often occurs against the background of genetic predisposition and endocrine pathologies. An autoimmune disease develops if the cells of a female fetus do not receive enough nutrients and hormones, without which the proper formation of the endocrine and reproductive systems is impossible. Reasons: poor diet during pregnancy, the influence of high doses of radiation, the expectant mother taking potent drugs, hormonal imbalances during gestation, endocrine diseases.

The risk of polycystic ovary syndrome can be reduced by a high-quality examination when planning pregnancy. If there are abnormalities in the functioning of the endocrine system, you need to undergo a course of therapy under the guidance of an experienced doctor. It is important to reduce the impact of chronic pathologies and ensure proper nutrition during pregnancy.

More information about the features of nutrition and diet during the treatment of polycystic ovary syndrome can be found in the following video:

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Polycystic ovary syndrome

Polycystic ovary syndrome (PCOS) is a pathology of the structure and function of the ovaries, the main criteria of which are chronic anovulation and hyperandrogenism. The frequency of PCOS in the structure of endocrine infertility reaches 75%.

Symptoms of polycystic ovary syndrome

Disorders of the menstrual cycle such as oligo-, amenorrhea. Since disruption of the hormonal function of the ovaries begins with puberty, cycle disturbances begin with menarche and do not tend to normalize. It should be noted that the age of menarche corresponds to that in the population - 12-13 years (in contrast to adrenal hyperandrogenism in adrenogenital syndrome, when menarche is delayed). In approximately 10-15% of patients, menstrual irregularities are characterized by dysfunctional uterine bleeding against the background of endometrial hyperplastic processes. Therefore, women with PCOS are at risk for developing endometrial adenocarcinoma, fibrocystic mastopathy and breast cancer, as well as problems with pregnancy.

Anovulatory infertility. Infertility is primary in nature, in contrast to adrenal hyperandrogenism, in which pregnancy is possible and is characterized by miscarriage.

Hirsutism of varying severity develops gradually from the period of menarche, in contrast to adrenogenital syndrome, when hirsutism develops before menarche, from the moment of activation of the hormonal function of the adrenal glands during the period of adrenarche.

Excess body weight is observed in approximately 70% of women and corresponds to II-III degree of obesity. Obesity is often universal in nature, as evidenced by a waist to hip ratio (W/H) of less than 0.85, which characterizes the female type of obesity. A WC/TB ratio of more than 0.85 characterizes the Cushingoid (male) type of obesity and is less common.

The mammary glands are developed correctly, every third woman has fibrocystic mastopathy, which develops against the background of chronic anovulation and hyperestrogenism.

In recent years, when they began to study the peculiarities of metabolism in PCOS, it was found that insulin resistance and compensatory hyperinsulinemia - disorders of carbohydrate and fat metabolism of the diabetoid type - often occur. Dyslipidemia with a predominance of lipoproteins of the atherogenic complex (cholesterol, triglycerides, LDL and VLDL) is also noted. This, in turn, increases the risk of developing cardiovascular diseases in the second and third decades of life, i.e., in age periods to which these diseases are not typical.

Causes of polycystic ovary syndrome

There is still no consensus on the causes of the development of the disease.

PCOS is a multifactorial pathology, possibly genetically determined, in the pathogenesis of which there are central mechanisms regulating the gonadotropic function of the pituitary gland from puberty, local ovarian factors, extraovarian endocrine and metabolic disorders that determine clinical symptoms and morphological changes in the ovaries.

Diagnosis of polycystic ovary syndrome

  • Stromal hyperplasia;
  • hyperplasia of theca cells with areas of luteinization;
  • the presence of many cystic atretic follicles with a diameter of 5-8 mm, located under the capsule in the form of a “necklace”;
  • thickening of the ovarian capsule.

A characteristic history, appearance and clinical symptoms facilitate the diagnosis of PCOS. In a modern clinic, the diagnosis can be made without hormonal studies, although they also have characteristic features.

The diagnosis of polycystic ovaries can be established by transvaginal ultrasound, as clear criteria for the echoscopic picture are described: the volume of the ovaries is more than 9 cm3, hyperplastic stroma makes up 25% of the volume, more than ten atretic follicles with a diameter of up to 10 mm, located along the periphery under a thickened capsule.

The volume of the ovaries is determined by the formula: V = 0.523 (L x Sx N) cm3, where V, L, S, H are the volume, length, width and thickness of the ovary, respectively; 0.523 is a constant coefficient. The increase in ovarian volume due to hyperplastic stroma and the characteristic location of the follicles help differentiate polycystic ovaries from normal (on the 5-7th day of the cycle) or multifollicular. The latter are characteristic of early puberty, hypogonadotropic amenorrhea, and long-term use of COCs. Multifollicular ovaries are characterized by ultrasound by a small number of follicles with a diameter of 4-10 mm located throughout the ovary, a normal pattern of stroma and, most importantly, a normal volume of the ovaries (4-8 cm3).

Thus, ultrasound is a non-invasive, highly informative method that can be considered the “gold standard” in the diagnosis of PCOS.

Hormonal characteristics of PCOS. The diagnostic criteria are: an increase in LH levels, an increase in the LH/FSH ratio of more than 2.5, an increase in the level of total and free T with normal levels of DHEA-S and 17-OHP.

After a test with dexamethasone, the androgen content decreases slightly, by about 25% (due to the adrenal fraction).

The ACTH test is negative, which excludes adrenal hyperandrogenism, characteristic of adrenogenital syndrome. An increase in insulin levels and a decrease in PSSG in the blood were also noted.

Metabolic disorders in PCOS are characterized by increased levels of triglycerides, LDL, VLDL and decreased HDL.

In clinical practice, a simple and accessible method for determining impaired glucose tolerance to insulin is the sugar curve. Blood sugar is determined first on an empty stomach, then within 2 hours after taking 75 g of glucose. If after 2 hours the blood sugar level does not return to the original values, this indicates impaired glucose tolerance, i.e. insulin resistance, which requires appropriate treatment.

Endometrial biopsy is indicated for women with acyclic bleeding due to the high incidence of endometrial hyperplastic processes.

The criteria for diagnosing PCOS are:

  • Timely age of menarche;
  • disturbance of the menstrual cycle from the period of menarche in the vast majority of cases as oligomenorrhea;
  • hirsutism and obesity since menarche in more than 50% of women;
  • primary infertility;
  • chronic anovulation;
  • increase in ovarian volume due to stroma according to transvaginal echography;
  • increased T levels;
  • increase in LH and LH/FSH ratio > 2.5.

