eMedicine Specialties > Endocrinology > Gonads

Hirsutism: Differential Diagnoses & Workup

Author: George T Griffing, MD, Professor of Medicine, St Louis University School of Medicine
Contributor Information and Disclosures

Updated: Aug 14, 2009

Differential Diagnoses

Adrenal Adenoma
Cushing Syndrome
Adrenal Carcinoma
Malignant Lesions of the Ovaries
C-11 Hydroxylase Deficiency
Ovarian Cancer
C-17 Hydroxylase Deficiency
Polycystic Ovarian Disease (Stein-Leventhal Syndrome)

Other Problems to Be Considered

Androgen-secreting adrenal tumors
Androgen-secreting ovarian tumors
Exogenous androgens
Congenital adrenal hyperplasia
Idiopathic hirsutism

Workup

Laboratory Studies

Approximately 50% of women with even minimal hirsutism have excessive androgen. Laboratory studies in hirsutism serve both to confirm the clinical impression of hyperandrogenism and to identify the source of excess androgens, either adrenal or ovarian. The workup described in the image below (see also Image 4) recommends 2 visits, a baseline evaluation followed by a 2-week dexamethasone treatment period. Specific discussion of the testing is below.

Etiologic diagnosis of hirsutism.

Etiologic diagnosis of hirsutism.

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Etiologic diagnosis of hirsutism.

Etiologic diagnosis of hirsutism.


  • Testosterone: The most important assay is the level of serum testosterone, the major circulating androgen. If the total serum testosterone level is normal, measure the free serum level because hyperandrogenism (and insulin resistance, if present) decreases sex steroid-binding globulin, such that the unbound, biologically active testosterone moiety may be elevated even if the total level is unremarkable. Extremely high testosterone levels are likely to be associated with adrenal or ovarian tumors, whereas idiopathic and benign etiologies result in very mild elevations. Indeed, in idiopathic hirsutism, the results from testing androgen levels are often normal. In some of these women, hirsutism is thought to be caused by increased skin sensitivity to androgen or by increased skin 5-alpha-reductase activity. This enzyme is located in the skin near the hair follicle, and it converts plasma testosterone to the androgen metabolite dihydrotestosterone.
  • Dehydroepiandrosterone sulfate (DHEAS): Because testosterone can originate in either the adrenal cortex or the ovary, an elevated testosterone level does not indicate the gland of origin. Accordingly, measurement of elevated plasma levels of DHEAS, an androgen synthesized almost exclusively by the adrenal cortex, can indicate excess adrenal function. Elevations in both testosterone and DHEAS suggest an adrenal origin, whereas an isolated testosterone elevation indicates an ovarian source.
  • Dexamethasone suppression (see Image 4): Laboratory testing of testosterone (free or total) and DHEAS can be performed on the initial visit. At the same time, a diagnostic trial of dexamethasone therapy for 7-14 days can be initiated to help exclude adrenocorticotropin hormone (ACTH)–dependent hirsutism. When the patient returns, free testosterone, DHEAS, and plasma cortisol levels are measured. Dexamethasone-mediated suppression of androgens is observed in healthy women who do not have hirsutism and in those with congenital adrenal hyperplasia (CAH) and idiopathic hirsutism.
  • Adrenocorticotropin stimulation: An ACTH-stimulation test (250 mcg for 30 min) can help differentiate between CAH and idiopathic hirsutism because CAH produces abnormal findings (elevations in metabolic precursors of cortisol).
    • Hirsutism caused by CAH is due to 1 of 3 cortisol biosynthetic defects, ie, 21-hydroxylase deficiency, 3 3 b -hydroxysteroid dehydrogenase, or 11-b -hydroxylase deficiency.
    • Because 21-hydroxylase deficiency accounts for the vast majority of cases of CAH (approximately 90%), the discussion is focused on this diagnosis. Investigate possible 21-hydroxylase deficiency by measuring plasma 17-hydroxyprogesterone levels obtained between 0700 and 0900 hours. Values of less than 7 nmol/L exclude the diagnosis, and values of greater than 45 nmol/L (in women who are nongestational) confirm 21-hydroxylase deficiency. When basal values of 17-hydroxyprogesterone are between 7 and 45 nmol/L, an ACTH-stimulated concentration of greater than 45 nmol/L is also diagnostic.
    • Although elevated basal plasma 17-hydroxyprogesterone levels (as high as 17 nmol/L) may be present during the luteal phase of the menstrual cycle and in PCOS, ACTH-stimulated increments are blunted.
  • Cortisol suppression: Investigation of subnormal dexamethasone suppression of androgens can be guided by the patient’s cortisol level, without the need for an ACTH-stimulation test. PCOS and adrenal and ovarian tumors are associated with normal suppression of cortisol by dexamethasone, whereas cortisol levels in patients with Cushing syndrome are not suppressed.

