Alopecia Areata – Autoimmune Inflammatory Disease and a New Targeted Treatment Option
Alopecia areata (AA) is one of the non-scarring focal alopecias. It is an autoimmune disease of the hair follicle, the etiopathogenesis of which is not entirely understood. At the hair root, a lymphocytic inflammatory infiltrate develops, resulting in follicle miniaturization and the growth of a thin dystrophic hair. Recently, however, a new strategy for the treatment of AA has emerged, focusing on reducing inflammation of the hair follicle by inhibiting Janus kinases (JAK). This is the first therapeutic modality officially approved for this indication.
Alopecia Areata
Alopecia areata is an autoimmune disease with a lifetime risk of occurrence of around 2%. It is characterized by non-scarring hair loss on defined areas of the scalp. Severe forms lead to complete hair loss (alopecia totalis), or complete body hair loss (alopecia universalis).
The disease can affect individuals of any age, but it most commonly appears between the ages of 25 and 37. Hair loss is often accompanied by psychological stress, which can manifest as anxiety, depression, and a reduced quality of life.
The cause of AA is unclear. Currently, it is believed to be a combination of environmental influences and genetic predispositions, such as variants of certain loci or genes involved in T lymphocyte signaling.
Pathophysiology of AA
AA affects hair follicles, which undergo a physiological cycle with 3 phases: anagen (growth, lasts 2–6 years), catagen (degenerative, lasts 2–3 weeks), and telogen (resting, lasts 3 months). The hair follicle in the anagen phase is in a state of so-called immune privilege. In patients with AA, dramatic changes occur in the microenvironment of the hair follicle in the anagen phase. This includes the expression of major histocompatibility complex (MHC) class I and II molecules, increased levels of pro-inflammatory cytokines, and a strong infiltration by immune cells, especially CD4+ and CD8+ T lymphocytes and NK cells.
Treatment Options for AA
In localized forms of AA, spontaneous remission occurs within 1 year in up to 80% of patients. In other cases, various off-label therapeutic modalities are used, such as local corticosteroids, minoxidil, anthralin, prostaglandin analogs, contact sensitizers, or phototherapy, though generally with uncertain effects. In the last decade, researchers have devised a new strategy for treating AA by suppressing inflammation via Janus kinase inhibition. Recently, baricitinib was approved for the indication of AA, making it the currently only officially approved treatment for AA in adult patients.
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Sources:
1. Lensing M., Jabbari A. An overview of JAK/STAT pathways and JAK inhibition in alopecia areata. Front Immunol 2022 Aug 30; 13: 955035, doi: 10.3389/fimmu.2022.955035.
2. Michalíková H. Alopecia and pharmacotherapy options. Remedia 2017; 27 (5): 471–476.
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