The disease may cause psychological stress. People are generally otherwise healthy. In a few cases, all the hair on the scalp is lost (alopecia totalis), or all body hair is lost (alopecia universalis), and loss can be permanent. It is distinctive from pattern hair loss, which is common among males.

Alopecia areata is believed to be an autoimmune disease resulting from a breach in the immune privilege of the hair follicles. Risk factors include a family history of the condition. Among identical twins, if one is affected, the other has about a 50% chance of also being affected. The underlying mechanism involves failure by the body to recognize its own cells, with subsequent immune-mediated destruction of the hair follicle.

No cure for the condition is known. Efforts may be used to try to speed hair regrowth, such as cortisone injections. Sunscreen, head coverings to protect from cold and sun, and glasses, if the eyelashes are missing, are recommended. In some cases, the hair regrows, and the condition does not reoccur. In others, hair loss and regrowth occurs over years. Among those in whom all body hair is lost, fewer than 10% recover.

About 0.15% of people are affected at any one time, and 2% of people are affected at some point in time. Onset is usually in childhood. Males and females have the condition in equal numbers. The condition does not affect a person’s life expectancy.

Typical first symptoms of alopecia areata are small bald patches. The underlying skin is unscarred and looks superficially normal. Although these patches can take many shapes, they are usually round or oval. Alopecia areata most often affects the scalp and beard, but may occur on any part of the body with hair. Different areas of the skin may exhibit hair loss and regrowth at the same time. The disease may also go into remission for a time, or may be permanent. It is common in children.

The area of hair loss may tingle or be painful.[8] The hair tends to fall out over a short period of time, with the loss commonly occurring more on one side of the scalp than the other.

Exclamation point hairs, narrower along the length of the strand closer to the base, producing a characteristic “exclamation point” appearance, are often present. These hairs are very short (3–4 mm), and can be seen surrounding the bald patches.

When healthy hair is pulled out, at most a few should come out, and ripped hair should not be distributed evenly across the tugged portion of the scalp. In cases of alopecia areata, hair tends to pull out more easily along the edge of the patch where the follicles are already being attacked by the body’s immune system than away from the patch where they are still healthy.

Nails may have pitting or trachyonychia.

Alopecia areata is thought to be a systemic autoimmune disorder in which the body attacks its own anagen hair follicles and suppresses or stops hair growth. For example, T cell lymphocytes cluster around affected follicles, causing inflammation and subsequent hair loss. Hair follicles in a normal state are thought to be kept secure from the immune system, a phenomenon called immune privilege. A breach in this immune privilege state is considered as the cause of alopecia areata. A few cases of babies being born with congenital alopecia areata have been reported.

Alopecia areata is not contagious. It occurs more frequently in people who have affected family members, suggesting heredity may be a factor. Strong evidence of genetic association with increased risk for alopecia areata was found by studying families with two or more affected members. This study identified at least four regions in the genome that are likely to contain these genes. In addition, alopecia areata shares genetic risk factors with other autoimmune diseases, including rheumatoid arthritis, type 1 diabetes, and celiac disease. It may be the only manifestation of celiac disease.

Endogenous retinoids metabolic defect is a key part of the pathogenesis of the alopecia areata.

In 2010, a genome-wide association study was completed that identified 129 single nucleotide polymorphisms that were associated with alopecia areata. The genes that were identified include those involved in controlling the activation and proliferation of regulatory T cells, cytotoxic T lymphocyte-associated antigen 4, interleukin-2, interleukin-2 receptor A, and Eos (also known as Ikaros family zinc finger 4), as well as the human leukocyte antigen. The study also identified two genes, PRDX5 and STX17, that are expressed in the hair follicle.

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