Other laboratory tests include the following:

  • Serum prolactin or FSH: Women with hirsutism and amenorrhea of unknown cause should have a serum prolactin or FSH test to evaluate for either a prolactinoma or ovarian failure.
  • Diabetes screening: Women with hirsutism, PCOS, obesity, or acanthosis nigricans may have insulin resistance, and screening for diabetes and hyperlipidemia is warranted. Approximately 50% of these women have increased insulin levels and 5% have undiagnosed diabetes mellitus.
  • Prostate-specific antigen (PSA): Ultrasensitive assays can detect PSA in women and is a potential marker for androgen excess. Studies thus far, however, have not shown a good correlation with the change in androgen levels after treatment. Therefore, further studies are needed.6

Imaging Studies

If indicated based on the findings from the clinical evaluation and laboratory testing, perform ovarian ultrasonography and adrenal computed tomography scanning or magnetic resonance imaging to evaluate for either ovarian or adrenal sources of androgen production.

More on Hirsutism

Overview: Hirsutism
Differential Diagnoses & Workup: Hirsutism
Treatment & Medication: Hirsutism
Follow-up: Hirsutism
Multimedia: Hirsutism
References
Further Reading
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Keywords

hirsutism, hirsute women, androgen excess, PCOS, ovarian polycystic syndrome, polycystic ovary syndrome, polycystic ovarian disease, PCOD, virilization, masculinization, excessive hairiness, excess body hair, endocrine disorders, androgen levels, congenital adrenal hyperplasia, CAH, androgen-secreting tumor, hyperandrogenism, Cushing syndrome, Cushing’s syndrome, Ferriman and Gallwey scale, idiopathic hirsutism

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Contributor Information and Disclosures

Author

George T Griffing, MD, Professor of Medicine, St Louis University School of Medicine
George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

Medical Editor

Stanley Wallach, MD, Executive Director, American College of Nutrition; Clinical Professor, Department of Medicine, New York University School of Medicine
Stanley Wallach, MD is a member of the following medical societies: American Society for Bone and Mineral Research, American Society for Clinical Investigation, American Society for Clinical Nutrition, American Society for Nutritional Sciences, Association of American Physicians, and Endocrine Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Don S Schalch, MD, Professor Emeritus, Department of Internal Medicine, Division of Endocrinology, University of Wisconsin Hospitals and Clinics
Don S Schalch, MD is a member of the following medical societies: American Diabetes Association, American Federation for Medical Research, Central Society for Clinical Research, and Endocrine Society
Disclosure: Nothing to disclose.

CME Editor

Mark Cooper, MBBS, PhD, FRACP, Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University
Disclosure: Nothing to disclose.

Chief Editor

Michel E Rivlin, MD, Professor, Coordinator of Quality Assurance/Quality Improvement, Department of Obstetrics and Gynecology, University of Mississippi School of Medicine
Michel E Rivlin, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, Mississippi State Medical Association, and Royal College of Surgeons of Edinburgh
Disclosure: Nothing to disclose.

 
 
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