Polycystic ovary syndrome is an increase in gonads due to cystic atresia of follicles. It is one of the signs of polycystic ovarian syndrome and is often used as a synonym for this pathology. Other symptoms of the disease include menstrual and reproductive dysfunction, signs of virilization, obesity. The diagnosis is based on anamnesis data, the results of general and gynecological examination, ultrasonography, hormonal analysis. The treatment is complex, includes correction of metabolic and endocrine disorders, wedge-shaped resection or cauterization of the ovaries.
E28.2 Polycystic ovarian syndrome
The term “polycystic ovary syndrome” can be interpreted as an ultrasound sign, polycystic gonadal changes observed normally or in a number of pathologies, or as a specific disease – polycystic ovary syndrome (PCOS). Its historical name is Stein–Leventhal syndrome, after Chicago gynecologists who most clearly described the symptoms of the classic form of the disease in 1935. Polycystic fibrosis is detected by ultrasound at 16-30 years of age, the frequency of occurrence is up to 54% among women of fertile age. Scleropolycystic disease is registered in 5-20% of women.
Causes of polycystic ovary syndrome
Common causes of asymptomatic transient polycystic ovaries (multifollicular gonads), which is the norm, are stress, physical activity, taking hormonal contraceptives. The provoking factors of secondary polycystic diseases that have arisen against the background of known diseases are different and are associated with the mechanism of development of these pathologies. The etiology of PCOS has been poorly studied. It is assumed that in 80% of the causes are congenital, in 20% – acquired. Possible risk factors:
- Exogenous: infectious and inflammatory diseases suffered in childhood and puberty (chronic tonsillitis, childhood infections, chronic inflammation of the internal genital organs), TBI (brain concussions, bruises, contusions), prolonged psycho-emotional stress (information stress, increased educational load).
- Endogenous: adverse effects on the fetus (androgens, epigenetic factors, consequences of the pathological course of pregnancy or childbirth), low birth weight, congenital genetically determined defect of the enzymatic systems of the gonads.
A special role is given to hereditary predisposition. There are cases of familial scleropolycystic disease. There is a high probability of pathology in women whose mothers or sisters suffer from this disease. The genetic risk of having a daughter with a tendency to PCOS in a sick mother is aggravated due to another reason – the fetus develops with an excess of testosterone. A risk factor for male line inheritance is early baldness in male blood relatives.
Polycystic ovaries are characterized by the accumulation of immature follicles due to anovulation. With random anovulatory cycles, such “cysts” resolve over time without consequences, with regular ones they provoke the development of pathology. The pathogenesis of PCOS has not yet been clarified, there are several theories on this. The primary defect of the feedback mechanism may come from the hypothalamic-pituitary system, ovaries, adrenal glands.
Desynchronization of endocrine gland functions leads to increased synthesis of androgens by gonads without their further aromatization into estradiol, lack of ovulation (as a consequence, infertility), progesterone deficiency, polycystic follicle changes, thickening of the ovarian capsule. Androstenediol is aromatized by adipose tissue and adrenal glands into estrone, there is a relative hyperestrogenism leading to endometrial hyperplasia.
The level of free testosterone in the blood increases, the result of hyperandrogenism is virilization. Hyperglycemia developed as a result of insulin resistance exacerbates the imbalance, contributing to increased synthesis of ovarian androgens, impaired binding of testosterone, which further increases the level of this hormone and estrone.
By origin, polycystic ovaries are classified as primary (PCOS) and secondary (concomitant with known nosological forms). Scleropolycystis is divided into two forms – with obesity and with normal or reduced body weight. In addition, there are 4 phenotypes of PCOS, which are based on symptoms that are diagnostic criteria (ESNRE/ASRM, 2007):
- Phenotype A (classical). Combination of hyperandrogenism with anovulation, polycystic disease. The frequency of occurrence is 54%.
- Phenotype B (anovulatory). With hyperandrogenism, ovulatory dysfunction, without polycystic disease. The prevalence is 29%.
- Phenotype C (ovulatory). Hyperandrogenism and polycystic disease. The frequency of occurrence is 9%.
