The molecular basis of alopecia areata and risk assessment of comorbid autoimmune diseases
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Abstract
Alopecia areata (AA) is a non-cicatricial autoimmune condition, resulting in a patchy loss of hair from the scalp. The hair loss is not limited to the scalp and can extend to ones eyebrows and eyelashes. AA can progress into the more severe subtypes; hair loss from the entire scalp (alopecia totalis) or the entire body (alopecia universalis). AA is a multifactorial disease, citing genes and environmental factors such as stress, climate, drugs and hair styling practices as causative factors. Histologically, CD8 (+) T cells invade and attack the hair follicle, leading to disturbances in hair growth. Treatment for AA aims to reduce the amount of inflammation and re-establish the normal hair loss cycle. Treatment options fall into 3 categories: local treatments, physical treatments and systemic treatments; none are FDA approved. Some patients do not require treatment, as spontaneous remission can occur. A number of studies have examined the comorbidity of AA with other autoimmune diseases genetically and phenotypically. There is a reported increased incidence of several autoimmune diseases occurring with AA such as rheumatoid arthritis, diseases of the thyroid, psoriasis, vitiligo and even type I diabetes. This hints at a relation occurring between the molecular pathways of AA and these comorbid diseases. As AA currently has no FDA approved treatment options, molecular investigation of where these pathways coincide may yield new, long-lasting treatment alternatives for patients with AA.