Virilization

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Chapter 179 Virilization

INTRODUCTION

Description: Virilization refers to the loss of female sexual characteristics such as body contour and the acquisition of masculine qualities such as increased muscle mass, temporal balding, deepening of the voice, and clitoromegaly.
Prevalence: Uncommon.
Predominant Age: Reproductive.
Genetics: No genetic pattern.

ETIOLOGY AND PATHOGENESIS

Causes: Idiopathic ovarian (polycystic ovary syndrome, hilus cell hyperplasia/tumor, arrhenoblastoma, adrenal rest), adrenal (congenital adrenal hyperplasia [10% to 15% of women with hirsutism], Cushing disease, virilizing carcinoma or adenoma), drugs (minoxidil, androgens including danazol [Danocrine], phenytoin, diazoxide), pregnancy (androgen excess of pregnancy, luteoma, or hyperreactio luteinalis).
Risk Factors: None known.

CLINICAL CHARACTERISTICS

Signs and Symptoms

• Amenorrhea (common but not universal)
• Temporal or frontal balding
• Deepening of the voice
• Clitoral enlargement
• Vaginal dryness
• Increased muscle mass
• Male-pattern hair growth

DIAGNOSTIC APPROACH

Differential Diagnosis

• Iatrogenic or exogenous steroid use
• Polycystic ovary syndrome
• Ovarian stromal hyperthecosis
• Ovarian tumors (Sertoli-Leydig tumors)
• Cushing’s disease (truncal obesity, facial rounding, cervicodorsal fat deposition [buffalo hump], and red or purple striae are often not fully developed)
• Adrenal tumors
• Congenital adrenal hyperplasia (especially in infants and children)

Associated Conditions: Defeminization, amenorrhea, obesity, menstrual irregularity, amenorrhea, infertility, acne, oily skin, increased libido, and alopecia.

Workup and Evaluation

Laboratory: Prolactin, follicle-stimulating hormone (FSH), thyroid screening. Patients suspected of having adrenal sources of hyperandrogenicity may be screened by measuring 24-hour urinary-free cortisol, by performing adrenocorticotropin hormone (ACTH) stimulation tests, or by performing an overnight dexamethasone suppression test. Dehydroepiandrosterone sulfate (DHEA-s) and testosterone should be measured. The circulating testosterone level is generally ≥2 ng/mL.
Imaging: Despite the ability of transvaginal ultrasonography and computerized tomography (CT) to detect 90% of virilizing tumors, 5% to 10% of tumors may not be detected, necessitating surgical exploration when these are suspected.
Special Tests: Clitoral index. (The clitoral index is defined as the vertical dimension times the horizontal dimension, in millimeters. The normal range is from 9 to 35 mm, with borderline values in the range of 36 to 99 mm. Values greater than 100 mm indicate severe hyperandrogenicity and should prompt aggressive evaluation and referral.)
Diagnostic Procedures: History, physical examination, and laboratory evaluation.

Pathologic Findings

Based on underlying pathophysiologic conditions.

MANAGEMENT AND THERAPY

Nonpharmacologic

General Measures: Evaluation and support, shaving, depilatories, or electrolysis. Topical treatment of acne (if present).
Specific Measures: Patients with polycystic ovary syndrome often do well with oral contraceptive suppression of ovarian function or with the use of spironolactone. Patients with hyperandrogenicity of adrenal origin respond well to cortisol administration, which results in a reduction of the production of androgenic precursors. Tumors require surgical removal.
Diet: No specific dietary changes indicated.
Activity: No restriction.

Drug(s) of Choice

Polycystic ovary syndrome—combination oral contraceptives, spironolactone (100 to 200 mg PO daily), medroxyprogesterone acetate (Depo-Provera 150 to 300 mg IM every 3 months).
Hyperandrogenicity of adrenal origin—cortisol administration.
Contraindications: Pregnancy. (Spironolactone is teratogenic; patients using it and able to become pregnant must use reliable contraception.)

FOLLOW-UP

Patient Monitoring: Normal health maintenance once diagnosis and management have been implemented. There is an increased risk of diabetes in patients with polycystic ovaries.
Prevention/Avoidance: None.
Possible Complications: Permanent loss of feminine attributes and induction of hirsutism, lowering of voice, and others. Chronic anovulation is associated with increased risk of endometrial hyperplasia and cancer.

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Expected Outcome: Good, with appropriate diagnosis and treatment.

MISCELLANEOUS

Pregnancy Considerations: No effect on pregnancy, although some metabolic causes of virilization of the mother may result in reduced fertility or virilization of a fetus.
ICD-9-CM Codes: 255.2 (others based on diagnosis).

REFERENCES

Level I

Azziz R, Ochoa TM, Bradley ELJr, et al. Leuprolide and estrogen versus oral contraceptive pills for the treatment of hirsutism: a prospective randomized study. J Clin Endocrinol Metab. 1995;80:3406.

Moghetti P, Tosi F, Tosti A, et al. Comparison of spironolactone, flutamide, and finasteride efficacy in the treatment of hirsutism: a randomized, double blind, placebo-controlled trial. J Clin Endocrinol Metab. 2000;85:89.

Level II

Coonrod DV, Rizkallah TH. Virilizing adrenal carcinoma in a woman of reproductive age: a case presentation and literature review. Am J Obstet Gynecol. 1995;172:1912.

