Alopecia areata (AA) is a chronic worldwide inflammatory disease that involves the hair follicle and sometimes the nails.1,2
The hair follicle is an immunologically privileged organ that is protected from the attack by cytotoxic T – lymphocytes (CTLS) by decreasing major histocompatibility complex (MHC) class I expression.3,4 Current evidence indicates that hair follicle inflammation in alopecia areata is caused by a T- cell mediated autoimmune mechanism occurring in genetically predisposed individuals .1,2 AA is a lymphocyte cell mediated inflammatory form of hair loss with research evidence suggesting an underlying autoimmune etiopathogenesis. The development of hair loss involves aberrant modulation of the hair growth cycle, resulting in dystrophic anagen hair follicles and/or increased frequency of telogen state follicles. Genetic susceptibility to the development of AA involves specific alleles of the HLA║ region though other non-HLA genes are also likely to be involved. Susceptibility to the development of AA may be modified by environmental factors, including exposure to proinflammatory agents and possibly other modulators, including stress and diet. 12
Alopecia areata is an immune mediated form of hair loss that occurs in all ethnic groups , ages , and both sexes , with an estimated life risk of 1.7% among the general population .1,5 Overall ,alopecia areata likely affects males and females equally. 6
In most patients , the onset is within the first decades of life , although alopecia areata can start at any age. 7 The disease prevalence peaks between the second and fourth decades . 9
The significance of genetic factors in alopecia areata is underlined by the high frequency of a positive family history in exaggerated individuals. In most reports , this range from 10% to 20% of cases, but mild cases are often over looked or hidden and the true figure may be larger 8 . In the United States, AA was estimated to occur in 0.1% to 0.2% of the general population .10
A wide range of clinical presentations can occur , from the loss of a single patch of hair to complete loss of hair on the scalp (AT) or over the entire body (AU) .3.4 AA can occur on virtually any hair-bearing area ,but it affects the scalp in approximately 90% of cases seen in dermatology clinic. 6 The natural history of Alopecia areata is not well known . Available information indicates that 34-50% of patients with Alopecia areata will recover within one year and 15- 25% will progress to total loss of scalp hair or loss of the entire scalp and body hair, from which full recovery is unusual (less than10%) .3.4 The histopathologic picture varies depending on disease duration. A peribulbar lymphocytic infiltrate ‘‘swarm of bees’’ characterizes the acute phase of AA. In subacute cases, large numbers of catagen and telogen hairs will be present. Hair follicle miniaturization with minimal or no inflammation is seen in chronic cases. 11 AA can be found in association with other autoimmune diseases. Thyroid autoimmunity is probably the main association with an incidence between 8% and 28% .12 The presence of thyroid autoantibodies has no clinical correlation with AA severity .13 Vitiligo may be another important association, with a 3% to 8% incidence in AA patients compared to a prevalence of 1% in the US population. 14 Atopy is twice as common in AA patients compared with the general population. 14 Other diseases and genetic disorders reported to be associated with AA include Down syndrome, Addison disease, autosomal recessive autoimmune polyglandular syndrome (APS-1)(chronic hypoparathyroidism , mucocutaneouscandidiasis-autoimmune adrenal insufficiency), pernicious anemia, psoriasis, lupus, celiac disease ,ulcerative colitis, and multiple sclerosis. These less common autoimmune diseases are more likely to be associated with AT/AU.15 There may be an increased risk of type 1 diabetes in family members of AA...