Alopecia Areata

Alopecia

Alopecia Areata:

  • AA is a common ,usually patchy, non-scarring hair loss condition affecting any hair bearing area.
  • It can affect 1.7% of the  population,

    with an equal distribution between males and females.

  • It is more common in children, with about 20% patients being children and reporting their first patch before age of 20.

Cause:

The exact cause of AA unknown and may be due to interaction of genetic and environmental factors

Possible causes may include:

  • Stress.
  • Infectious agents (such as Cytomegalovirus)
  • Vaccinations.
  • Hormonal factors.
  • Genetics: There is positive family history (gene CTLA4, ULBP3/6, IL2/21 & IL2RA).

Autoimmunity is major pathogenetic process in AA and can been seen as an organ specific autoimmune condition characterized by T cell-mediated attacks on the hair follicle

Differential Daignosis:

  • Andogenic alopecia.
  • Telogen effluvium
  • Tricotillomania.
  • Syphilitic alopecia.

Clinical Features:

  • Abrupt loss of hairs and marked hair shedding.
  • The characteristic lesions of AA are oval or round, totally bald, and smooth patches involving the scalp and any hair-bearing area on the body.
  • The scalp and beard are the most affected areas.
  • The patch may be mild peachy or pinkish-red  color.
  • Nail dystrophy may be associated with AA.

Laboratory Test:

  • Thyroid function test.
  • Tests for ferritin, Vitamin-D, B12, Selenium, Zinc, and Copper may be useful.

Corticosteroids:

Mechanism of action: Immunosuppression is main mechanism of action.

Intralesional Corticosteriods: Intralesional corticosteriods injection is first-line therapy for adult patients with less than 50 % scalp involvement. For circumscribed lesions, intralesional corticosteroids are the first-line treatment.
Triamcinolone acetonide is the drug of choice. A 5mg/mL solution with a maximum of 3ml of  triamcinolone acetonide is injected intralesionally with a 30-gauge needle.
Initial growth is often seen in 4 to 8 weeks, and treatment is repeated every 4 to 6 weeks.
The main side effect is atrophy of the scalp.
Children below 10 years are usually are not treated with intralesional corticosteroids.
If there is no response after 6 months, discontinue the treatment.
The use of 0.05% Betamethasone dipropionate cream, 0.05% clobetasol propionate, and 0.2% fluocinolone acetonide cream has been advised for hair growth.
Primary complications from the use of steroids are skin atrophy, telangiectasia and folliculitis, which are reversible on cessation of treatment. Little is known about adrenal suppression with the use of topical steroids.
Oral steroids may be useful in active disease. Oral prednisone is most commonly used drug. The dose is usually 0.8 mg/kg with a tapering dose regime over period of 6 weeks.
Methylprednisolone injection may used for extensive and recent disease

Side effects of steroids include :

  • Weight gain.
  • Osteoporosis.
  • Hypertension.
  • Psychological changes.
  • Suppression of the adrenal cortical axis.
  • Striae.
  • Acne hypertricosis.
  • Purpura.

Topical Sensitizers:

Diphencyprone is the most commonly used topical sensitizer. Sensitization is started with a 2% solution over a 2-week period. It may take 2 years to show results.

Side effects are vesicular or bullous reactions, dissemination of allergic dermatitis, urticarial, enlargement of retroauricular lymph nodes, and altered skin pigmentation.

Minoxidil : Topical and Oral:

Patients with patchy alopecia areata have been reported acceptable regrowth of hairs with 2% application of minoxidil.

Light Therapy:

Psoralene –Ultraviolet A (PUVA) can be used for patchy alopecia areata.

Anthralin:

It can have used for treatment of AA

Biologics:

Not recommended for AA
Combination Therapy
Most commonly Topical steroid and Minoxidil is used in treatment of AA. With promising results.

Combination Therapy:

The most commonly used combination therapy in the treatment of AA is topical steroid and minoxidil, which has shown promising results.

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