Treatise Index
- 1. The PCOS Spectrum
- 2. Diagnosis: Rotterdam Criteria
- 3. Pathophysiology: Insulin and Androgens
- 4. Clinical Manifestations and Phenotypes
- 5. Long-Term Metabolic Risks
- 6. Nutritional Management and PCOS Diet
- 7. Pharmacotherapy: Beyond the Pill
- 8. Infertility Management
- 9. Conclusion
- Selected References
It's Not About Cysts
The name "Polycystic Ovary Syndrome" is technically inaccurate. The "cysts" seen on ultrasound are actually antral follicles (immature eggs) that have stopped growing due to hormonal imbalance. PCOS is not an isolated ovarian disease, but a complex endocrine and metabolic disorder that affects the entire body, from skin to pancreas.
1. Introduction: The PCOS Spectrum
Polycystic Ovary Syndrome (PCOS) is the most common endocrinopathy in women of reproductive age, affecting between 6% to 20% of the global female population, depending on the diagnostic criteria used. Frequently underdiagnosed, PCOS is the leading cause of anovulatory infertility worldwide.
More than a reproductive or aesthetic issue, PCOS represents a state of chronic low-grade inflammation and metabolic dysfunction. Women with PCOS have increased risks for type 2 diabetes, cardiovascular disease, hypertension, and endometrial cancer, requiring a medical approach that goes far beyond prescribing contraceptives.
2. Diagnosis: The Rotterdam Criteria
The current international consensus for PCOS diagnosis is the Rotterdam Criteria (2003). To confirm the diagnosis, the patient must present at least two of the three criteria below, after excluding other etiologies (such as congenital adrenal hyperplasia, thyroid disorders, or hyperprolactinemia):
- Ovulatory Dysfunction: Oligo-ovulation (long cycles, >35 days) or Anovulation (absence of menstruation/ovulation).
- Hyperandrogenism:
- Clinical: Hirsutism (excess hair in male areas - Ferriman-Gallwey Score), severe acne, androgenetic alopecia.
- Biochemical: Elevated levels of total/free testosterone or DHEA-S in the blood.
- Polycystic Ovarian Morphology (on Ultrasound): Presence of 12 or more follicles (2-9 mm) in at least one ovary and/or increased ovarian volume (>10 cm³).
3. Pathophysiology: The Insulin Vicious Cycle
Although the exact cause is multifactorial (genetic + environment), Insulin Resistance (IR) is considered the central driver of the syndrome in about 70-80% of patients (even in lean ones).
The Molecular Mechanism
IR leads to compensatory hyperinsulinemia (excess insulin in the blood). Elevated insulin acts directly on two targets:
- Ovaries (Theca Cells): Insulin stimulates excessive production of androgens (testosterone), which block follicular maturation, causing anovulation.
- Liver: Insulin inhibits the production of SHBG (Sex Hormone Binding Globulin). With less SHBG, more free testosterone is left circulating to cause acne and hirsutism.
4. Clinical Manifestations and Phenotypes
PCOS presentation is heterogeneous. Not every patient has acne, not every patient is obese. Four main phenotypes (A, B, C, and D) are recognized, varying in severity:
| Sign/Symptom | Description and Impact |
|---|---|
| Menstrual Irregularity | Unpredictable cycles, amenorrhea (going months without menstruating), or dysfunctional uterine bleeding. Reflects lack of ovulation. |
| Hirsutism | Growth of thick, pigmented hair on the face (chin, upper lip), chest, abdomen, and back. Causes great psychosocial distress. |
| Resistant Acne | Acne that persists into adulthood, often located on the jawline and neck, refractory to common topical treatments. |
| Acanthosis Nigricans | Dark, velvety patches in skin folds (neck, armpits, groin). It is a direct dermatological sign of severe insulin resistance. |
5. Long-Term Metabolic Risks
PCOS does not end at menopause; its metabolic risks persist. Patients with PCOS have:
- 4x higher risk of developing Type 2 Diabetes.
- High prevalence of Metabolic Syndrome (central obesity, dyslipidemia, hypertension).
- Higher risk of Hepatic Steatosis (fatty liver).
- Increased risk of Endometrial Cancer due to prolonged exposure to estrogen without the opposition of progesterone (which is only produced upon ovulation).
6. Nutritional Management: The First Line of Treatment
Lifestyle change is the first-line therapy in all international consensuses. The main goal is to improve insulin sensitivity.
Dietary Strategies
- Low Glycemic Index (GI): Prioritize complex carbohydrates rich in fiber to avoid insulin spikes.
- Anti-inflammatory Diet: Rich in omega-3, antioxidants, vegetables, and low in trans fats and ultra-processed foods.
- Seed Cycling: Complementary strategy for hormonal support, although with more limited scientific evidence.
7. Pharmacotherapy: Beyond the Pill
Treatment should be individualized according to the patient's main complaint (irregularity, androgenic symptoms, or desire to conceive).
- Insulin Sensitizers: Metformin is the gold standard for treating insulin resistance in PCOS, improving ovulation and reducing androgens.
- Inositol (Myo-inositol): Natural supplement that improves insulin signaling and oocyte quality, with fewer side effects than metformin.
- Combined Oral Contraceptives (COCs): Regulate the cycle and reduce androgens, protecting the endometrium. They do not "cure" PCOS, only control symptoms.
- Anti-androgens: Spironolactone or Cyproterone can be used to treat severe hirsutism and acne.
8. Infertility Management
For women wishing to conceive, the focus is on inducing ovulation. Weight loss of just 5-10% can restore spontaneous ovulation in many patients.
Inducing medications like Letrozole (aromatase inhibitor) are today the first pharmacological choice, surpassing Clomiphene in efficacy and safety for PCOS patients.
9. Conclusion
Polycystic Ovary Syndrome is a chronic condition that accompanies women throughout their lives. Early diagnosis and intervention focused on metabolic health are crucial not only for fertility but for the prevention of cardiovascular diseases and diabetes in the future. The approach should always be multidisciplinary, integrating gynecologist, endocrinologist, nutritionist, and dermatologist.