Stages of treatment for polycystic ovary syndrome

As a rule, patients with PCOS consult a doctor with complaints of infertility. Therefore, the goal of treatment is to restore ovulatory cycles.

In PCOS with obesity and with normal body weight, the sequence of therapeutic measures is different.

If you are obese:
  • The first stage of therapy is normalization of body weight. Reducing body weight against the background of a reduction diet leads to normalization of carbohydrate and fat metabolism. The diet for PCOS involves reducing the total caloric content of food to 2000 kcal per day, of which 52% comes from carbohydrates, 16% from proteins and 32% from fats, and saturated fats should make up no more than 1/3 of the total amount of fat. An important component of the diet is limiting spicy and salty foods and liquids. A very good effect is observed when using fasting days; fasting is not recommended due to protein consumption in the process of gluconeogenesis. Increasing physical activity is an important component not only for normalizing body weight, but also for increasing the sensitivity of muscle tissue to insulin. Most importantly, it is necessary to convince the patient of the need to normalize body weight as the first stage in the treatment of PCOS.
  • The second stage of therapy is drug treatment of metabolic disorders (insulin resistance and hyperinsulinemia) in the absence of effect from a reduction diet and physical activity. A drug that increases the sensitivity of peripheral tissues to insulin is metformin. Metformin leads to a decrease in peripheral insulin resistance, improving glucose utilization in the liver, muscles and adipose tissue; normalizes the blood lipid profile, reducing the level of triglycerides and LDL. The drug is prescribed at 1000-1500 mg per day for 3-6 months under the control of a glucose tolerance test.
  • The third stage of therapy is stimulation of ovulation after normalization of body weight and in PCOS with normal body weight. Stimulation of ovulation is carried out after excluding tubal and male factors of infertility.

Therapeutic methods for stimulating ovulation in PCOS

After normalization of body weight and in PCOS with normal body weight, stimulation of ovulation is indicated. Stimulation of ovulation is carried out after excluding tubal and male factors of infertility.

Most doctors begin ovulation induction with the use of Clomiphene. It should be noted that the long-used method of stimulating ovulation using estrogen-progestin drugs, based on the rebound effect after their withdrawal, has not lost its popularity. If there is no effect from therapy with estrogen-gestagens and Clomiphene, it is recommended to prescribe gonadotropins or surgical stimulation of ovulation.

"Clomiphene" refers to non-steroidal synthetic estrogens. Its mechanism of action is based on blockade of estradiol receptors. After discontinuation of Clomiphene, the feedback mechanism increases the secretion of GnRH, which normalizes the release of LH and FSH and, accordingly, the growth and maturation of follicles in the ovary. Thus, Clomiphene does not stimulate the ovaries directly, but has an effect through the hypothalamic-pituitary system. Stimulation of ovulation with Clomiphene begins from the 5th to the 9th day of the menstrual cycle, 50 mg per day. With this regimen, the drug-induced increase in gonadrtropin levels occurs at a time when the selection of the dominant follicle has already been completed. Earlier use may stimulate the development of multiple follicles and increases the risk of multiple pregnancies. In the absence of ovulation according to ultrasound and basal temperature, the dose of Clomiphene can be increased in each subsequent cycle by 50 mg, until reaching 200 mg per day. However, many clinicians believe that if there is no effect when prescribing 100-150 mg of Clomiphene, further increasing the dose is not advisable. If there is no ovulation at the maximum dose for 3 months, the patient can be considered resistant to the drug.

The criteria for the effectiveness of ovulation stimulation are:

  • Restoration of regular menstrual cycles with hyperthermic basal temperature for 12-14 days;
  • progesterone level in the middle of the second phase of the cycle is 5 ng/ml or more, preovulatory LH peak;
  • Ultrasound signs of ovulation on the 13-15th day of the cycle:
  • the presence of a dominant follicle with a diameter of at least 18 mm;
  • endometrial thickness is at least 8-10 mm.

If these indicators are present, it is recommended to administer an ovulatory dose of 7500-10000 IU of human chorionic gonadotropin - hCG (Profazi, Horagon, Pregnil), after which ovulation is noted after 36-48 hours. When treating with Clomiphene, it should be taken into account that it has antiestrogenic properties, reduces the amount of cervical mucus (“dry cervix”), which prevents the penetration of sperm and inhibits the proliferation of the endometrium and leads to implantation failure in the event of fertilization of the egg. In order to eliminate these undesirable effects of the drug, it is recommended, after finishing taking Clomiphene, to take natural estrogens in a dose of 1-2 mg or their synthetic analogues (Microfollin) from the 10th to the 14th day of the cycle to increase the permeability of cervical mucus and endometrial proliferation .

The frequency of ovulation induction during treatment with Clomiphene is approximately 60-65%, pregnancy occurs in 32-35% of cases, the frequency of multiple pregnancies, mainly twins, is 5-6%, the risk of ectopic pregnancy and spontaneous miscarriages is not higher than in populations. In the absence of pregnancy against the background of ovulatory cycles, it is necessary to exclude peritoneal factors of infertility during laparoscopy.

If there is resistance to Clomiphene, gonadotropic drugs are prescribed - direct ovulation stimulants. Human menopausal gonadotropin (hMG), prepared from the urine of postmenopausal women, is used. hMG preparations contain LH and FSH, 75 IU each (Pergonal, Menogon, Menopur, etc.). When prescribing gonadotropins, the patient should be informed about the risk of multiple pregnancy, the possible development of ovarian hyperstimulation syndrome, as well as the high cost of treatment. Treatment of polycystic ovary syndrome should be carried out only after excluding pathology of the uterus and tubes, as well as male factor infertility. During the treatment process, transvaginal ultrasound monitoring of folliculogenesis and the condition of the endometrium is mandatory. Ovulation is initiated by a single injection of hCG at a dose of 7500-10000 IU, when there is at least one follicle with a diameter of 17 mm. If more than 2 follicles with a diameter of more than 16 mm or 4 follicles with a diameter of more than 14 mm are detected, the administration of hCG is undesirable due to the risk of multiple pregnancy.

