Information on the following diseases can be found in the Related Disorders section of this report:

• Trichotillomania
• Hypotrichiasis (Alopecia Congenitalis, Alopecia Adnata, Congenital
• Baldness, Congenital Alopecia)
• Alopecia Medicamentosa
• Alopecia Mucinosa
• Alopecia Neurotica
• Postpartum Alopecia
• Premature Alopecia
• Alopecia Presenilis
• Alopecia Symptomatica
• Syphilitic Alopecia
• Alopecia Toxica (Toxic Alopecia)
• Alopecia Triangularis Congenitalis

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.

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.

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.

Loss of hair (alopecia) can occur from a wide variety of causes. Symptoms of the following disorders can be similar to those of alopecia areata. Comparisons may be useful for a differential diagnosis:

Trichotillomania, also known as hair pulling, is a neurotic habit that usually appears in children. It may remain undiagnosed for a long time. The hairs may be broken off or pulled out. Stubby regrowth may replace damaged hair or bald areas. This mental illness may be hard to distinguish from alopecia areata without careful observation of the affected child's habits. Hair can be similarly damaged by permanent wave solutions, softeners or hot combs. (For more information on this disorder, choose "trichotillomania" as your search term in the Rare Disease Database.)

Hypotrichiasis (hypotrichosis, alopecia congenitalis, alopecia adnata, congenital alopecia, congenital baldness) is a condition characterized by the absence of hair at birth. This disorder is usually inherited as a dominant trait, but can also be due to a recessive gene. It often occurs in association with other surface skin layer (ectodermal) defects.

Alopecia medicamentosa is characterized by widespread hair loss, most commonly of the scalp, caused by a reaction to various types of drugs in sensitive or allergic individuals. It may also be a result of chemotherapy used in treating various disorders (e.g., cancer).

Alopecia mucinosa, also known as follicular mucinosis, occurs in children and young adults. Hard, reddish, well defined plaques underlie the areas of hair loss. A fine scaling may develop on the face, scalp, trunk, arms or legs. A loss of sensation may occur as the plaques develop. The exact cause of this form of hair loss in not known, although a skin inflammation is suspected. Symptoms often spontaneously resolve after a few months in many cases.

Alopecia neurotica is characterized by hair loss caused by injury to the nerves in the area where balding occurs.

Postpartum alopecia is characterized by temporary loss of hair at the termination of a pregnancy. The cause is not known.

Premature alopecia is characterized by male pattern baldness occurring at an abnormally early age.

Alopecia presenilis is characterized by ordinary or common baldness occurring in early or middle life without any apparent disease of the scalp. This condition is very common in males, but rare in females.

Alopecia symptomatica is characterized by hair loss associated with other illnesses or conditions, most commonly following prolonged illnesses marked by high fever.

Alopecia toxica, also known as toxic alopecia, is characterized by hair loss thought to be caused only by fever.

Alopecia triangularis congenitalis is a congenital defect consisting of a triangular patch of baldness on the front of the scalp.

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.

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.

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

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

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
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.
http://www.naaf.org/