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Androgenetic Alopecia Clinical Presentation

  • Author: Robert P Feinstein, MD; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
 
Updated: Jun 24, 2016
 

History

The onset of androgenetic alopecia 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 with androgenetic alopecia 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.[13]

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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 androgenetic alopecia 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.

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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.[14] In addition, an association between androgenetic alopecia and chromosome 20pll and the androgen-receptor gene has been reported.[15]

Androgen is necessary for progression of androgenetic alopecia, as it is not found in males castrated prior to puberty. The progression of androgenetic alopecia 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.[16] This suggests that systemic or external factors may play a role in androgenetic alopecia. Interestingly, female androgenetic alopecia has been reported in a patient with complete androgen insensitivity syndrome. This suggests that factors other than direct androgen action contribute to patterned hair loss.[17]

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.[18] Whether this will be helpful in the treatment of androgenetic alopecia remains to be seen.

As to the question of whether iron deficiency plays a role in female pattern hair loss, a study by Olsen et al indicated iron deficiency is common in women but is not significantly increased in patients with female patterns of hair loss or chronic telogen effluvium when compared with control subjects.[19]

Lattouf et al have described a case of connubial androgenetic alopecia in a 52-year-old woman secondary to contact with the skin of her husband who was being treated with topical testosterone for hypogonadism. She developed severe androgenetic alopecia involving the crown and the frontotemporal areas. Her spouse had been applying transdermal testosterone gel to his upper arms once daily. The patient was evaluated for evidence of hyperandrogenism, and no other signs of this disorder were identified. She was advised to ask her husband to apply his testosterone gel on a less exposed area of his body. The authors go on to state that it is possible that cases of connubial androgenetic alopecia may be underreported.[20]

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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, Phi Beta Kappa

Disclosure: Nothing to disclose.

Specialty Editor Board

David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

David F Butler, MD is a member of the following medical societies: American Medical Association, Alpha Omega Alpha, Association of Military Dermatologists, American Academy of Dermatology, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Phi Beta Kappa

Disclosure: Nothing to disclose.

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, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Chief Editor

Romesh Khardori, MD, PhD, FACP Professor of Endocrinology, Director of Training Program, Division of Endocrinology, Diabetes and Metabolism, Strelitz Diabetes and Endocrine Disorders Institute, Department of Internal Medicine, Eastern Virginia Medical School

Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, Endocrine Society

Disclosure: Nothing to disclose.

Additional Contributors

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.

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