Pathogenetic forms and development mechanisms
The development of endocrine disorders is based on several forms:
- Mixed form: The triggering mechanism is adrenal disorders or androgen excess during adrenarche. Peripheral conversion in adipose tissue enhances luteinizing hormone synthesis, disrupting the gonadotropin ratio and triggering a vicious cycle of hyperandrogenism.
- Central form: Develops due to stress, infections, or intoxications. Endogenous opioid levels rise, and dopaminergic regulation of gonadotropin-releasing hormone is impaired.
- Metabolic factor: Chronic hyperinsulinemia stimulates insulin-like growth factor 1, increasing androgen synthesis in the theca cells and decreasing sex hormone-binding globulin levels.
Clinical features and symptoms
The clinical presentation depends on the form of the disease, but shares common patterns:
- Cycle disorders: Hypomenorrhea, opsomenorrhea, oligomenorrhea, and amenorrhea are characteristic, as well as primary or secondary infertility due to folliculogenesis disorders.
- Hirsutism: The main symptom for young patients. Moderate in the typical form, observed in all patients in the mixed form, and appears several years after cycle disruption against the background of obesity in the central form.
- Metabolic disorders: Dyslipidemia, obesity, striae, as well as long-term risks of arterial hypertension and atherosclerosis are possible.
Diagnostic criteria
Diagnosis is based on a comprehensive analysis of medical history, hormonal profile, and instrumental data:
- Ultrasound examination: Reveals bilateral ovarian enlargement (volume greater than 9 cm³), hyperplastic stroma, and an accumulation of more than 10 atretic follicles peripherally («string of pearls» sign).
- Hormonal profile: The LH to FSH ratio rises above 2.5–3. DHEA and DHEA-S levels are elevated in the mixed form.
- Laparoscopy: Visualizes a thickened pearly-white ovarian capsule without signs of ovulatory stigmata.
Principles and stages of treatment
The therapeutic strategy is selected individually depending on the patient's age and main complaints:
- Weight management: In case of concomitant obesity, diet therapy combined with physical therapy is indicated; therapeutic fasting is strictly contraindicated.
- Medical support: In central genesis, drugs that normalize neurotransmitter metabolism are used (phenytoin, beclamide), and for weight loss — orlistat or sibutramine.
- Reproductive function: To restore ovulation in subsequent stages, the first-line drug clomifene is used.
Pathogenesis formula: Stress or adrenals $\rightarrow$ LH/FSH disruption $\rightarrow$ hyperandrogenism + insulin resistance $\rightarrow$ anovulation and infertility.
Class and exam questions
What are the main sonographic signs characteristic of the pathology?
Pathognomonic signs include an ovarian volume increase of more than 9 cm³, stromal hyperplasia, the presence of more than 10 atretic follicles, and their peripheral arrangement beneath a thickened capsule.
What is the difference in hirsutism manifestations between the typical and central forms?
In the typical form, hirsutism develops gradually from menarche and is moderately expressed. In the central form, it occurs 3–5 years after menstrual dysfunction against the background of pronounced obesity.
How does insulin affect the level of free androgens?
Chronic hyperinsulinemia stimulates the synthesis of IGF-1, which increases androgen production in the ovaries and inhibits hepatic synthesis of sex hormone-binding globulins, increasing the free testosterone fraction.
What else to study on this topic
- Differential diagnosis with hormone-secreting ovarian and adrenal tumors
- Histological picture of ovarian biopsy during laparoscopy
- The role of growth hormone in normal-weight patients
- Pathogenetic features of early pregnancy loss
- Methods for preventing endometrial hyperplastic processes
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