Guido M, Romualdi D, Giuliani M, et al. Drospirenone for the treatment of hirsute women with polycystic ovary syndrome: a clinical, endocrinological, metabolic pilot study. J Clin Endocrinol Metab. 2004;89:2817.

Ibanez L, Potau N, Marcos MV, de Zegher F. Treatment of hirsutism, hyperandrogenism, oligomenorrhea, dyslipidemia, and hyperinsulinism in nonobese, adolescent girls: effect of flutamide. J Clin Endocrinol Metab. 2000;85:3251.

Level III

American College of Obstetricians and Gynecologists. Polycystic ovary syndrome. ACOG Practice Bulletin 41. Obstet Gynecol. 2002;100:1389.

Azziz R. The evaluation and management of hirsutism. Obstet Gynecol. 2003;101:995.

Bailey-Pridham DD, Sanfilippo JS. Hirsutism in the adolescent female. Pediatr Clin North Am. 1989;36:581.

Bergfeld WF. Hirsutism in women. Effective therapy that is safe for long-term use. Postgrad Med. 2000;107:93. 99.

Chang RJ. A practical approach to the diagnosis of polycystic ovary syndrome. Am J Obstet Gynecol. 2004;191:713.

Conn JJ, Jacobs HS. Managing hirsutism in gynaecological practice. Br J Obstet Gynaecol. 1998;105:687.

Curran DR, Moore C, Huber T. Clinical inquiries. What is the best approach to the evaluation of hirsutism? J Fam Pract. 2005;54:465.

Ehrmann DA. Polycystic ovary syndrome. N Engl J Med. 2005;352:1223.

Ehrmann DA, Rosenfield RL. Clinical review 10: an endocrinologic approach to the patient with hirsutism. J Clin Endocrinol Metab. 1990;71:1.

Ginsburg J, White MC. Hirsutism and virilisation. Br Med J. 1980;280:369.

Gordon CM. Menstrual disorders in adolescents. Excess androgens and the polycystic ovary syndrome. Pediatr Clin North Am. 1999;46:519.

Harborne L, Fleming R, Lyall H, et al. Metformin or antiandrogen in the treatment of hirsutism in polycystic ovary syndrome. J Clin Endocrinol Metab. 2003;88:4116.

Karp L, Herrmann WL. Diagnosis and treatment of hirsutism in women. Obstet Gynecol. 1973;41:283.

Lobo RA. Hyperandrogenism. In: Katz VL, Lentz GM, Lobo RA, Gershenson DM, editors. Comprehensive Gynecology. 5th ed. Philadelphia: Mosby/Elsevier; 2007:979.

Marshburn PB, Carr BR. Hirsutism and virilization. A systematic approach to benign and potentially serious causes. Postgrad Med. 1995;97:99. 105.

Rosenfield RL. Clinical practice. Hirsutism. N Engl J Med. 2005;353:2578.

Tagatz GE, Kopher RA, Nagel TC, Okagaki T. The clitoral index: a bioassay of androgenic stimulation. Obstet Gynecol. 1979;54:562.

[/level-membership-for-obstetrics-gynecology-category][not-level-membership-for-obstetrics-gynecology-category]

Chapter 179 Virilization

INTRODUCTION

Description: Virilization refers to the loss of female sexual characteristics such as body contour and the acquisition of masculine qualities such as increased muscle mass, temporal balding, deepening of the voice, and clitoromegaly.
Prevalence: Uncommon.
Predominant Age: Reproductive.
Genetics: No genetic pattern.

ETIOLOGY AND PATHOGENESIS

Causes: Idiopathic ovarian (polycystic ovary syndrome, hilus cell hyperplasia/tumor, arrhenoblastoma, adrenal rest), adrenal (congenital adrenal hyperplasia [10% to 15% of women with hirsutism], Cushing disease, virilizing carcinoma or adenoma), drugs (minoxidil, androgens including danazol [Danocrine], phenytoin, diazoxide), pregnancy (androgen excess of pregnancy, luteoma, or hyperreactio luteinalis).
Risk Factors: None known.

CLINICAL CHARACTERISTICS

Signs and Symptoms

• Amenorrhea (common but not universal)
• Temporal or frontal balding
• Deepening of the voice
• Clitoral enlargement
• Vaginal dryness
• Increased muscle mass
• Male-pattern hair growth

DIAGNOSTIC APPROACH

Differential Diagnosis

• Iatrogenic or exogenous steroid use
• Polycystic ovary syndrome
• Ovarian stromal hyperthecosis
• Ovarian tumors (Sertoli-Leydig tumors)
• Cushing’s disease (truncal obesity, facial rounding, cervicodorsal fat deposition [buffalo hump], and red or purple striae are often not fully developed)
• Adrenal tumors
• Congenital adrenal hyperplasia (especially in infants and children)

Associated Conditions: Defeminization, amenorrhea, obesity, menstrual irregularity, amenorrhea, infertility, acne, oily skin, increased libido, and alopecia.

Workup and Evaluation

Laboratory: Prolactin, follicle-stimulating hormone (FSH), thyroid screening. Patients suspected of having adrenal sources of hyperandrogenicity may be screened by measuring 24-hour urinary-free cortisol, by performing adrenocorticotropin hormone (ACTH) stimulation tests, or by performing an overnight dexamethasone suppression test. Dehydroepiandrosterone sulfate (DHEA-s) and testosterone should be measured. The circulating testosterone level is generally ≥2 ng/mL.
Imaging:

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