• Disease Overview
  • Synonyms
  • Subdivisions
  • Signs & Symptoms
  • Causes
  • Affected Populations
  • Disorders with Similar Symptoms
  • Standard Therapies
  • Clinical Trials and Studies
  • References
  • Programs & Resources
  • Complete Report

Alopecia Areata

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No longer considered rare

Last updated: July 12, 2022
Years published: 1987, 1988, 1989, 1995, 1997, 1998, 1999, 2000, 2004


Disease Overview

Alopecia areata is a disorder characterized by loss of hair. Sometimes, this means simply a few bare patches on the scalp. In other cases, hair loss is more extensive. Although the exact cause is not known, this is thought to be an autoimmune disorder in which the immune system, the body’s own defense system, mistakenly attacks the hair follicles, the tiny structures from which hairs grow. Unpredictable hair loss is the only noticeable symptom of this disorder. Regrowth of hair may or may not occur. Hair loss is usually confined to the head and face, although the entire body may be involved.

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Synonyms

  • Alopecia Celsi
  • Alopecia Cicatrisata
  • Alopecia Circumscripta
  • Cazenave's Vitiligo
  • Celsus' Vitiligo
  • Jonston's Alopecia
  • Porrigo Decalvans
  • Vitiligo Capitis
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Subdivisions

  • Alopecia Seminuniversalis
  • Alopecia Totalis
  • Alopecia Universalis
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Signs & Symptoms

Alopecia areata often begins suddenly with oval or round bald patches appearing most commonly on the scalp. Other areas of hairy skin may also be involved. Gradually, the affected skin becomes smooth. New patches may spread by joining existing bald patches. These larger bald areas can appear while hair is regrowing in older hairless patches. Loss of hair can be permanent in some cases. Hair follicles may deteriorate, but oil producing glands in the skin (sebaceous glands) usually change very little. The skin does not become hard or atrophied. In a very few cases, all body hair may be lost. Cases beginning during childhood tend to be more severe than cases with an onset during adulthood.

The physical manifestations of this disorder may not be as difficult to handle for some individuals as the emotional ones. Most people with alopecia areata are generally healthy otherwise, and the disorder itself is not a sign of a serious or life-threatening disease.

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Causes

The exact cause of alopecia areata is not known. An autoimmune mechanism is suspected in this disorder. Autoimmune disorders are caused when the body’s natural defenses against “foreign” or invading organisms (e.g., antibodies) begin to attack healthy tissue for unknown reasons. Some cases may be linked to abnormal reactions by blood cells (serum antibodies) to a thyroid protein (thyroglobulin), stomach (parietal) cells, or adrenal cells.

In 20 percent of cases, a familial pattern has been proposed, suggesting that some individuals may have a genetic predisposition to alopecia areata. A genetic predisposition means that a person may carry a gene for a disease but it may not be expressed unless something in the environment triggers the disease. It is not known whether this trigger comes from outside the body, such as a virus, or is internal. People who develop alopecia areata for the first time after age 30 are less likely to have other family members who also have the disorder.

The gene responsible for alopecia universalis (total absence of hair on the body) is located on the short arm of chromosome 8 (8p12).

Chromosomes are found in the nucleus of all body cells. They carry the genetic characteristics of each individual. Pairs of human chromosomes are numbered from 1 through 22, with an unequal 23rd pair of X and Y chromosomes for males and two X chromosomes for females.

Each chromosome has a short arm designated as “p” and a long arm identified by the letter “q”. Chromosomes are further subdivided into bands that are numbered. For example, chromosome 8p12 refers to band 12 on the short arm of chromosome 8.

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Affected populations

Alopecia areata affects males and females in equal numbers. It may appear at any age, but most typically begins during childhood. There are approximately 2.5 million individuals in the United States affected by alopecia areata.

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Standard Therapies

Treatment of alopecia areata is directed at producing regrowth of hair. Although there is no cure for alopecia areata at the present time, the hair may sometimes return by itself. In some cases, it may also fall out again after returning. The course of this disorder varies among individuals, and is difficult to predict.

