Hirsutism¶
Chapter 406 | Part 12: Endocrinology
KEY CLINICAL POINTS¶
- Hirsutism is defined as excessive terminal hair growth in women, typically assessed using the Ferriman-Gallwey scale (score <8 is normal).
- Polycystic ovary syndrome (PCOS) is the most common cause of androgen excess, while adrenal hyperplasia, tumors, and medications (e.g., minoxidil, phenytoin) are other etiologies.
- Diagnostic evaluation includes hormonal testing (testosterone, DHEAS, SHBG), imaging (ultrasound, MRI), and the dexamethasone suppression test to differentiate ovarian vs. adrenal androgen sources.
- Treatment options include antiandrogens (cyproterone acetate, spironolactone), combined hormonal contraceptives, and non-pharmacologic hair removal methods.
- Management must consider pregnancy risks, drug interactions, and long-term monitoring for complications like hyperprolactinemia or Cushing’s syndrome.
1. DEFINITION & OVERVIEW¶
Hirsutism refers to excessive terminal hair growth in women, typically in androgen-sensitive areas (face, chest, back). It is differentiated from hypertrichosis (generalized hair growth) by the Ferriman-Gallwey scale. Androgen excess, either from ovarian or adrenal sources, is the primary pathophysiological mechanism.
Table 406-1: Causes of Hirsutism¶
| Category | Causes |
|---|---|
| Gonadal Hyperandrogenism | Polycystic ovary syndrome, Ovarian hyperthecosis, Ovarian neoplasms |
| Adrenal Hyperandrogenism | Premature adrenarche, Congenital adrenal hyperplasia, Adrenal tumors |
| Peripheral Factors | Obesity, Insulin resistance, Medications (minoxidil, phenytoin, cyclosporine) |
| Other Endocrine Disorders | Cushing’s syndrome, Hyperprolactinemia, Acromegaly |
1.1 Clinical Differentiation¶
Hirsutism is distinct from hypertrichosis (generalized hair growth) and androgenic alopecia (hair thinning). The Ferriman-Gallwey scale grades hair growth across nine sites (face, chest, abdomen, etc.) on a 0–4 scale, with scores >8 indicating excess androgen-mediated growth.
1.2 Hormonal Mechanisms¶
Androgens (testosterone, DHT) drive terminal hair growth. DHT, a more potent androgen, binds strongly to androgen receptors in hair follicles. Insulin resistance and obesity may exacerbate androgenic effects by reducing SHBG and increasing free testosterone.
2. EPIDEMIOLOGY¶
Approximately 10% of reproductive-age women have hirsutism. Ethnicity influences hair growth: Asians and Native Americans typically have less hirsutism than Mediterranean or European populations. PCOS accounts for ~70% of cases, with obesity and insulin resistance as contributing factors.
2.1 Risk Factors¶
Family history of hirsutism, PCOS, obesity, insulin resistance, and certain medications (e.g., minoxidil, phenytoin) increase risk. Adrenal or ovarian tumors may present with sudden hirsutism progression.
3. ETIOLOGY & PATHOPHYSIOLOGY¶
Androgen excess from ovarian (PCOS, hyperthecosis) or adrenal (Cushing’s, congenital adrenal hyperplasia) sources drives hirsutism. DHT, produced via 5 α -reductase, is the primary mediator. Insulin resistance reduces SHBG, increasing free testosterone and exacerbating androgenic effects.
3.1 Hormonal Pathways¶
Testosterone is converted to DHT via 5 α -reductase. DHT binds to androgen receptors in hair follicles, promoting terminal hair growth. SHBG levels decrease with insulin resistance, increasing free testosterone availability.
4. CLINICAL FEATURES¶
Symptoms include acne, hair thinning, and excessive hair growth in androgen-sensitive areas. Physical signs may include clitoromegaly, voice deepening, and virilization in severe cases. The Ferriman-Gallwey scale is used to quantify hair distribution.
4.1 Differential Diagnosis¶
Distinguish hirsutism from hypertrichosis, androgenic alopecia, and other endocrine disorders (e.g., Cushing’s, PCOS). Virilization may indicate adrenal or ovarian tumors.
5. INVESTIGATIONS & DIAGNOSIS¶
Diagnostic workup includes hormonal testing (total/testosterone, DHEAS, SHBG), imaging (transvaginal ultrasound for PCOS, MRI for adrenal masses), and the dexamethasone suppression test to differentiate ovarian vs. adrenal androgen sources.
Ferriman-Gallwey Hirsutism Scale¶
| Body Area | Score (0–4) |
|---|---|
| Upper lip | 0–4 |
| Chin | 0–4 |
| Chest | 0–4 |
| Abdomen | 0–4 |
| Pelvis | 0–4 |
| Body Area | Score (0–4) |
|---|---|
| Upper arms | 0–4 |
| Thighs | 0,4 |
| Upper back | 0–4 |
| Lower back | 0–4 |
5.1 Hormonal Evaluation¶
Measure total and free testosterone, DHEAS, and SHBG. A dexamethasone suppression test (0.5 mg every 6 h for 4 days) helps identify adrenal vs. ovarian androgen excess.
6. MANAGEMENT & TREATMENT¶
Treatment combines pharmacologic (antiandrogens, contraceptives) and non-pharmacologic (hair removal) approaches. Hormonal suppression, SHBG augmentation, and androgen receptor blockade are key mechanisms.
6.1 Pharmacologic Therapies¶
Cyproterone acetate (antiandrogen), spironolactone (mineralocorticoid antagonist), and combined oral contraceptives (e.g., drospirenone/ethinyl estradiol) are first-line. Finasteride and dutasteride inhibit 5 α -reductase but are contraindicated in pregnancy.
6.2 Non-Pharmacologic Approaches¶
Hair removal methods include shaving, waxing, electrolysis, laser, and IPL. These are adjunctive to hormonal therapy and do not address underlying androgen excess.
7. PROGNOSIS & COMPLICATIONS¶
Hirsutism may persist or improve with treatment. Complications include PCOS-related infertility, metabolic syndrome, and virilization from tumors. Long-term monitoring is needed for hormonal imbalances and treatment side effects.
8. SPECIAL CONSIDERATIONS¶
Pregnancy is contraindicated with cyproterone acetate and spironolactone. Obesity and insulin resistance should be managed alongside hirsutism. Hormonal therapies require regular follow-up for efficacy and safety.
9. KEY POINTS & CLINICAL PEARLS¶
- Use the Ferriman-Gallwey scale to quantify hirsutism.
- Distinguish ovarian vs. adrenal androgen sources with dexamethasone suppression testing.
- Combined hormonal contraceptives are first-line for PCOS-related hirsutism.
- Antiandrogens (spironolactone, cyproterone acetate) are effective but require monitoring for side effects.
- Non-pharmacologic hair removal is adjunctive and does not address underlying pathophysiology.