- Phenotype D (nonandrogenic). Anovulation and polycystic disease. The occurrence is 8%.
Symptoms of polycystic ovary syndrome
Transient cystic changes usually occur without external signs. With scleropolycystosis, symptoms can manifest with menarche, less often – against the background of an established cycle. 85% of women have menstrual disorders: first, proyomenorrhea alternates with opsomenorrhea, acyclic bleeding, hypo- and oligomenorrhea is recorded. Then the intervals between bleeding lengthen, hypomenstrual syndrome and amenorrhea develop.
A few years after the onset of menstruation, hirsutism occurs, skin symptoms of hyperandrogenism: seborrhea, acne. In 30-40% of patients, obesity is formed. Persistent anovulation leads to infertility. In 10-15% of patients, spontaneous pregnancy may occur, which most often ends in miscarriage. There may be symptoms such as galactorrhea, psychoemotional and vegetative-vascular disorders similar to menopausal syndrome.
The most threatening complication of untreated scleropolycystic is hormone-dependent endometrial cancer, which develops in 19-25% of patients. Other long-term consequences include various types of cerebrovascular insufficiency (the risk increases by 2.8-3.4 times), glucose tolerance, which occurs in 40% of patients after 40 years and progresses in half of them to type 2 diabetes for six years.
Obstetric complications are typical for patients of reproductive age – gestational diabetes mellitus, preeclampsia, premature birth (the risk of these pathologies increases threefold, fourfold and twice, respectively). The risk of perinatal mortality is tripled. Complications are often caused by some methods of treating the disease: after ovulation induction, ovarian hyperstimulation syndrome develops, surgical intervention entails tubal-peritoneal infertility.
Polycystic ovaries as a morphological change is not a diagnosis, but a sign of a possible pathology. The diagnosis is made by a gynecologist with the participation of an ultrasound diagnostics doctor, an endocrinologist. PCOS is indicated by the following symptoms (at least two are required): laboratory or visual signs of hyperandrogenism; oligo- or anovulation; polycystic changes. Diagnostic methods include:
- Clinical examination. During a conversation with the patient, a general examination of scleropolycystis can be assumed from complaints of menstrual cycle disorders and infertility, the presence of PCOS in close relatives, an increased body mass index, virilization (hirsutism, hypertrichosis, oily, acne-prone skin). During gynecological examination – for enlarged ovaries.
- Ultrasonography. With transvaginal ultrasound of the ovaries, polycystic is characterized by an increased (over 9-10 cubic cm) volume of gonads; enlarged (2-10 mm) atretic follicles (more than 10) located under the thickened capsule without dominant; hyperplastic (up to a quarter of the total volume) stroma. Folliculometry reveals less than 6 ovulations per year.
- Laboratory tests. In androgenemia, hormone analysis confirms an increase in the level of luteinizing hormone and its ratio to follicle-stimulating hormone (more than 2.5), an increase in the free testosterone index. Concomitant insulin resistance is indirectly indicated by the results of a biochemical blood test – an increase in triglycerides, a decrease in HDL, hyperglycemia.
Additionally, a biochemical blood test, hysteroscopy with endometrial biopsy, ultrasound of the adrenal glands, thyroid gland, radiography or MRI of the Turkish saddle are prescribed. Some clinicians recommend to distinguish polycystic ovaries according to ultrasound data from multifollicular ovaries, characterized by a smaller size of “cysts”, unchanged capsule and stroma, normal volume and echogenic structure of gonads. Such changes are often a variant of the norm.
Primary polycystic ovaries should be differentiated from secondary, the most common causes of which are congenital pathologies (adrenogenital syndrome, congenital hyperplasia of the adrenal cortex), neurotransmitter-endocrine syndrome, Itsenko-Cushing’s disease, as well as virilizing tumors of the ovaries and adrenal glands. To exclude the tumor process, it may be necessary to consult an oncogynecologist, oncourologist.
The choice of therapeutic tactics depends on the cause that caused this condition and the existing symptoms. Polycystic ovaries, not manifested by any disorders, does not require treatment. With secondary polycystic disease, correction of disorders caused by the underlying disease is prescribed. Therapeutic measures for PCOS are determined by the clinical picture of pathology.