When ovulation is stimulated by gonadotropins, the pregnancy rate increases to 60%, the risk of multiple pregnancies is 10-25%, ectopic - 2.5-6%, spontaneous miscarriages in cycles ending in pregnancy reach 12-30%, ovarian hyperstimulation syndrome is observed in 5 -6% of cases.

Surgical methods to stimulate ovulation in PCOS

The surgical method of stimulating ovulation (wedge resection of the ovaries) has been performed laparoscopically in recent years, thereby ensuring minimal invasive intervention and reducing the risk of adhesions. In addition, the advantage of laparoscopic resection is the ability to eliminate the often associated peritoneal factor of infertility. In addition to wedge resection, during laparoscopy it is possible to cauterize the ovaries using various types of energy (thermo-, electric-, laser), which is based on the destruction of the stroma with a point electrode. From 15 to 25 punctures are produced in each ovary; the operation is less traumatic and time-consuming compared to wedge resection.

In most cases, in the postoperative period, a menstrual-like reaction is observed after 3-5 days, and ovulation is observed after 2 weeks, which is tested by basal temperature. The absence of ovulation for 2-3 cycles requires additional administration of Clomiphene. As a rule, pregnancy occurs within 6-12 months, then the frequency of pregnancy decreases. The absence of pregnancy in the presence of ovulatory menstrual cycles dictates the need to exclude tubal factor infertility.

The frequency of ovulation induction with any laparoscopic technique is approximately the same and amounts to 84-89%; pregnancy occurs on average in 72% of cases.

Despite the fairly high effect in stimulating ovulation and pregnancy, most clinicians note a relapse of clinical symptoms after about 5 years. Therefore, after pregnancy and childbirth, prevention of recurrence of PCOS is necessary, which is important given the risk of developing endometrial hyperplastic processes. For this purpose, it is most advisable to prescribe COCs, preferably monophasic ones (Marvelon, Femoden, Diane, Mercilon, etc.). If COCs are poorly tolerated, which happens with excess body weight, gestagens can be recommended in the second phase of the cycle: Duphaston at a dose of 20 mg from the 16th to the 25th day of the cycle.

For women who are not planning a pregnancy, after the first stage of ovulation stimulation with Clomiphene, aimed at identifying the reserve capabilities of the reproductive system, it is also recommended to prescribe COCs or gestagens to regulate the cycle, reduce hirsutism and prevent hyperplastic processes.

Technique of wedge resection of the ovary

Indications: sclerocystic ovarian syndrome. In this case, the ovaries are enlarged 2-5 times, sometimes smaller than normal, covered with a dense, thick fibrous membrane of a whitish or gray color.

Characteristic features are also the absence of corpora lutea in the ovaries and a very small number of small immature follicles.

In sclerocystic ovary syndrome, despite their large mass, which is many times greater than the mass of normal ovaries, their hormonal function is often reduced. Clinically, this often manifests itself as menstrual dysfunction, hypomenstrual syndrome or amenorrhea. In some patients, maturation and rupture of follicles are sometimes observed. In these cases, reproductive function may not be impaired, although, as a rule, with sclerocystic ovary syndrome, menstrual dysfunction and infertility are observed.

A generally accepted method of surgical treatment of sclerocystic ovary syndrome is marginal wedge resection of both ovaries; It is recommended to excise two-thirds of the mass of each ovary.

The surgical technique is simple. After laparotomy, first one, then the second ovary is removed from the abdominal cavity. The tubular end of the ovary is sutured (taken on a “holder”) for ease of manipulation and the main part of the operation begins.

Holding the ovary with the fingers of the left hand, a significant part of its tissue is excised along the free edge - from half to two-thirds - with the right hand. This is best done with a scalpel. It should be remembered that if the scalpel blade penetrates very deeply in the direction of the ovarian hilum, blood vessels may be damaged, the ligation of which causes the development of ischemia of the remaining ovarian tissue. This will immediately negatively affect the results of the operation. If the injury to the ovarian vessels remains unnoticed during surgery, internal bleeding will occur in the postoperative period, to stop which it will inevitably be necessary to perform a relaparotomy and suturing the bleeding vessels. When suturing the ovary, you should not try to carefully connect the edges of the wound.

If they diverge a little, ovulation will be easier in the future.

After toileting the abdominal cavity, they begin to restore the integrity of the anterior abdominal wall by layer-by-layer suturing the edges of the surgical wound and finally apply an aseptic bandage.

The main points of the operation of marginal wedge resection of the ovary after laparotomy are the following:

  1. Examination of the uterus, both ovaries and fallopian tubes;
  2. suturing the tubal end of each ovary (taking them on “holds”);
  3. marginal wedge-shaped resection of two-thirds of the mass of both ovaries in case of small cystic degeneration of them, caused by the persistence of follicles, or in case of sclerocystic degeneration of the ovaries (Stein-Leventhal syndrome);
  4. if a tumor is detected during surgery, excision is performed within healthy tissue;
  5. puncturing or diathermopuncture of persistent follicles;
  6. restoration of the integrity of the ovaries by applying a continuous catgut suture or knotted sutures;
  7. abdominal toilet;
  8. layer-by-layer suturing of the surgical wound;
  9. aseptic dressing.

Treatment of hyperplastic processes in PCOS

Treatment of endometrial hyperplastic processes (see endometrial hyperplasia, as well as the article on its treatment). Recurrent hyperplastic processes of the endometrium in PCOS are an indication for ovarian resection.

Treatment of hirsutism

Treatment of hirsutism is the most difficult task, which is due not only to the hypersecretion of androgens, but also to their peripheral metabolism.

At the level of the target tissue, in particular the hair follicle, T is converted into active dihydrotestosterone under the influence of the enzyme 5α-reductase. An increase in free androgen fractions is of no small importance, which aggravates the clinical manifestations of hyperandrogenism.

Treatment of hirsutism involves blocking the action of androgens in various ways:

  • Inhibition of synthesis in the endocrine glands;
  • an increase in the concentration of PSSG, i.e. a decrease in biologically active androgens;
  • inhibition of dihydrotestosterone synthesis in the target tissue due to inhibition of the activity of the enzyme 5α-reductase;
  • blockade of androgen receptors at the level of the hair follicle.