For mild, patchy alopecia areata, in which less than 50% of the scalp hair is gone, cortisone may be injected locally into areas of bare skin. These injections are done with tiny needles, and repeated once a month. Topical solutions, creams and ointments may also help.

For more extensive alopecia areata, cortisone pills are sometimes given. However, these pills may have undesirable side effects that should be discussed with a physician beforehand.

In 2022, the U.S. Food and Drug Administration (FDA) approved baricitinib (Olumiant) oral tablets as a treatment option for adult patients with severe alopecia areata, being the first FDA approval of a systemic treatment for the disorder.

Treatment tends to be less effective for more extensive alopecia areata than in cases of mild, patchy alopecia areata.

For cosmetic reasons, wigs and hairpieces may be necessary, especially for affected women and children.

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Clinical Trials and Studies

Information on current clinical trials is posted on the Internet at www.clinicaltrials.gov. All studies receiving U.S. government funding, and some supported by private industry, are posted on this government web site.

For information about clinical trials being conducted at the NIH Clinical Center in Bethesda, MD, contact the NIH Patient Recruitment Office:

Tollfree: (800) 411-1222

TTY: (866) 411-1010

Email: prpl@cc.nih.gov

For information about clinical trials sponsored by private sources, contact:

www.centerwatch.com

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References

TEXTBOOKS

Beers MH, Berkow R, eds. The Merck Manual, 17th ed. Whitehouse Station, NJ: Merck Research Laboratories; 1999:814-15.

Berkow R, ed. The Merck Manual-Home Edition.2nd ed. Whitehouse Station, NJ: Merck Research Laboratories; 2003:975-76.

Larson DE, ed. Mayo Clinic Family Health Book. New York, NY: William Morrow and Company, Inc; 1996:1018-19.

Bennett JC, Plum F, eds. Cecil Textbook of Medicine. 20th ed. W.B. Saunders Co., Philadelphia, PA; 1996:2215.

Thompson W, Shapiro J. Alopecia Areata: Understanding and Coping with Hair Loss. Johns Hopkins University Press. Baltimore, MD. 1996.

REVIEW ARTICLES

Freyschmidt-Paul P, Happle R, McElwee KJ, et al. Alopecia areata: treatment of today and tomorrow. J Investig Sermatol Symp Proc. 2003;8:12-17.

Springer K, Brown M, Stulberg DL. Common hair loss disorders. Am Fam Physician. 2003;68:93-102.

Namazi MR. Nitric acid donors as potential additions to anti-alopecia areata armamentarium. Inflamm Res. 2003;52:227-29.

Skurkovich B, Skurkovich S. Anti-interferon-gamma antibodies in the treatment of autoimmune diseases. Curr Opin Mol Ther. 2003;5:52-57.

Thiedke CC. Alopecia in women. Am Fam Physician. 200367:1007-14.

Chartier MB, Hoss DM, Grant-Kels JM. Approach to the adult female patient with diffuse nonscarring alopecia. J Am Acad Dermatol. 2002;47:809-18.

McDonagh AJ, Tazi-Ahnini R. Epidemiology and genetics of alopecia areata. Clin Exper Dermatol. 2002;27:405-09.

Hordinsky M, Sawaya M, Roberts JL. Hair loss and hirsutism in the elderly. Clin Geriatr Med. 2002;18:121-33.

Papadopoulos AJ, Schwartz RA, Janniger CK. Alopecia areata. Pathogenesis, diagnosis, and therapy. Am J Clin Dermatol. 2000;1:101-05.

FROM THE INTERNET

McKusick VA, ed. Online Mendelian Inheritance in Man (OMIM). The Johns Hopkins University. Entry Number; 104000: Last Edit Date; 9/5/2003.

Alopecia areata. MedlinePlus. Medical Encylopedia. Update Date1/11/2003. 3pp.

www.nlm.nih.gov/medlineplus/ency/article/001450.htm

Questions and Answers About Alopecia Areata. NIAMS. Publication Date: February 2003. 11 pp.

www.niams.nih.gov/hi/topics/alpecia/alopecia.htm

What is Alopecia Areata? National Alopecia Areata Foundation. nd. 2pp.

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