An overview of alopecia areata, what it is and how it is treated

What causes this disease is still unknown. Many studies show it to be an immune mediated disease. The immune system, meant to attack the viruses and bacterias, mistakenly attacks the hair follicles, causing hair loss. Other studies point at the genes. This is supported by the fact that families of affected people show a history of alopecia areata.

According to some, environmental factors like chemicals, vaccines and desensitizing injections may also trigger this disease. Some skin specialists opine that viral and bacterial diseases could cause the immune system to behave aberrantly against the hair follicles. Then there are cases which show stress and anxiety can cause this disease.

Clinical Features of Alopecia Areata

Hair growth progresses in cycles, which have three phases. They are called anagen, catagen and telogen. Anagen is the active growth phase when the hair fibers are produced. In the catagen phase the hair follicle undergoes a controlled regression phase. In the final, telogen phase it is in a resting state. The hair follicle then enters the anagen phase of the next growth cycle.

Alopecia areata occurs when the hair follicle growth cycle is disturbed as it enters the anagen phase. The hair follicles in anagen, bypass the catagen state and prematurely enter the telogen state. The hair follicles may then enter anagen phase of the next cycle but produce poor quality fibers. Hair follicles are then said to be in a dystrophic anagen state. Examination of fallen hairs shows them having telogen roots.

Alopecia areata usually shows up as a bald patch, one to two centimeters in diameter, on any hair bearing part of the body but commonly on the scalp. These patches may increase in size or numbers. The patterns of hair loss are as follows:

• Oval or round patches
• Alopecia totalis or total loss of terminal scalp hair
• Alopecia universalis or total loss of all body hair
• Ophiasis or band like pattern of hair loss

Often, at the fringes of the patches, 1 to 2 mm long broken hairs are found. These are called exclamation hairs because their distal ends taper to a point. The less damaged hairs remain in anagen but go on to produce defective dystrophic hairs.

Alopecia areata affects only pigmented hairs and not un-pigmented or white hair. The course of the disease is unpredictable. It may last a short time with normal hair growth quickly recovered. It may also last years with some re-growth or it may remain in the two phase cycle of anagen and telogen. This disturbed cycle may, initially, cause growth of white fuzzy hairs, which is strange, considering that alopecia areata affects only pigmented hairs. This paradox is still to be explained.

In some cases, hair changes color during or after the period of hair loss. Sometimes the change can be permanent.

About 10% to 66% people affected by alopecia areata also have distorted nail formations, of which pitting is the most common. Other aberrations are brittle nails, spotting of the lunae or crescent shaped mark at the base of the nail and concave outer surface of the nail. Loosening or complete shedding of nails has also been observed.

Diagnosis of Alopecia Areata

Presently there is no foolproof diagnostic method for alopecia areata. Dermatologists diagnose, by a process of elimination of other causes showing similar clinical features. Lesion examination and hair pull tests are also conducted. For a more reliable diagnosis, skin biopsy tests are also done.

Pathology of Alopecia Areata

Lymphocytic infiltrates and granulamatous inflammation have been seen around late anagen hairs and within the hair follicles in the acute stage of the disease. The inflammatory infiltrate contains, mainly, activated T lymphocytes with some CD4 and Langerhans cells. It may be present above the hair follicle bulb and enter follicular streamers, but usually does not enter the bulge area containing stem cells. Probably this is why follicles are not destroyed in alopecia areata.

Light and electron microscope techniques show that nail changes in alopecia areata are linked to changes inside the proximal matrix.

Treatment of Alopecia Areata

Treatment depends on the age of the patient and the spread of the disease. As yet, there is no evidence showing medication can change the course of the disease. All alopecia areata patients have the potential to re-grow their hair even after years of hair loss. There is no permanent cure for this disease nor is there any universally proven treatment.

Corticosteroids are most commonly used for treatment. They hinder activation of T- lymphocytes. They are administered in four ways:

• Topically as cream or lotion only on the affected parts: It is a mild treatment and gives mixed results. For long term treatment the risk of systemic absorption and side effects must be weighed.
• As intralesional steroid injections into the bald patch and below the epidermis where the inflammatory infiltrate is present. Growth is seen after 2 to 6 weeks. Side effects are pain from the injection and atrophy of the skin around it. This atrophy is normally reversible unless the region has been repeatedly injected. Here also there is a risk of side effects through systemic absorption if injected doses are too high or too frequent.
• Systemically as injections into the muscles

Oral treatment is a last resort, since risk of serious side effects is high in this case. Studies show that a combination of topical and oral treatment and injection can be quite effective. Steroids normally cause temporary hair re-growth. There is a relapse once they are stopped.

PUVA or photochemotherapy is being used to treat alopecia areata. Here psoralen (P) drug is taken two hours before measured exposure to long-wave ultraviolet light. Hair growth may occur after 40-80 treatments. Total recovery takes one to two years.

Contact sensitizers are also used for alopecia areata. Hair growth takes 8 to 10 weeks. For total recovery weekly treatments are necessary.

Today the focus is on gene therapy. It is hoped that the future will introduce better treatments, which are immunosuppressive and immunomodulatory. These will be more effective in dealing with this immune mediated disease and in protecting the follicles from inflammation.