Polycystic Ovarian Syndrome - PCOS
Polycystic ovary syndrome (PCOS) is the most common, and one of the most complex, endocrine and metabolic disorders in women of reproductive age, affecting 6% to 20% depending on the diagnostic criteria used. Although PCOS is a multisystem condition involving both reproduction and metabolism, a dermatologist is often the first doctor these patients see, because excess androgens (hyperandrogenism) show up so visibly on the skin: persistent, treatment-resistant acne, excess hair growth, female pattern hair loss (androgenetic alopecia) and acanthosis nigricans.
At Haute-Derma, managing PCOS goes well beyond cosmetic skin treatments. It calls for a thorough hormonal workup, systemic medication and targeted procedures, all aimed at addressing the underlying cause of the disease.
How PCOS Develops: Biology and Pathogenesis
PCOS is driven by a self-reinforcing cycle in which a disturbed neuroendocrine axis and a disturbed metabolic axis feed into each other:
- Androgen excess (hyperandrogenism):
- GnRH is released from the hypothalamus in faster pulses, which pushes the pituitary to favor luteinizing hormone (LH) over FSH (LH/FSH ratio > 2).
- High LH levels act directly on the ovarian theca cells, which respond by producing more androgens (testosterone and androstenedione).
- Insulin resistance and hyperinsulinemia:
- Around 70–80% of women with PCOS, whether overweight or lean, have peripheral insulin resistance.
- High insulin levels cause harm in two ways: (1) they stimulate the ovaries to make more testosterone, and (2) they suppress the liver's production of SHBG (sex hormone-binding globulin), the protein that carries sex hormones. With less SHBG available, the share of free testosterone in the blood rises sharply, and it is this biologically active form that triggers the skin symptoms.
- Androgen conversion in hair follicles and sebaceous glands:
- Sebaceous gland cells and hair follicles contain the enzyme 5-alpha-reductase (mainly type 1), which converts testosterone into dihydrotestosterone (DHT), an androgen that binds the androgen receptor (AR) 5–10 times more strongly.
- DHT enlarges the sebaceous glands and increases oil production. On the face and body it turns fine vellus hairs into coarse terminal hairs, yet on the scalp it shrinks the follicles, leading to hair loss.
Rotterdam Criteria (2003) and Clinical Signs
PCOS is diagnosed when a patient meets at least 2 of the 3 Rotterdam criteria, once other conditions such as non-classic congenital adrenal hyperplasia, Cushing's syndrome and hyperprolactinemia have been ruled out:
- Ovulatory dysfunction / menstrual irregularity: infrequent periods (cycles longer than 35 days) or no periods at all for more than 6 months.
- Hyperandrogenism (clinical or biochemical):
- Polycystic ovarian morphology on ultrasound: ≥ 12 small follicles (2–9 mm in diameter) per ovary under the original Rotterdam criteria (≥ 20 follicles under the 2018 international guideline with modern probes), and/or an ovarian volume > 10 mL.
Skin Manifestations of PCOS
| Skin Manifestation | Underlying Hormonal Mechanism | Assessment Scale / Clinical Features |
|---|---|---|
| Recalcitrant acne | DHT enlarges the sebaceous glands, increases production of thick sebum and causes keratinization of the follicular opening | Concentrated on the lower third of the face, jawline, neck and chest/back. Resistant to antibiotics or isotretinoin used alone |
| Hirsutism | DHT converts vellus hairs into terminal hairs (coarse, dark, long) at androgen-sensitive sites | Assessed with the modified Ferriman-Gallwey (mFG) score ≥ 8 (face, chin, chest, abdomen, back, thighs) |
| Female pattern hair loss (androgenetic alopecia, AGA) | DHT shortens the anagen phase and miniaturizes follicles on the crown | Graded with the Ludwig scale (diffuse thinning along a widening part, with the frontal hairline preserved) |
| Acanthosis nigricans | High insulin levels bind IGF-1 receptors, stimulating keratinocyte and melanocyte proliferation | Gray to dark brown, velvety, thickened plaques in skin folds (neck, armpits, groin, under the breasts) |
Our Multidisciplinary PCOS Treatment Pathway at Haute-Derma
History Taking and Baseline Screening Tests
- Review of the menstrual cycle, BMI and waist-to-hip ratio (WHR).
- Ferriman-Gallwey scoring for hirsutism and Ludwig grading for hair loss.
- Blood tests on days 2–4 of the cycle: total and free testosterone, SHBG, DHEAS, LH, FSH, estradiol, prolactin, an oral glucose tolerance test (OGTT) and fasting insulin.
Systemic Medical Therapy
- Combined oral contraceptives (OCPs):
- We choose pills that pair ethinyl estradiol with a strongly anti-androgenic progestin such as cyproterone acetate or drospirenone.
- How they help: they suppress pituitary LH release and prompt the liver to make more SHBG, bringing free testosterone down quickly within 3–6 months.
- Androgen receptor blockers (anti-androgens):
- Spironolactone (50–200 mg/day): displaces DHT from androgen receptors in the sebaceous glands and hair follicles and also inhibits 5-alpha-reductase. Acne and hirsutism improve clearly after about 6 months.
- Insulin sensitizers:
- Metformin (500–1500 mg/day): reduces glucose output from the liver and improves insulin sensitivity in muscle. Lower insulin levels in turn reduce ovarian androgen production and noticeably improve acanthosis nigricans.
In-Office Procedures and Aesthetic Treatments
- Acne and post-acne marks: medical-grade comedone extraction and Biolight/IPL light therapy to kill C. acnes, combined with chemical peels (20% azelaic acid, 30% salicylic acid) to clear blocked follicles.
- Hirsutism control: 808 nm diode laser or broadband IPL hair removal over 6–8 sessions, destroying the dermal papilla of follicles in the anagen phase.
- Resurfacing acanthosis nigricans: creams containing 10–20% urea and salicylic acid, combined with low-energy fractional CO2 or picosecond laser to lighten pigmentation and thin the thickened skin in body folds.
Lifestyle Changes and Regular Monitoring
- Low-GI / low-carb diet: lowering the glycemic load of meals helps blunt insulin spikes.
- Exercise to reduce visceral fat: losing 5–10% of body weight can restore natural ovulation and significantly lower free androgen levels in the blood.