Given the important role that JAK pathways play in the pathogenesis of AA, JAK inhibitors (JAKi) have been investigated as a promising therapy for AA. IL-15 then binds to the surface of CD8 + NKG2D + T cells, further promoting the production of IFN-γ via JAK1/3 pathways to amplify the inflammatory response and impair the hair growth cycle ( 6, 7). Evidence from the studies on mouse models of AA has shown that CD8 + NKG2D + T cells release IFN-γ via Janus kinase (JAK)1/2 pathways to stimulate interleukin-15 (IL-15) production in follicular epithelial cells. Interferon-γ (IFN-γ) and CD8 + NKG2D + T cells have been identified as the key contributors to the pathogenesis of AA ( 5). Breakdown of the immune privilege of hair follicles has been thought to be the prerequisite of AA ( 4). The etiology of AA is related to a complex interaction between genetic and immune abnormalities, which induced inflammation targeting the hair follicles. The traditional treatments, such as systemic corticosteroids (SCs) and immunosuppressants, are limited in terms of treatment efficacy and high risk of adverse effects ( 2, 3). There is still no reliable therapy for severe AA. The majority of patients with moderate-to-severe AA will experience unpredictable episodes of relapsing and remitting courses or long-term persistence. Efficacy significantly decreased in patients with a current episode of disease for more than 2 years.Īlopecia areata (AA) is an autoimmune non-scarring hair loss, presenting as focal hairless patches to entire scalp loss or loss involving other body hairs ( 1). A combination of tofacitinib and SCs may have higher efficacy than SCs alone. There were 66.7% patients in the SCs group, 35.0% patients in the tofacitinib group, and 56.5% patients in the combined group that showed adverse effects.Ĭonclusion: Tofacitinib was an effective treatment for patients with moderate-to-severe AA, and it was more tolerated than SCs. The ratio of patients who achieved SALT 50 was significantly higher in patients with a short duration of current hair loss episode (≤2 years) than in those with a duration of current hair loss episode (>2 years) in all the three groups. There were 12 (66.7%) of 18 patients in the SCs group, 12 (60.0%) of 20 patients in the tofacitinib group, and 18 (78.3%) of 23 patients achieved SALT 50, with no significant difference among the three groups. Results: Sixty-one patients with moderate-to-severe AA were included in this study. The efficacy and adverse events of these treatments were retrospectively analyzed. Methods: Patients with moderate-to-severe AA, who have been treated with at least 3 months of monotherapy of tofacitinib or SCs, or in their combination, were included in this study. Objective: To compare the efficacy and safety of monotherapy of oral tofacitinib and SCs, as well as their combination in patients with moderate-to-severe AA. Evidence on the combination use of oral tofacitinib and systemic corticosteroids (SCs) for AA is still lacking. Janus kinase inhibitors, such as tofacitinib, have been recently investigated as a promising treatment option for AA. Treatment for moderate-to-severe AA is still challenging. Introduction: Alopecia areata (AA) is an autoimmune hair loss mediated by CD8 + T cells. Reyes Memorial Medical Center, Manila, Philippines
1Department of Dermatology, Peking University People’s Hospital, Beijing, China.Wenxin Zhang 1 Xiangqian Li 1 Baifu Chen 1 Jianzhong Zhang 1 Kara Melissa T.
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