Aetiology

The aetiology of AA has not been determined. However, it is hypothesised to be an organ-specific autoimmune disease mediated by T lymphocytes directed at hair follicles.[10] With respect to the genetics of AA, there seem to exist both susceptibility and severity genes.[11]

Pathophysiology

The autoimmune nature of AA is supported by the inflammatory infiltrate of activated CD4+ and CD8+ lymphocytes around affected anagen-phase hair bulbs and by the ability to transfer AA by T lymphocytes from involved scalp to human scalp explants on severe combined immunodeficiency (SCID) mice.[12][13] As in many other autoimmune diseases, there is a strong association of AA with with human leukocyte antigen (HLA) class II alleles.[13][14] A genome-wide search has revealed evidence of at least 4 susceptibility loci on chromosomes 6, 10, 16, and 18.[15] There also appears to be a link between AA and Down’s syndrome, suggesting that chromosome 21 may also be involved.[16]

Classification

Severity in alopecia tool (SALT)[3]

This categorises the pattern or extent of hair loss and prognostic factors, such as duration of hair loss, loss of body hair, nail changes, and type of hair left on the scalp:

  • Patchy alopecia areata

  • Alopecia totalis, indicating total loss of scalp hair

  • Alopecia universalis, referring to loss of hair over the entire scalp and body.

Use of this content is subject to our disclaimer