Given the role of adipose tissue in the synthesis of androgens, an indispensable condition in the treatment of hirsutism in obese women is normalization of body weight. A clear positive correlation has been shown between androgen levels and body mass index. In addition, given the role of insulin in hyperandrogenism in women with PCOS, therapy for insulin resistance is necessary.

Combined oral contraceptives are widely used to treat hirsutism, especially in mild forms. The mechanism of action of COCs is based on the suppression of LH synthesis, as well as an increase in the level of PSSH, which reduces the concentration of free androgens. The most effective, based on clinical studies, are COCs containing desogestrel, gestodene, and norgestimate.

One of the first antiandrogens was cyproterone acetate (Androcur), the mechanism of action of which is based on the blockade of androgen receptors in the target tissue and the suppression of gonadotropic secretion. Diane-35 is also an antiandrogen, combining 2 mg of cyproterone acetate with 35 mcg of ethinyl estradiol, which also has a contraceptive effect. Strengthening the antiandrogenic effect of “Diane” can be achieved by additionally prescribing “Androcur” - 25-50 mg from the 5th to the 15th day of the cycle. The duration of treatment ranges from 6 months to 2 years or more. The drug is well tolerated; side effects sometimes include lethargy, pastiness, mastalgia, weight gain and decreased libido at the beginning of treatment.

Spironolactone (Veroshpiron) also has an antiandrogenic effect. Blocks peripheral receptors and androgen synthesis in the adrenal glands and ovaries, promotes weight loss. With long-term use of 100 mg per day, a decrease in hirsutism is noted. Side effects: weak diuretic effect (in the first 5 days of treatment), lethargy, drowsiness. The duration of treatment is from 6 months to 2 years or more.

Flutamide is a nonsteroidal antiandrogen used in the treatment of prostate cancer. The mechanism of action is based primarily on inhibition of hair growth by blocking receptors and slight suppression of T synthesis. No side effects were noted. Prescribed 250-500 mg per day for 6 months or more. After 3 months, a pronounced clinical effect was noted without changing the level of androgens in the blood.

Gonadotropic releasing hormone agonists (Zoladex, Diferelin Depot, Buserelin, Decapeptil) are rarely used to treat hirsutism. They can be prescribed for high LH levels. The mechanism of action is based on blockade of the gonadotropic function of the pituitary gland and, consequently, LH-dependent synthesis of androgens in theca cells of the ovaries. The disadvantage is the appearance of complaints characteristic of menopausal syndrome, caused by a sharp decrease in ovarian function. These drugs are rarely used to treat hirsutism.

Drug treatment of hirsutism is not always effective, so various types of hair removal (electrical, laser, chemical and mechanical) have become widespread.

Hyperandrogenism and chronic anovulation are observed in endocrine disorders such as adrenogenital syndrome, neurometabolic-endocrine syndrome, Cushing's disease and hyperprolactinemia. In this case, morphological changes similar to polycystic ovary syndrome develop in the ovaries, and hyperandrogenism occurs. In such cases, we are talking about so-called secondary polycystic ovaries and the main principle of treatment is the therapy of the above diseases.

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How polycystic ovary syndrome manifests itself and what causes it: symptoms and causes

A woman’s health is extremely important for her full life and good mood. However, patients often have no idea that they have any disease.

Thus, neoplasms in the ovaries lead to many harmful consequences. Therefore, it is necessary to know the symptoms of polycystic ovary syndrome and the causes that cause it. What causes this pathology and what the threat is we will consider later in the article.

What it is?

Polycystic ovary syndrome is a disease of the female reproductive glands of hormonal etiology, characterized by multiple formation of cysts in their tissue.

Cysts are located both distantly from each other and in clusters. They also affect not only the surface of the organ, but also its internal space.

The ovaries are the female reproductive organs in which eggs are formed. They consist of a body and a tunica albuginea. It is in the membrane that follicles are formed, one of which becomes dominant, matures and subsequently bursts. An egg is released from such a follicle, which starts the ovulation process.

Healthy ovaries have the following sizes:

  • width – about 25 mm;
  • length - about three centimeters;
  • thickness - about one and a half centimeters;
  • volume – no more than 80 cubic meters. mm.

However, with polycystic disease, a dominant one does not stand out among the follicles, and therefore all the eggs remain immature. Ovulation does not occur, and the woman cannot become pregnant. In rare cases, when conception is successful, due to hormonal imbalance, a natural termination of pregnancy occurs at an early stage.

With the disease, the volume of the ovaries becomes over 9 cubic meters. see, which helps in diagnosing polycystic disease.

(The picture is clickable, click to enlarge)

Based on its origin, polycystic disease is divided into the following types:

  • Primary - has a genetic predisposition and can be congenital or debuts in teenage girls with the onset of the development of secondary sexual characteristics.
  • Secondary - develops as a complication of other diseases and is more of a syndrome than a pathology. Its development occurs after the onset of menstruation.

This disease is often confused with multifollicular ovaries. It is important to understand that these are different conditions and there is a difference.

Thus, multifollicular ovaries are a type of normal, treatment is not always required. This phenomenon is accompanied by the development of a large number of follicles, which is typical for the first week of the menstrual cycle. With polycystic disease, it is not follicles that develop, but cysts - pathological formations filled with liquid content.

This disease also differs from ovarian cysts. With the latter, the formation in the gland is single and often affects only one organ, while polycystic disease spreads to both sides. The causes of pathologies also differ.

According to statistics, 5–10% of women of reproductive age suffer from polycystic disease. It is this disease that leads to 25% of cases of female infertility. According to the International Classification of Diseases, tenth reissue ICD-10, polycystic ovarian disease refers to ovarian dysfunction and has code E28.2.

  • Excess androgens and insulin interfere with ovulation.
  • Obesity increases the amount of estrogen. The body tries to restore balance and produces more testosterone.
  • Chronic inflammation. Because of it, the body becomes less sensitive to insulin, which leads to an increase in its level.
  • Genetic predisposition for primary polycystic disease.

In addition to the causes, there are also factors that trigger the development of the disease:

  • excess weight;
  • constant stress;
  • irregular sex life;
  • a large number of abortions.

In adolescence, polycystic disease is especially affected by:

  • smoking;
  • unbalanced diet;
  • early sexual life;
  • little physical activity.

Psychosomatic factors in the development of the disease should not be excluded. Thus, anxious and stressed women suffer more than others from polycystic disease. Psychological reasons are:

  • problems with menstruation;
  • dissatisfaction with one's appearance;
  • unhealthy relationship with partner;
  • inability to get pregnant, or loss of a child.

