eMedicine Specialties > Dermatology > Diseases of the Adnexa

Androgenetic Alopecia

Robert P Feinstein, MD, Associate Clinical Professor, Department of Dermatology, Columbia University College of Physicians and Surgeons

Updated: Jan 22, 2009

Introduction

Background

Androgenetic alopecia is an extremely common disorder affecting both men and women. The incidence is generally considered to be greater in males than females, although some evidence suggests that the apparent differences in incidence may be a reflection of different expression in males and females.

Pathophysiology

This genetically determined disorder is progressive through the gradual conversion of terminal hairs into indeterminate hairs and finally to vellus hairs. Patients have a reduction in the terminal-to-vellus hair ratio, normally at least 2:1. Following miniaturization of the follicles, fibrous tracts remain. Patients with this disorder usually have a typical distribution of hair loss.

Frequency

International

This is an extremely common disorder that affects roughly 50% of men and perhaps as many women older than 40 years. As many as 13% of premenopausal women reportedly have some evidence of androgenetic alopecia. However, the incidence increases greatly in women following menopause, and, according to one author, it may affect 75% of women older than 65 years.

Mortality/Morbidity

This is essentially a cosmetic disorder. Other than affecting the patient psychologically,¹ the disorder is significant only in that it allows ultraviolet light to reach the scalp and, thus, increases the amount of actinic damage. Males with androgenetic alopecia may have an increased incidence of myocardial infarction.² An increase in benign prostatic hypertrophy has also been associated.³ If these associations are proven conclusively, this disorder will be of greater clinical significance.

Race

The incidence and the severity of androgenetic alopecia tend to be highest in white men, second highest in Asians and African Americans, and lowest in Native Americans and Eskimos.

Age

Almost all patients have an onset prior to age 40 years, although many of the patients (both male and female) show evidence of the disorder by age 30 years.

Clinical

History

The onset is gradual. Men present with gradual thinning in the temporal areas, producing a reshaping of the anterior part of the hairline. For the most part, the evolution of baldness progresses according to the Norwood/Hamilton classification of frontal and vertex thinning. Women usually present with diffuse thinning on the crown. Bitemporal recession does occur in women but usually to a lesser degree than in men. In general, women maintain a frontal hairline.⁴

Physical

In both males and females with androgenetic alopecia, the transition from large, thick, pigmented terminal hairs to thinner, shorter, indeterminate hairs and finally to short, wispy, nonpigmented vellus hairs in the involved areas is gradual. As the disorder progresses, the anagen phase shortens with the telogen phase remaining constant. As a result, more hairs are in the telogen phase, and the patient may notice an increase in hair shedding. The end result can be an area of total denudation. This area varies from patient to patient and is usually most marked at the vertex.

Women with androgenetic alopecia generally lose hair diffusely over the crown. This produces a gradual thinning of the hair rather than an area of marked baldness. The part is widest anteriorly. The frontal hairline is often preserved in women with this disorder, whereas men note a gradual recession of the frontal hairline early in the process.

Causes

Androgenetic alopecia is a genetically determined condition. In 2008, 95 families were studied genetically, and the locus with strongest evidence for linkage to androgenetic alopecia was the 3q26 site on the X chromosome.⁵
 
Androgen is necessary for progression of the disorder, as it is not found in males castrated prior to puberty. The progression of the disorder is stopped if postpubertal males are castrated. Androgenetic alopecia is postulated to be a dominantly inherited disorder with variable penetrance and expression. However, it may be of polygenic inheritance. It has been noted that follicles from balding areas of persons with androgenetic alopecia are able to produce terminal hairs when implanted into immunodeficient mice.⁶ This suggests that systemic or external factors may play a role in this disorder.

As reported in 2005, it was noted in adult mouse skin that the hedgehog (Hh) family of intercellular signaling proteins can stimulate the transition from the resting (telogen) state to the growth phase (anagen) of the hair cycle.⁷ Whether this will be helpful in the treatment of androgenetic alopecia remains to be seen.