PCOS treatment includes several stages aimed at normalization of metabolic disorders, restoration of the ovulatory cycle and generative function, elimination of endometrial hyperplastic processes and manifestations of hyperandrogenism. First of all, the treatment of metabolic syndrome and endometrial hyperplasia (if any) is carried out, then, if the patient wants to have children, ovulation induction is started.
- Correction of metabolic disorders. All obese patients are recommended to modify their lifestyle – physical activity, a diet with a restriction of spicy and salty dishes, liquids – up to 1.5 liters per day. The caloric content of the daily diet is up to 2,000 kcal, 52% of calories should come from carbohydrates, 16% from proteins, 32% from fats, two thirds of the latter are unsaturated. With insulin resistance, hyperinsulinemia, insulin sensitizers are prescribed.
- Therapy of endometrial hyperplasia. With obesity, recurrent hyperplastic processes, adenomyosis, the use of progestogens is preferable, with normal body weight and primary hyperplasia – estrogen-progestogens. Drugs can be prescribed in a cyclic or continuous mode. Adenomyosis is also treated with gonadoliberin analogues.
- Infertility treatment. Not the most effective, but the safest method is the use of estrogen–progestin drugs (the “rebound effect” after their cancellation can lead to ovulation). In case of anovulatory infertility, ovulation induction is carried out by clomiphene, letrozole, in case of their ineffectiveness – gonadotropins. IVF technologies can be used for pregnancy.
- Treatment of hirsutism and acne. To eliminate the external manifestations of hyperandrogenism, hormonal contraceptives (orally, in the form of patches or vaginal rings) spironolactone are used. Preference is given to combined hormonal drugs without androgenic action or with an antiandrogenic effect. Laser and photoepilation are used to enhance the cosmetic effect.
In most cases, only surgical treatment can restore menstrual and reproductive function. Ovarian interventions are performed by laparoscopic access, which minimizes the risk of adhesions. Surgical treatment for recurrent endometrial hyperplasia is also prescribed to women who are not planning pregnancy.
- Ovarian drilling. Destruction of hyperplastic stroma by a point electrode. It is used to stimulate ovulation with a slight increase in the gonads. It includes various techniques – electro-, laser-, diathermocauterization. The disadvantage of the method is the relative short–term therapeutic effect.
- Wedge-shaped resection. Excision of the wedge-shaped area, including the cortical and medullary layers. It is performed to induce ovulation with a pronounced increase in the ovaries or to prevent relapses of endometrial hyperplasia. The disadvantage is a decrease in ovarian reserve, early or premature menopause is possible.
The success of surgical intervention is evidenced by the restoration of ovulatory function in the first weeks after surgery. If ovulation does not occur within two to three cycles, it is medically stimulated. Pregnancy usually occurs within 6-12 months. The probability of a favorable outcome decreases in direct proportion to the time since the operation.
Prevention of relapse
Existing methods of treating polycystic ovary syndrome most often do not allow achieving a lasting cure. The reason is the inability to eliminate the main pathogenetic links of the disease. Symptoms and structural ovarian changes resume within five years after surgery, which necessitates supportive treatment.
To regulate the menstrual cycle, prevent endometrial hyperplasia, hirsutism and hyperandrogenic dermatopathy on a permanent basis until menopause, patients are prescribed combined hormonal contraceptives or progestogens in the second phase of the cycle. This tactic also contributes to the preservation of reproductive function in some patients.
Prognosis and prevention
With polycystic ovaries, the prognosis for life is favorable in the absence of malignant transformation of the endometrium. The prognosis of the realization of reproductive function depends on how early treatment was started, what causes underlie the pathology. Thus, infertility treatment is most effective in the absence of virile and metabolic syndrome, pronounced hypothalamic-pituitary disorders.
Primary and secondary prevention of polycystic ovaries is to combat obesity, timely detection and correction of hypothalamic-pituitary, adrenal, ovarian dysfunction. Women suffering from PCOS are at high risk of developing cancer of the uterine body, therefore they are subject to follow–up, including control studies (ultrasound, hysteroscopy, if necessary, therapeutic and diagnostic curettage of the endometrium).