The last factor is the most important, since the feeling of losing such a close person leads to functional changes in the body. If a child dies, has a miscarriage, or is unable to become pregnant, the woman’s body reacts to the feeling of loss by forming a cyst in the ovary.

With a lot of stress and anxiety, polycystic disease forms.

  • menstrual irregularities;
  • an increase in the amount of hair (hirsutism) in the perineum, on the abdomen and inner thighs, the appearance of a mustache above the upper lip (see photo);
  • excess weight.

With further development of polycystic disease, the patient's condition worsens. This is caused by an increase in the level of male hormones in the body. The disease is accompanied by the following symptoms:

  • scanty or profuse discharge during menstruation;
  • different duration of menstruation;
  • acne;
  • low voice;
  • male pattern bald spots;
  • mastopathy;
  • high insulin levels;
  • uterine bleeding (may be perceived as menstruation);
  • brown discharge (stained with blood);
  • pain in the lower abdomen;
  • mood lability;
  • infertility.

This will help to diagnose the disease in a timely manner and prescribe therapy.

  • type II diabetes;
  • malignant tumors in the uterus and mammary glands;
  • atherosclerosis;
  • rheumatic diseases;
  • hepatitis due to fat accumulation in the liver;
  • the risk of heart attack and stroke increases.

In addition, disruption of the endocrine glands worsens, which further worsens the course of the disease:

  • thyroid;
  • hypothalamus;
  • adrenal glands;
  • pituitary.

Polycystic ovary syndrome is a disease that worsens a woman’s well-being and self-perception. Along with unpleasant symptoms, it leads to harmful and even dangerous consequences and complications. This explains the need for its timely diagnosis and treatment.

Read our article on how polycystic ovary syndrome is treated.

Find out the main causes of polycystic ovary syndrome from the video:

opochke.com

2018 Blog about women's health.

Polycystic ovary syndrome is a gynecological disease combined with dysfunction of the endocrine system. The absence of a full-fledged dominant follicle provokes problems with conception. Against the background of PCOS, obesity often develops; women complain of irregular menstruation, the appearance of acne, and excessive hair growth.

What to do if polycystic ovary syndrome is diagnosed? What treatments are effective? What measures help you get pregnant with PCOS? The answers are in the article.

Polycystic ovary syndrome: what is it?

With polycystic ovary syndrome, many small, underdeveloped follicles appear. The number of bubbles can reach a dozen or more. In the absence of a full-fledged dominant follicle, there are disruptions in the ovulation process, the egg does not mature, and the regularity of the cycle is disrupted.

In patients with PCOS due to anovulation, doctors diagnose primary infertility. Carrying out full hormonal therapy and stimulating ovulation in many cases allows you to restore the level of fertility, increasing the chance of full conception and gestation.

Amenorrhea (lack of monthly bleeding) or oligomenorrhea (scanty, infrequent menstruation) often develops. Sometimes bleeding due to endometrial tissue rejection is accompanied by severe pain, and the blood volume is significantly higher than normal.

Causes of disturbances and discomfort: long-term influence of estrogens on the inner layer of the uterus and anovulation. In combination with a decrease in level, the development of hyperplastic processes is possible, which sometimes leads to pathological uterine bleeding. In the absence of treatment and inattention to the symptoms of PCOS, a negative effect on the uterus and appendages occurs over a long period, which can cause a malignant process.

Polycystic ovary syndrome ICD code - 10 - E28.2.

Reasons for the development of pathology

PCOS develops with severe disruption of the endocrine system. The pathological process develops when there is a malfunction in the functioning of the ovaries, pituitary gland, and adrenal glands.

With the progression of chronic autoimmune pathology, the levels of female sex hormones noticeably decrease: progesterone production is higher than normal. occurs against the background of excessive synthesis and, which is produced by the pituitary gland.

Note! Autoimmune pathology is congenital; hormonal disorders during fetal development are often associated with poor nutrition of the mother. With a meager diet, the growing body lacks many important substances, without which the full formation of the endocrine and reproductive systems in a female embryo is impossible.

First signs and symptoms

The first menstruation in girls occurs at the right time - from 12 to 13 years, but the cycle is not established for a long time. Scanty periods or absence of bleeding for six months indicates ovulation. During puberty, excessive hair growth is noticeable, acne often appears, and examination shows a bilateral increase in the size of the ovaries. A characteristic feature is the uniform accumulation of fat in different parts of the body, which leads to an increase in body weight, sometimes 10-20% above normal.

Dyshormonal disorders can be identified not only during a gynecological ultrasound and the results of a blood test for hormones, but also by external manifestations. With PCOS, a woman often gains extra pounds, and hirsutism increases psycho-emotional discomfort. As you get older, acne often disappears, but obesity and hair growth due to excess testosterone remain. Sometimes the male hormone levels are not much higher than normal, and the manifestations of hirsutism are minimal.

Specific symptoms of polycystic ovary syndrome:

  • menstrual irregularities;
  • absence or rare occurrence of ovulation;
  • primary infertility;
  • obesity, development of prediabetes;
  • increased cholesterol levels in the blood;
  • hair thinning or active growth on the body;
  • acne;
  • During the examination, the doctor notes the appearance of multiple cysts and enlarged ovaries.

Diagnostics

The presence of PCOS in a woman can be confirmed based on a comprehensive examination, based on a combination of echoscopic and clinical symptoms. When making a diagnosis, the basis is a prolonged absence of ovulation in combination with high testosterone levels and hyperandrogenism syndromes.

On bimanual examination, the paired organs are dense and larger than usual in size. Multiple cysts in the body of the ovaries in the absence of a mature dominant follicle are a characteristic sign of polycystic disease (“poly” means “many”).

Be sure to conduct hormone tests: it is important to know the level of progesterone, estrogen, testosterone, LH. Often, estrogens are practically normal, androgen values ​​are slightly increased, which reduces the diagnostic value of a blood test if PCOS is suspected. You cannot refuse tests: when selecting hormonal drugs, you need to see the indicators of the main regulators that affect the state of the reproductive and reproductive systems.

In difficult cases, ovarian laparoscopy is prescribed for an in-depth examination of the affected organs. If necessary, the doctor performs a tissue biopsy for research.