Differential Diagnoses

Alopecia Areata
Anagen Effluvium
Telogen Effluvium

Other Problems to Be Considered

• Alopecia of senescence
• Alopecia associated with virilizing disorders of women, in whom it may be seen in association with hirsutism and menstrual problems
• Anagen effluvium after exposure to toxic chemicals, including chemotherapeutic agents
• Alopecia associated with hypothyroidism or hyperthyroidism
• Telogen effluvium: This condition may accelerate androgenetic alopecia, and causes, such as iron deficiency and papulosquamous diseases of the scalp, must be considered.
• Hypertension and/or smoking: A strong association of androgenetic alopecia with hypertension was noted in a study of 250 white men aged 35-65 years. In this French study, a definite familial tendency to androgenetic alopecia was also described, but no association was noted with diabetes mellitus, hyperlipidemia, or smoking.⁸  However, a study of 740 Taiwanese men aged 40-91 years indicated an association between androgenetic alopecia and smoking. Smoking status, current amount of cigarette smoking, and smoking intensity were statistically significant in this report.⁹

Workup

Laboratory Studies

• The most important aspects are the history and the physical examination.
  • In the case of a woman, if virilization is evident, laboratory analysis of dehydroepiandrosterone (DHEA)-sulfate and testosterone may need to be obtained. Some authors have suggested that total testosterone level alone may be adequate to screen for a virilizing tumor.
  • If a thyroid disorder is suspected, obtaining a thyrotropin level is indicated.
• If telogen effluvium is present, laboratory analysis of serum iron levels or a biopsy to note an underlying papulosquamous disorder may be indicated. Telogen effluvium may accelerate the course of pattern alopecia. Iron deficiency is a common and reversible cause of telogen effluvium. A normal CBC count does not exclude iron deficiency as a cause of hair loss. While a low ferritin level is always a sign of iron deficiency, ferritin behaves as an acute phase reactant, and levels may be normal despite iron deficiency. Iron, total iron-binding capacity, and transferrin saturation are inexpensive and sensitive tests for iron deficiency.
• Diffuse alopecia areata may mimic pattern alopecia. The presence of exclamation point hairs, pitted nails, or a history of periodic regrowth or tapered fractures noted on hair counts suggests the diagnosis of diffuse alopecia areata.

Procedures

• A biopsy is rarely necessary to make the diagnosis. If a single biopsy specimen is obtained, it should generally be sectioned transversely if pattern alopecia is suspected. Some dermatopathologists recommend that if a biopsy is to be performed, a sample should be obtained from 2 sites: one for horizontal sectioning and one for vertical sectioning of the hair follicles. Other dermatopathologists point out that one may commonly obtain sufficient information from serial vertical sections to diagnose the condition.

Histologic Findings

In pattern alopecia, hairs are miniaturized. In evolving-pattern alopecia, the diameter of hair shafts varies. Fibrous tract remnants (so-called streamers) can be found below miniaturized follicles. Although androgenetic alopecia is considered a noninflammatory form of hair loss, at times, a superficial, perifollicular, inflammatory infiltrate is noted. A mildly increased telogen-to-anagen ratio is often observed.

Treatment

Medical Care

Only 2 proven, food and drug administration (FDA)–approved medications are currently available for treatment of androgenetic alopecia: minoxidil and finasteride.

• Minoxidil¹⁰
  • Although the method of action is essentially unknown, minoxidil appears to lengthen the duration of the anagen phase, and it may increase the blood supply to the follicle. Regrowth is more pronounced at the vertex than in the frontal areas and is not noted for at least 4 months. Continuing topical treatment with the drug is necessary indefinitely because discontinuation of treatment produces a rapid reversion to the pretreatment balding pattern.
  • Patients who respond best to this drug are those who have a recent onset of androgenetic alopecia and small areas of hair loss. The drug is marketed as a 2% or a 5% solution, with the 5% solution being somewhat more effective. A 48-week study compared the 2 strengths in men.¹¹ Findings indicated that 45% more regrowth occurred with the 5% compared with the 2% solution. In general, women respond better to topical minoxidil than men. The increase in effectiveness of the 5% solution was not evident for women in the FDA-controlled studies. Subsequent studies have shown at best a modest advantage to the higher concentration in women. In addition, the occurrence of facial hair growth appears to be increased with the use of the higher-concentration formulation.
• Finasteride¹²
  • Finasteride is given orally and is a 5 alpha-reductase type 2 inhibitor. It is not an antiandrogen. The drug can be used only in men because it can produce ambiguous genitalia in a developing male fetus. Finasteride has been shown to diminish the progression of androgenetic alopecia in males who are treated, and, in many patients, it has stimulated new regrowth.
  • Although it affects vertex balding more than frontal hair loss, the medication has been shown to increase regrowth in the frontal area as well. Finasteride must be continued indefinitely because discontinuation results in gradual progression of the disorder. A study in postmenopausal women indicated no beneficial effect of the medication in treating female androgenetic alopecia.

