Summary
Hirsutism is a common clinical problem with diverse etiologies ranging from benign familial patterns to serious androgen-secreting tumors. A structured diagnostic approach focusing on the site and severity of androgen excess is essential. Patient centered treatment balancing medical therapy, cosmetic interventions, and management of underlying conditions offers the best outcomes for both physical and emotional well-being
Definition
Hirsutism is defined as the excessive growth of androgen-dependent (sexual) terminal hair in women in areas typically seen in males such as the face (upper lip, chin), chest, abdomen, back, and limbs. It becomes clinically significant when the hair growth is distressing to the patient, interfering with her psychological or social well-being. Hirsutism affects approximately 5–10% of women of reproductive age.
Unlike;
-
Hypertrichosis: excessive hair growth in areas not necessarily androgen-dependent.
- Virilization, a more severe condition, includes hirsutism along with masculinizing features such as deep voice, clitoromegaly, male-pattern baldness, and increased muscle mass.
Pathophysiology
Hirsutism results from the conversion of vellus (fine, non-pigmented) hair to terminal (thick, pigmented) hair in androgen-sensitive areas. This transformation is mediated by androgens particularly dihydrotestosterone (DHT), a more potent derivative of testosterone, produced within the hair follicle by the enzyme 5α reductase.
Androgens in women are produced by:
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Adrenal glands (25%)
-
Ovaries (25%)
-
Peripheral conversion of precursors such as androstenedione (50%)
DHEAS (dehydroepiandrosterone sulfate) is exclusively adrenal in origin, whereas testosterone comes from both adrenal and ovarian sources. SHBG regulates the free (active) portion of circulating testosterone; conditions like obesity, PCOS, hypothyroidism, and liver disease lower SHBG, enhancing free testosterone.
Types and Causes of Hirsutism
|
Type |
Description |
|
Idiopathic Hirsutism |
Most common type. Normal androgen levels and regular ovulatory cycles. Likely due to increased peripheral sensitivity to androgens or altered 5α reductase activity. |
|
PCOS Related Hirsutism |
Associated with menstrual irregularity, obesity, acne, and polycystic ovaries on imaging. Characterized by hyperandrogenism and insulin resistance. |
|
Congenital Adrenal Hyperplasia (CAH) |
Especially late-onset 21-hydroxylase deficiency. Presents with elevated 17OH progesterone and hirsutism without virilization. |
|
Tumor Related Hirsutism |
Rapid onset and virilization suggest an ovarian (e.g., Sertoli Leydig tumor) or adrenal tumor. Markedly elevated testosterone or DHEAS levels are red flags. |
|
Medication Induced Hirsutism |
Caused by drugs like steroids, danazol, phenytoin, minoxidil, and cyclosporine. |
|
Endocrinopathies |
Includes Cushing syndrome, acromegaly, prolactinomas, and hypothyroidism, all of which may contribute to hirsutism by affecting androgen production or SHBG levels. |
|
Aromatase Deficiency (Rare) |
Leads to prenatal virilization in XX females, delayed puberty, and hyperandrogenism due to the inability to convert androgens to estrogens. |
Diagnostic Approach
|
Investigation |
Purpose |
|
Serum Testosterone |
Mild elevation → PCOS; marked elevation → ovarian tumor |
|
DHEAS |
Markedly elevated in adrenal tumors |
|
17OH Progesterone |
Elevated in late-onset CAH |
|
LH/FSH Ratio |
Increased in PCOS |
|
TFTs (Thyroid Function Tests) |
Evaluate for hypothyroidism |
|
Prolactin Levels |
Rule out pituitary adenoma |
|
Cortisol Studies |
If Cushing syndrome suspected |
|
Pelvic Ultrasound or MRI/CT |
To identify ovarian or adrenal masses |
Treatment of Hirsutism
Treatment is unnecessary for women without signs of underlying endocrine disorders and who are not bothered by the hair growth.
-
Lifestyle modification
-
Cosmetic methods: laser hair removal, electrolysis.
-
Hormonal therapy:
- Oral contraceptives (OCPs): First-line; increase SHBG and suppress ovarian androgen production.
-
Antiandrogens: Spironolactone, cyproterone acetate (used with OCPs to avoid teratogenicity).
-
Other medication:
-
Finasteride: 5α-reductase inhibitor for resistant cases.
-
Glucocorticoids: For CAH.
-
Levothyroxine: For hypothyroidism.
-
Dexamethasone: To suppress adrenal androgen production in select cases.
-
-
Surgical management: Indicated for androgen-secreting tumors (adrenal or ovarian); prompt resection is curative.
احصل على التجربة الكاملة
اشترك للوصول لفيديوهات الشرح التفصيلي والبطاقات التعليمية التفاعلية وأسئلة الممارسة مع تتبع التقدم.