Objectives and main directions of therapy

Treatment goals for polycystic ovary syndrome:

  • restore the menstrual cycle;
  • reduce negative symptoms that worsen a woman’s appearance and health;
  • achieve ovulation if a woman is planning a pregnancy;
  • protect the walls of the uterus from excessive accumulation of endometrial cells that were not rejected during menstruation, which did not occur on time;
  • stabilize weight;
  • prevent long-term complications due to PCOS.

Go to the address and find out about the reasons for the development of ovarian oophoritis and the features of treatment of the disease.

Main methods of therapy:

  • taking combined oral contraceptives to stabilize menstrual function. Depending on the testosterone level, the gynecologist selects the optimal type of COC: Jazz, Janine, Diane 35, Yarina, Marvelon;
  • To achieve pregnancy, ovulation is stimulated. There are several schemes, but the most effective and in demand is the combination of the drug Clomiphene in the first phase of the cycle and for 10 days in the luteal (second) phase. Ovarian hyperstimulation requires strict adherence to the medication regimen, timely testing, and an ovulation test as recommended by a doctor;
  • diet correction is an essential element of treatment. If you have polycystic ovaries, you need to stabilize your weight at levels that are optimal for your height, age, and body type. You cannot starve, adhere to strict diets, or eat only vegetables or buckwheat. An unbalanced diet increases hormonal fluctuations, which interferes with the treatment process. You should not eat sugar, smoked meats, baked goods, fatty foods, you need to limit salt and spices. It is useful to eat five to six times throughout the day, drink up to one and a half to two liters of water to maintain water balance;
  • baths with pine elixir, herbal infusions, sea salt are useful;
  • As prescribed by your doctor, you need to take a complex of vitamins: tocopherol, ascorbic acid, riboflavin, biotin, cyanocobalamin. Vitamin therapy is needed to stimulate metabolic processes, normalize progesterone synthesis, strengthen the immune system, and improve the condition of blood vessels;
  • Surgical treatment with removal of multiple cysts is carried out when the effectiveness of conservative therapy is low. Endoscopic surgery is low-traumatic, the result after the procedure is in most cases positive - the likelihood of pregnancy against the backdrop of maturation of a full-fledged follicle increases several times.

Possible consequences

Against the background of long-term malfunctions of the reproductive and endocrine systems, an increased risk of negative processes in various parts of the body has been confirmed. The more attention a woman pays to her health, the lower the likelihood of complications, but the development of pathologies cannot be completely excluded: arterial hypertension, endometrial hyperplasia, oncopathology of the uterus and appendages.

Polycystic ovary syndrome and pregnancy

Is it possible to get pregnant with polycystic ovary syndrome? Some “specialists” provide inaccurate information in their materials: with PCOS, infertility inevitably develops, and the likelihood of getting pregnant is extremely low. After reading such articles, women diagnosed with polycystic ovary syndrome panic, despair, and become depressed. Nervous overload, taking tranquilizers, and depressed mood cause even more active hormonal fluctuations, which does not help restore the ability to conceive.

Reproduction doctors recommend that women with PCOS do not despair and go to a clinic with modern diagnostic equipment and qualified personnel. To achieve the long-awaited pregnancy, you will have to undergo a course of drug therapy or undergo endoscopic surgery to remove multiple cysts. To achieve a positive result, time must pass: most often, conception occurs six months to a year after the start of treatment, sometimes therapy lasts longer. In some cases, it is possible to stabilize the menstrual cycle in a shorter period of time if ovulation occurs periodically.

A woman will need patience and accuracy in plotting her basal temperature chart. It is important to take antiandrogenic COCs strictly on schedule.

To stimulate the ovaries, in which a full-fledged egg must mature, on certain days the woman receives hormonal injections (chorionic gonadotropin). Under the influence of regulators, a healthy follicle is formed in the ovary, which bursts and allows the prepared egg to be released. It is during this period that you need to do an ovulation test to confirm the optimal period for conception. Sexual intercourse is required (also the next day) for sperm to penetrate the mature egg.

Before ovarian stimulation, you need to pass a test for tubal patency (the procedure is called hysterosalpinography); free passage into the uterine cavity from the ovaries is important. A man must have a spermogram to confirm a sufficient number of motile and healthy sperm. If the conditions are met and there are no obstacles or pathological changes in the ejaculate and fallopian tubes, ovarian hyperstimulation can be performed.

If the ovaries are unresponsive to the standard dose, the reproductologist increases the rate of Clomiphene or, when the level reaches 200 mg, prescribes drugs from another group. It is important to monitor with ultrasound to ensure there is no overstimulation of the ovaries.

A positive result in the treatment of infertility due to PCOS is provided by “drilling” the ovaries - a laparoscopic operation during which the surgeon removes part of the thickened capsule with multiple cysts, freeing the passage for the follicle. After surgery, the production of testosterone decreases, an excess of which often makes it difficult to get pregnant. After ovarian laparoscopy, pregnancy can occur as early as the next full menstrual cycle. In most cases, conception occurs within a year after ovarian surgery.

After pregnancy, a woman with PCOS is under medical supervision. It is important to monitor hormonal levels to avoid spontaneous abortion, gestational diabetes, and other complications.

Prevention

Damage to the endocrine system often occurs against the background of genetic predisposition and endocrine pathologies. An autoimmune disease develops if the cells of a female fetus do not receive enough nutrients and hormones, without which the proper formation of the endocrine and reproductive systems is impossible. Reasons: poor diet during pregnancy, the influence of high doses of radiation, the expectant mother taking potent drugs, hormonal imbalances during gestation, endocrine diseases.

The risk of polycystic ovary syndrome can be reduced by a high-quality examination when planning pregnancy. If there are abnormalities in the functioning of the endocrine system, you need to undergo a course of therapy under the guidance of an experienced doctor. It is important to reduce the impact of chronic pathologies and ensure proper nutrition during pregnancy.

More information about the features of nutrition and diet during the treatment of polycystic ovary syndrome can be found in the following video:

), adrenal cortex (hypersecretion of adrenal androgens), hypothalamus and pituitary gland.