Some drugs are not approved by the FDA but are potentially helpful medications.¹³ In women with androgenetic alopecia, especially those with a component of hyperandrogenism, drugs that act as androgen suppressants or antagonists (eg, spironolactone, oral contraceptives) may be beneficial. Evidence exists of an association between androgenetic alopecia, hypertension, and hyperaldosteronism. Spironolactone could play a dual role in treatment.
 
Phase III US Food and Drug Administration (FDA) trials of dutasteride to treat androgenetic alopecia are currently on hold. This drug inhibits both type I and type II 5-a reductase isoenzymes and is felt to be 3 times as potent as finasteride in inhibiting the type II enzyme and 100 times as potent in inhibiting the type I enzyme.

Low-level laser light therapy, in particular a red light hairbrush-like device has been marketed as an over-the-counter technique for hair growth. Marketed as the HairMax LaserComb, it has obtained 510K FDA approval for use as a medical device. Note that this approval refers to safety rather than actual efficacy.

Androgenetic alopecia is very common; therefore, not surprisingly, it may accompany other forms of hair loss. Cases of telogen effluvium often occur in patients with underlying androgenetic alopecia. Therefore, a search for treatable causes of telogen effluvium (eg, anemia, hypothyroidism), especially in patients with an abrupt onset or a rapid progression of their disease, is indicated.

Surgical Care

Surgical treatment of androgenetic alopecia has been successfully performed for the past 4 decades. Although the cosmetic results are often satisfactory, the main problem is covering the bald area with donor plugs (or follicles) sufficient in number to be effective. Micrografting produces a more natural appearance than the old technique of transplanting plugs. Patients with less than 40 follicular units/cm² in their donor areas are poor candidates for the procedure. Scalp reduction has been attempted to decrease the size of the scalp to be covered by transplanted hair. However, the scars produced by the reduction technique often spread and become more noticeable with time.

Hair weaving techniques are available, and, together with hairpieces, they offer the patient a prosthetic method of coverage.

Medication

Only 2 medications have been shown to be effective in the treatment of androgenetic alopecia: minoxidil and finasteride. Minoxidil is applied topically and available as 2% or 5% solutions. Finasteride is taken orally.

Vasodilators

This drug is indicated to improve hair growth by stimulating vasodilation.

Minoxidil (Rogaine)

Relaxes arteriolar smooth muscle, causing vasodilation. Hair growth effects are secondary to vasodilation.
Available as 2% and 5% solutions.

Dosing

Adult

1 mL applied to affected area bid

Pediatric

Not established

Interactions

Concurrent use with guanethidine, diuretics, or hypotensive agents may result in additive hypotension

Contraindications

Documented hypersensitivity; pheochromocytoma; women

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May exacerbate angina pectoris; caution in pulmonary hypertension, congestive heart failure, coronary artery disease, and significant renal failure

Antiandrogens

Finasteride is the agent in this category known to promote hair growth.

Finasteride (Propecia)

Inhibits conversion of testosterone to dihydrotestosterone, causing serum dihydrotestosterone levels to decrease. However, effects in hair growth are not clearly understood.

Dosing

Adult

1 mg PO qd

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity; women of childbearing age

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in hepatic impairment; may cause a large residual urinary volume; avoid use in patients with severely diminished urinary flow

Follow-up

Prognosis

• The prognosis of androgenetic alopecia is unknown.
  • Some patients progress to the point where they lose almost all of the hair on the scalp.
  • Others have a patterned or nonpatterned thinning but retain a considerable number of scalp hairs.
  • Women with the disorder usually show thinning of the crown rather than developing truly bald areas.

Patient Education

• For excellent patient education resources, visit eMedicine's Skin, Hair, and Nails Center. Also see eMedicine's article Hair Loss.

References

1. Stough D, Stenn K, Haber R, et al. Psychological effect, pathophysiology, and management of androgenetic alopecia in men. Mayo Clin Proc. Oct 2005;80(10):1316-22. [Medline].

2. Lesko SM, Rosenberg L, Shapiro S. A case-control study of baldness in relation to myocardial infarction in men. JAMA. Feb 24 1993;269(8):998-1003. [Medline].

3. Oh BR, Kim SJ, Moon JD, et al. Association of benign prostatic hyperplasia with male pattern baldness. Urology. May 1998;51(5):744-8. [Medline].

