Pocket ObGyn – Hyperandrogenism / Hirsutism
See Abbreviations
Adrenal Hyperandrogenism
- Definition: primary adrenal androgens (DHEA & DHEA-S). Converted to androstenedione ® testosterone (& also to estrogen). adrenarche = DHEA + DHEA-S ® pubic hair Can have ± hyperaldo, ± Cushing’s syn.
- Etiology: Adrenal tumors (adenoma, carcinoma, bilateral macronodular adrenal hyperplasia), CAH (ACTH hypersecretion). Also in diff: Exogenous androgens, hyperprolactinemia, placental aromatase deficiency, See also Ch. 6 (CAH) & Ch. 8 (PCOS).
- Dx: Clinical exam (hirsutism, androgenic alopecia, oily skin, acne, muscle hypertrophy, clitoromegaly, virilization, acanthosis nigricans)
Labs: serum testosterone, DHEA-S (>500 mg/dL in sugg adrenal tumor),
17-OHP (nml 100–300 ng/dL), prolactin (nml <20 ng/mL; prolactin acting on receptors in adrenal ® DHEA-S), thyroid fxn tests, gluc tol testing (fasting +2-h OGTT). Fasting gluc:insulin ratio <4.5 sugg insulin resistance.
Imaging: MRI or CT
- Rx: Depends on etiology; Surg is recommended for adrenal tumors
Polycystic Ovary Syndrome (See Ch. 8) Ovarian Hyperthecosis
- Definition: Ovarian interstitial cells differentiate into islands of luteinized theca cells
® steroid production. periph conversion to estrogen ® endometrial hyperplasia.
- Dx: Menstrual irregularities, obesity, Can be postmenopausal
(unlike PCOS only in younger).
- Rx: Combination OCPs, weight loss, GnRH agonist (øLH secretion), surgical
Other ovarian tumors: See Ch. 21 for other sex hormone producing tumors (teratoma, gonadoblastoma, granulosa cell, Sertoli-Leydig cell)
Hirsutism
Definition, Pathophysiology, and Epidemiology
- Excessive male pattern growth of coarse terminal hair in
- Conversion of testosterone to DHT by 5a-reductase ® irreversible conversion of soft, vellus hair to coarse terminal
- Ethnicity-related trends in hair follicle conc & thus propensity toward hirsutism; distinguish hypertrichosis from Mediterranean descent > northern Europeans > Asians.
- Overall 5–10% of reproductive age . Typical onset in adolescence to early 20’s.
Etiology
- PCOS (70–80%), meds (anabolic steroids, danazol, progestins, metoclopramide, methyldopa), idiopathic, nonclassical 21-OH CAH, adrenal tumors, hyperthecosis, ovarian tumors, Cushing’s syn, hyperprolactinemia
Clinical Presentation
- Terminal hair on lip, chin, chest, abd, arms, legs, Ferriman–Gallwey score to grade (95% of are nml w/ score <8; score >8, consider androgen-excess).
Figure 17.5 Ferriman-Gallwey scoring chart
Modified Ferriman–Gallwey scale for assessing hirsutism. Score nine body areas and sum. If no excess terminal hair, score is zero (Modified from Hatch, et al. Hirsutism: Implications, etiology, and management. Am J Obstet Gynecol. 1981;140:815–830)
Diagnosis – See Hyperandrogen/PCOS Workup (Chap. 8) Treatment
- Combined OCPs 1st line (use lower androgenic progest products) ® other treatments as for hyperandrogenism. Mechanical hair removal (shaving, waxing, laser).
- Antiandrogens effective but only monotherapy in reproductive aged w/ contraception. Spironolactone (also aldosterone receptor antag), flutamide, cyproterone, drospirenone (very weak antiandrogen, only available in combined OCP).