Nomenclature

Other names for this syndrome are:

  • polycystic ovary disease (incorrect, since this condition is characterized not as a disease, a separate nosological form, but as a clinical syndrome, the causes of which may be different);
  • functional ovarian hyperandrogenism (or functional ovarian hyperandrogenism);
  • hyperandrogenic chronic anovulation;
  • ovarian dysmetabolic syndrome;
  • polycystic ovary syndrome;
  • polycystic ovary syndrome.

Definitions

There are two definitions of polycystic ovary syndrome most commonly used in clinical practice.

The first definition was developed last year by consensus of an expert commission formed by the American National Institutes of Health (NIH). According to this definition, a patient should be diagnosed with polycystic ovary syndrome if she simultaneously has:

  1. Symptoms of excessive activity or excessive secretion of androgens (clinical and/or biochemical);
  2. Oligoovulation or anovulation

The second definition was formulated last year by a consensus of European experts formed in Rotterdam. By this definition, a diagnosis is made if the patient has any two of the following three signs simultaneously:

  1. Symptoms of excessive activity or excessive secretion of androgens (clinical or biochemical);
  2. Oligoovulation or anovulation;
  3. Polycystic ovaries with ultrasound examination of the abdominal organs

and if other causes that can cause polycystic ovaries are excluded.

The Rotterdam definition is much broader and includes significantly more patients in the group suffering from this syndrome. In particular, it includes patients without clinical or biochemical evidence of androgen excess (since any two of the three signs are mandatory, not all three), while in the American definition, excess secretion or excess activity of androgens is a prerequisite for the diagnosis polycystic ovary syndrome. Critics of the Rotterdam definition argue that findings from patients with androgen excess cannot necessarily be extrapolated to patients without symptoms of androgen excess.

Symptoms

Common symptoms of polycystic ovary syndrome are as follows:

  • Oligomenorrhea, amenorrhea - irregular, rare menstruation or complete absence of menstruation; those menstruation that does occur can be pathologically scanty or, on the contrary, excessively abundant, as well as painful;
  • Infertility, usually the result of chronic anovulation or oligoovulation (complete absence of ovulation or ovulation does not occur in every cycle);
  • Elevated blood levels of androgens (male hormones), especially free fractions of testosterone, androstenedione and dehydroepiandrosterone sulfate, which causes hirsutism and sometimes masculinization;
  • Central obesity is “spider-shaped” or “apple-shaped” obesity of the male type, in which the bulk of adipose tissue is concentrated in the lower abdomen and abdominal cavity;
  • Androgenic alopecia (significant male pattern baldness or hair loss with receding hairline on the sides of the forehead, above the forehead line, on the crown, occurring due to hormonal imbalance);
  • Acanthosis (dark pigment spots on the skin, from light beige to dark brown or black);
  • Acrochordons (skin folds) - small folds and wrinkles of the skin;
  • Striae (stretch marks) on the skin of the abdomen, usually as a consequence of rapid weight gain;
  • Long periods of symptoms resembling those of premenstrual syndrome (swelling, mood swings, pain in the lower abdomen, lower back, pain or swelling of the mammary glands);
  • Night apnea - stopping breathing during sleep, leading to frequent awakenings of the patient at night;
  • Depression, dysphoria (irritability, nervousness, aggressiveness), often drowsiness, lethargy, apathy, complaints of “fog in the head.”
  • Multiple ovarian cysts. Sonographically, they may appear as a “pearl necklace,” a collection of whitish vesicles or “fruit pits” scattered throughout the ovarian tissue;
  • Enlarged ovaries, usually 1.5 to 3 times larger than normal, resulting from multiple small cysts;
  • Thickened, smooth, pearly white outer surface (capsule) of the ovaries;
  • Thickened, hyperplastic endometrium of the uterus as a result of a chronic excess of estrogen, not balanced by adequate progesterone influences;
  • Chronic pain in the lower abdomen or lower back, in the pelvic region, probably due to compression of the pelvic organs by enlarged ovaries or due to hypersecretion of prostaglandins in the ovaries and endometrium; The exact cause of chronic pain in PCOS is unknown;
  • Elevated LH levels or increased LH/FSH ratio: when measured on the 3rd day of the menstrual cycle, the LH/FSH ratio is greater than 1:1;
  • Reduced levels of sex steroid binding globulin;
  • Hyperinsulinemia (increased fasting blood insulin level), impaired glucose tolerance, signs of tissue insulin resistance when tested using the sugar curve method.

Health risks and complications

Women with PCOS are at increased risk of developing the following complications:

  • Endometrial hyperplasia and endometrial cancer due to the absence or irregularity of menstruation and the “accumulation” of non-exfoliating endometrium, as well as due to the absence or insufficiency of progesterone effects, leading to prolonged hyperstimulation of endometrial cells unbalanced by progesterone with increased levels of estrogen;
  • Insulin resistance and type 2 diabetes mellitus;
  • Thrombosis, thromboembolism, thrombophlebitis due to increased blood clotting;
  • Dyslipidemia (metabolism disorders of cholesterol and triglycerides with the possible development of vascular atherosclerosis);
  • Cardiovascular diseases, myocardial infarction, stroke.

Data from a number of researchers indicate that women with polycystic ovary syndrome have an increased risk of miscarriage or premature birth, and miscarriage. In addition, many women with this syndrome cannot conceive or have difficulty conceiving due to irregular menstrual cycles and absent or infrequent ovulation. However, with proper treatment, these women can normally conceive, carry and give birth to a healthy child.

Epidemiology

Although ultrasound examination of the abdominal cavity reveals polycystic-appearing ovaries in up to 20% of women of reproductive age (including those who do not present any complaints), only 5-10% of women of reproductive age show clinical signs that allow a diagnosis of polycystic ovary syndrome . Polycystic ovary syndrome is equally common in different ethnic groups. It is the most common hormonal disorder in women of childbearing age and one of the leading causes of female infertility.

Etiology and pathogenesis

The exact reasons for the development of the syndrome are unknown, but great importance is attached to the pathological decrease in insulin sensitivity of peripheral tissues, especially adipose and muscle tissue (the development of their insulin resistance) while maintaining insulin sensitivity of ovarian tissue. A situation of pathologically increased insulin sensitivity of ovarian tissue while maintaining normal insulin sensitivity of peripheral tissues is also possible.

In the first case, as a consequence of the body's insulin resistance, compensatory hypersecretion of insulin occurs, leading to the development of hyperinsulinemia. And a pathologically elevated level of insulin in the blood leads to ovarian hyperstimulation and increased secretion of androgens and estrogens by the ovaries and impaired ovulation, since the ovaries retain normal sensitivity to insulin.