4. Ludwig E. Classification of the types of androgenetic alopecia (common baldness) occurring in the female sex. Br J Dermatol. Sep 1977;97(3):247-54. [Medline].

5. Hillmer AM, Flaquer A, Hanneken S, et al. Genome-wide scan and fine-mapping linkage study of androgenetic alopecia reveals a locus on chromosome 3q26. Am J Hum Genet. Mar 2008;82(3):737-43. [Medline].

6. Krajcik RA, Vogelman JH, Malloy VL, Orentreich N. Transplants from balding and hairy androgenetic alopecia scalp regrow hair comparably well on immunodeficient mice. J Am Acad Dermatol. May 2003;48(5):752-9. [Medline].

7. Paladini RD, Saleh J, Qian C, Xu GX, Rubin LL. Modulation of hair growth with small molecule agonists of the hedgehog signaling pathway. J Invest Dermatol. Oct 2005;125(4):638-46. [Medline].

8. Ahouansou S, Le Toumelin P, Crickx B, Descamps V. Association of androgenetic alopecia and hypertension. Eur J Dermatol. May-Jun 2007;17(3):220-2. [Medline].

9. Su LH, Chen TH. Association of androgenetic alopecia with smoking and its prevalence among Asian men: a community-based survey. Arch Dermatol. Nov 2007;143(11):1401-6. [Medline].

10. Headington JT, Novak E. Clinical and histological studies of male pattern baldness treated with topical minoxidil. Curr Ther Res Clin Exp. 1984;36:1098-106.

11. Olsen EA, Dunlap FE, Funicella T, et al. A randomized clinical trial of 5% topical minoxidil versus 2% topical minoxidil and placebo in the treatment of androgenetic alopecia in men. J Am Acad Dermatol. Sep 2002;47(3):377-85. [Medline].

12. Rittmaster RS. Finasteride. N Engl J Med. Jan 13 1994;330(2):120-5. [Medline].

13. Rogers NE, Avram MR. Medical treatments for male and female pattern hair loss. J Am Acad Dermatol. Oct 2008;59(4):547-66; quiz 567-8. [Medline].

14. Hamilton JB. Patterned loss of hair in man; types and incidence. Ann N Y Acad Sci. Mar 1951;53(3):708-28. [Medline].

15. Kaufman KD. Androgen metabolism as it affects hair growth in androgenetic alopecia. Dermatol Clin. Oct 1996;14(4):697-711. [Medline].

16. Muller SA. Alopecia: syndromes of genetic significance. J Invest Dermatol. Jun 1973;60(6):475-92. [Medline].

17. Olsen EA. Androgenetic alopecia. In: Olsen EA ed. Disorders of Hair Growth: Diagnosis and Treatment. New York, NY: McGraw-Hill; 1994:257-83.

18. Olsen EA, Messenger AG, Shapiro J, et al. Evaluation and treatment of male and female pattern hair loss. J Am Acad Dermatol. Feb 2005;52(2):301-11. [Medline].

19. Otberg N, Finner AM, Shapiro J. Androgenetic alopecia. Endocrinol Metab Clin North Am. Jun 2007;36(2):379-98. [Medline].

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21. Sperling LC. Evaluation of hair loss. Curr Probl Dermatol. 1996;8:97-136.

22. Sperling LC, Lupton GP. Histopathology of non-scarring alopecia. J Cutan Pathol. Apr 1995;22(2):97-114. [Medline].

23. Stern Rl, Heymann WR. Androgenetic alopecia. Clin Dermatol. 1997;2(32):1-6.

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Keywords

androgenetic alopecia, common baldness, familial baldness, hereditary baldness, male pattern baldness, female pattern baldness, pattern baldness, hair loss, androgenic alopecia

Contributor Information and Disclosures

Author

Robert P Feinstein, MD, Associate Clinical Professor, Department of Dermatology, Columbia University College of Physicians and Surgeons
Robert P Feinstein, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Noah Worcester Dermatological Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Medical Editor

Leonard Sperling, MD, Chair, Professor, Department of Dermatology, Uniformed Services University of the Health Sciences
Leonard Sperling, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: 3M Pharmaceutical Grant/research funds Other; Graceway Pharmaceuticals Grant/research funds Other

Managing Editor

Edward F Chan, MD, Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania School of Medicine
Edward F Chan, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

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