On physical examination, there is a near-complete loss of scalp hair, with preservation of hair at other bodily sites, including the eyelashes, eyebrows, axilla, and pubic area. Comorbidities in order of highest frequency include autoimmune thyroid disease, vitiligo, type I diabetes mellitus, atopy, and inflammatory bowel disease.

Comorbid conditions are common in patients with AA and might be slightly more frequent in those with AT, affecting about 20% of patients. There is a positive family history of hair loss in about 20% of cases. įamily history and past medical history are also important to obtain. The time from the initial development of AA to progression to AT is, on average one year, and within 4 years in 90% of patients. For patients with AT, the most common initial presentation is multifocal AA, defined as 5 or more discrete patches. Most patients presenting with AT will have a history of discrete, patchy hair loss, which has progressed to total scalp involvement, though only 5%-10% of patients with AF progress to totalis or universalis. Įlucidating a thorough history is critical in patients presenting with extensive hair loss. JAK3 is overexpressed in patients with AA. Downstream, these cytokines signal the Janus kinase signal transducer and activator of transcription (JAK/STAT) pathway. IL-15 suppresses regulatory T-cells, promoting the proliferation of natural killer cells.

These T-cells produce interferon (IFN)-gamma, which activates interleukin (IL)-2, IL-7, IL-15, and IL-21 cytokines. ĬD8+ T-cells, in particular, are known to play a key role in the pathogenesis. When this is disturbed, and MHC expression is increased, immune privilege is lost as previously hidden antigens may be presented to T-cells. In normal conditions, healthy anagen hair follicles express major histocompatibility complex (MHC) class I at low levels, which prevents molecular presentation as autoantigens. Central to these is the loss of the immune privilege of the hair follicle leading to attack of the follicle by the immune system. The loss of immune privilege may occur secondary to an environmental insult such as a virus, or it may be a spontaneous autoimmune phenomenon. There are multiple theories on the pathogenesis of alopecia areata.

Alopecia universalis women