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.

DIAGNOSTIC APPROACH

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.

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).

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