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Androgenetic Alopecia

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

Practice Essentials

Androgenetic (or pattern) alopecia is a genetically determined disorder characterized by the gradual conversion of terminal hairs into indeterminate, and finally into vellus, hairs. It is an extremely common disease that affects men and women.

Signs and symptoms

Signs of androgenetic alopecia include the following:

  • Gradual onset
  • Increased hair shedding
  • Transition in the involved areas from large, thick, pigmented terminal hairs to thinner, shorter, indeterminate hairs and finally to short, wispy, nonpigmented vellus hairs
  • End result can be an area of total denudation; this area varies from patient to patient and is usually most marked at the vertex

Diffuse alopecia areata may mimic the androgenetic form. 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.

Males

  • Men note a gradual recession of the frontal hairline early in the process
  • Men present with gradual thinning in the temporal areas, producing a reshaping of the anterior part of the hairline

Females

  • Hair generally is lost 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
  • Bitemporal recession does occur in women but usually to a lesser degree than in men

See Clinical Presentation for more detail.

Diagnosis

Laboratory studies

History and the physical examination are the most important aspects of diagnosis in patients with androgenetic alopecia. The following laboratory tests, however, can play a role in patient assessment:

  • Dehydroepiandrosterone (DHEA)-sulfate and testosterone analysis: In women, if virilization is evident
  • Iron, total iron-binding capacity, and transferrin saturation: To test for iron deficiency, if telogen effluvium is present
  • Thyrotropin level: If a thyroid disorder is suspected

Biopsy and histology

A biopsy is rarely necessary to make the diagnosis of androgenetic alopecia. If a single biopsy specimen is obtained, it should generally be sectioned transversely if pattern alopecia is suspected.

In androgenetic alopecia, hairs are miniaturized. Although the condition is considered a noninflammatory form of hair loss, a superficial, perifollicular, inflammatory infiltrate is noted at times. A mildly increased telogen-to-anagen ratio is often observed.

See Workup for more detail.

Management

The following drugs have been approved by the FDA for the treatment of androgenetic alopecia:

  • Minoxidil: Androgen-independent hair-growth stimulator
  • Finasteride: 5-Alpha reductase type 2 inhibitor

The cosmetic results of surgical treatment for androgenetic alopecia are often satisfactory. Micrografting produces a more natural appearance than does the old technique of transplanting plugs.

See Treatment and Medication for more detail.

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Background

Androgenetic alopecia, or pattern alopecia, is an extremely common disorder affecting both men and women. The incidence of androgenetic alopecia 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.

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Pathophysiology

Androgenetic alopecia is a genetically determined disorder and is progressive through the gradual conversion of terminal hairs into indeterminate hairs and finally to vellus hairs. Patients with androgenetic alopecia have a reduction in the terminal-to-vellus hair ratio, normally about 4:1. Following miniaturization of the follicles, fibrous tracts remain. Patients with this disorder usually have a typical patterned distribution of hair loss.

In androgenetic alopecia, studies have indicated a self-renewal of the hair follicle via keratinocyte stem cells located at the area of the bulge of the hair follicle. In addition, a series of studies using mice has indicated that interfollicular keratinocyte stem cells could generate de novo hair follicles in adult mouse skin. These regenerated hair follicles cycled through stages of telogen to anagen. However, these transitions between bulge and epidermal keratinocytes have not been seen yet in human studies.[1]

Another report has indicated that mice lacking in functional vitamin D receptors develop a functional first coat of hair, but lack the cyclic regeneration of hair follicles leading to the development of alopecia.[2] Whether these findings will lead to a new area of exploration into the cause of androgenetic alopecia in humans is unknown at this time.

A lymphocytic microfolliculitis targeting the bulge epithelium, along with deposits of epithelial basement membrane zone immunoreactants, are frequently seen in androgenetic alopecia in both sexes. Those cases with a positive immunoreactant profile respond better to combined-modality therapy than do those with a negative result.[3]

Numerous studies have identified 2 major genetic risk loci for androgenetic alopecia. These are the X-chromosomal AR/EDA2R locus and the PAX1/FOXA2 locus on chromosome 20. A recent genome-wide association study compared move than 1100 severely affected cases of androgenetic alopecia and controls to note differences in the 2 groups. The study indicated that HDAC9 is the third androgenetic alopecia susceptibility gene. The results of this German study were further analyzed by fine-mapping and then individually replicated in an Australian sample.[4]

A Japanese study of the sebaceous glands was performed to note whether the distribution of the bulge stem cells play a role in the development of androgenetic alopecia.[5] Biopsies from 250 cases of men with androgenetic alopecia were reviewed. Twenty-three vertical sections of areas of androgenetic alopecia were studied, and each sebaceous gland area was measured and statistically analyzed. For identification of the bulge area, immunochemical study was carried out in the cases of androgenetic alopecia. The result of the study was that the sebaceous gland area of the androgenetic alopecia group was noticeably increased, while the size of each sebaceous gland remained unchanged. This suggests that overgrowth of the sebaceous gland and relative preservation of the follicular stem cells could be an important factor in the pathology of androgenetic alopecia.

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Epidemiology

Frequency

Androgenetic alopecia 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 of androgenetic alopecia increases greatly in women following menopause, and, according to one author, it may affect 75% of women older than 65 years.

A community-based study of androgenetic alopecia in 6 cities in China indicated that the prevalence of androgenetic alopecia in both Chinese males and females was lower than that seen in whites but similar to the incidence among Koreans.[6]

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 with androgenetic alopecia 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.

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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 androgenetic alopecia usually show thinning of the crown rather than developing truly bald areas.

Along with affecting the patient psychologically,[7] androgenetic alopecia is significant in that it allows ultraviolet light to reach the scalp and, thus, increases the amount of actinic damage. In addition, males with androgenetic alopecia may have an increased incidence of myocardial infarction.[8]

An increase in benign prostatic hypertrophy has also been associated with androgenetic alopecia.[9] Arias-Santiago et al measured prostatic volume by transrectal ultrasound and urinary flow by urinary flowmetry in order to study this hypothesis. Their findings suggest that a relationship exists between early onset androgenetic alopecia and prostate growth associated urinary symptoms, most likely owing to their pathophysiological similarity. They suggest that future studies may clarify whether treatment of patients with androgenetic alopecia might benefit concomitant benign prostatic hypertrophy.[10]

If these associations are proven conclusively, androgenetic alopecia will be of greater clinical significance.

A study by Sanke et al indicated that early androgenetic alopecia (ie, prior to age 30 years) in males is the phenotypic equivalent of polycystic ovarian syndrome (PCOS) and that these males may be at risk of developing complications found in association with PCOS, such as obesity, metabolic syndrome, insulin resistance, cardiovascular disease, and infertility. The investigators reported that the endocrinologic profile of the males with early androgenetic alopecia was similar to that of females with PCOS. Compared with controls, mean levels of testosterone, dehydroepiandrosterone (DHEA)-sulfate, luteinizing hormone, and prolactin were significantly higher in individuals with early androgenetic alopecia, while the mean free androgen index was also higher and mean levels of follicle-stimulating hormone were lower.[11]

A study by Polat et al indicated that men with androgenetic alopecia have a higher likelihood of developing urolithiasis than do those with no hair loss, with the risk being 1.3-fold greater in males with vertex-pattern alopecia, and 2.1-fold greater in those with total alopecia. The study included 200 men with urolithiasis and 168 males with no history of renal stones.[12]

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Patient Education

For patient education resources, see the Skin, Hair, and Nails Center, as well as Hair Loss.

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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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