In the second case, the level of insulin in the blood is normal, but the response of the ovaries to stimulation by normal levels of insulin is pathologically increased, which leads to the same result - hypersecretion of androgens and estrogens by the ovaries and impaired ovulation.

Pathological tissue insulin resistance, hyperinsulinemia and insulin hypersecretion in polycystic ovary syndrome are often (but not always) a consequence of obesity or overweight. At the same time, these phenomena themselves can lead to obesity, since the effects of insulin are an increase in appetite, an increase in fat deposition and a decrease in its mobilization.

In the pathogenesis of polycystic ovary syndrome, importance is also attached to disturbances in the regulatory hypothalamic-pituitary influences: excessive secretion of LH, abnormally increased LH/FSH ratio, increased “opioidergic” and decreased dopaminergic tone in the hypothalamic-pituitary system. The condition may be aggravated and more difficult to treat in the presence of concomitant hyperprolactinemia, subclinical or clinically significant thyroid insufficiency. Such combinations occur in these women much more often than in the general population, which may indicate the polyendocrine or polyetiological nature of Stein-Leventhal syndrome.

Some researchers attach importance to the increased level of prostaglandins and other inflammatory mediators in the thecal tissue of the ovaries and in the follicular fluid in patients with polycystic ovary syndrome and believe that the “cold”, aseptic inflammation of the ovarian tissue that occurs for unknown reasons may play a role in the pathogenesis of polycystic ovary syndrome. inflammatory diseases of the female genital area or autoimmune mechanisms. It is known that the introduction of prostaglandin E1 into the ovary or into the vessel supplying it causes a significant increase in the secretion of androgens and estrogens by the thecal tissue of the ovary in laboratory rats.

Treatment

Story

Historically, the very first attempts to treat polycystic ovary syndrome consisted of surgical intervention - decapsulation of the ovaries or their partial resection with removal of the tissue most affected by cystosis, or excision of the ovarian bed (ovarian wedge resection), or the careful use of diathermy (heating) of the ovaries. In a number of cases, such operations led to success and made it possible to restore a woman’s fertility, as well as to achieve a sharp decrease in the secretion of androgens by the ovaries, normalization of the menstrual cycle, etc. However, surgical intervention is not always possible, and did not always lead to success. In addition, complications are possible, such as the formation of adhesions. Therefore, experts were looking for conservative, non-surgical methods for treating polycystic ovary syndrome.

Traditional conservative treatment consisted of prescribing antiandrogens, estrogens, progestins with antiandrogenic activity, or a combination of these (for example, in the form of birth control pills such as Diane-35). Such treatment usually normalized the menstrual cycle, but was insufficiently effective against skin manifestations (acne, sebaceous skin, androgen-dependent alopecia), did not restore ovulation and fertility, and did not eliminate the causes of polycystic ovary syndrome (impaired insulin secretion and insulin sensitivity tissues, functions of the hypothalamic-pituitary axis, etc.). Moreover, treatment with estrogens, progestins and antiandrogens was often accompanied by further weight gain in patients, worsening existing problems with carbohydrate metabolism and the thyroid gland, hyperprolactinemia, and depression.

The next attempt to improve methods of treating polycystic ovary syndrome was made with the advent of anti-estrogenic drugs - clostilbegit (clomiphene citrate) and tamoxifen - in the arsenal of doctors. The use of clomiphene citrate or tamoxifen in the middle of the cycle made it possible to successfully induce ovulation in approximately 30% of cases, restore women's fertility and achieve a stable ovulatory menstrual cycle without the use of exogenous hormones (estrogens, progestins and antiandrogens). However, the effectiveness of clostilbegit and tamoxifen against other symptoms of polycystic ovary syndrome, in particular manifestations of hyperandrogenism, was limited. The effectiveness of combination therapy (estrogens and progestins or antiandrogens during the cycle, clostilbegit or tamoxifen in the middle of the cycle) turned out to be higher, but also insufficient.

Attempts to improve the effectiveness of treatment of women with polycystic ovary syndrome by correcting authentically existing or suspected concomitant endocrine disorders (correction of concomitant hyperprolactinemia with bromocriptine, concomitant subclinical thyroid insufficiency with the prescription of thyroid hormones, suppression of hypersecretion of androgens by the adrenal glands by prescribing small doses of dexamethasone) were partly successful, but success was individual and not constant and predictable enough.

Real changes in the effectiveness of treatment of polycystic ovary syndrome occurred when it was possible to penetrate deeper into the understanding of the pathogenesis of polycystic ovary syndrome and when they began to attach primary importance in the development of this state to insulin hypersecretion and pathological tissue insulin resistance with preserved ovarian insulin sensitivity. Since that time, for the treatment of polycystic ovary syndrome, drugs that normalize tissue sensitivity to insulin and reduce insulin secretion - metformin, glitazones (pioglitazone, rosiglitazone) have become widely used as first-line drugs. This approach turned out to be very successful - in 80% of women with polycystic ovary syndrome on monotherapy with metformin or one of the glitazones, ovulation was spontaneously restored, the menstrual cycle was normalized, the secretion of androgens by the ovaries was reduced and the symptoms of hyperandrogenism disappeared or decreased, body weight decreased, carbohydrate metabolism was normalized, and the mental state improved . Most of these women were then able to carry and give birth to healthy children.

An even higher success rate, exceeding 90%, was given by combination therapy - a combination of metformin or glitazones with previously known methods (estrogens, antiandrogens and progestins, and/or with antiestrogens in the middle of the cycle and/or, possibly, correction of concomitant disorders of prolactin secretion, thyroid hormones, adrenal androgens). The introduction of such a combined approach to the treatment of polycystic ovary syndrome into the practice of gynecologists-endocrinologists has made it possible to almost completely eliminate, except for rare multidrug-resistant cases, the need for surgical intervention for polycystic ovary syndrome, and also make the need for ovulation induction with gonadotropins and artificial insemination of women much less common with polycystic ovary syndrome.

Current state of the issue

Today, the first-line drugs for the treatment of polycystic ovary syndrome are metformin and glitazones (pioglitazone, rosiglitazone). Antiandrogenic drugs can be added to them, if necessary (