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Background: Efficacy of the Janus kinase (JAK) inhibitor baricitinib for severe alopecia areata (AA) continuously increased over 52 weeks in two Phase 3 trials. There are limited long‐term data on JAK inhibitors in AA. Objectives: To evaluate efficacy and safety of baricitinib for severe AA through 104 weeks of continuous therapy. Methods: Integrated data from the BRAVE‐AA1 and BRAVE‐AA2 Phase 3 trials included adults with Severity of Alopecia Tool (SALT) scores ≥50 (≥50% scalp hair loss) randomized to and continuously treated with 2‐mg or 4‐mg baricitinib through Week 104. Patients who qualified to remain on continuous treatment included subjects who achieved SALT score ≤20 at Week 52 (Week‐52 responders; 2‐mg: N = 65; 4‐mg: N = 129) and baricitinib 4‐mg‐treated patients who had SALT score >20 at Week 52 but achieved SALT score ≤20 at prior visit(s) and/or had significant improvement in eyebrow or eyelash hair growth relative to baseline by Week 52 (Week‐52 mixed responders; N = 110). Week‐104 outcomes included the proportion of patients achieving SALT score ≤20 (≤20% scalp hair loss). Data were censored after treatment discontinuation. Results: Among baricitinib 4‐mg‐treated and baricitinib 2‐mg‐treated Week‐52 responders, 90.7% and 89.2%, respectively, maintained SALT score ≤20 at Week 104. Among Week‐52 mixed responders, 39.1% reached SALT score ≤20 by Week 104. Continued improvement in eyebrow and eyelash regrowth was observed across groups. The most frequent treatment‐emergent adverse events were COVID‐19, upper respiratory tract infection, headache, nasopharyngitis, acne, urinary tract infection and creatine phosphokinase increase. Conclusions: Baricitinib demonstrated a high level of maintenance of efficacy over 104 weeks in patients with severe AA. Efficacy increased in Week‐52 mixed responders, illustrating that long‐term treatment is necessary to observe maximum benefit in some patients. No new safety signals were observed. [ABSTRACT FROM AUTHOR]

Background Atopic dermatitis ( AD) is a commonly encountered inflammatory skin disease. Although acute lesions of acute AD are characterized by intense inflammation, the hallmarks of chronic AD lesions include lichenified fibrosis and thickening of the upper dermis. The increased expression of transforming growth factor beta 1 ( TGF-β1), a well-known fibrogenic cytokine, is observed in chronic AD lesions. Tacrolimus ( FK506) ointment has been reported to be effective for treating AD as well as some TGF-β1-induced fibrotic diseases. Objectives To evaluate the effect of tacrolimus on TGF-β1-stimulated cultured normal human dermal fibroblasts and explore the potential signalling pathways involved. Methods Fibroblasts cultured from healthy adult human foreskins were treated with TGF-β1 with or without tacrolimus. The impact on cell viability and proliferation were assessed by [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] (MTT) assay and BrdU incorporation assay respectively. Reverse transcription-polymerase chain reaction (RT-PCR), quantitative real-time PCR, enzyme-linked immunosorbent assay (ELISA) and western blotting were performed to evaluate the relevant expressions of m RNA or proteins in fibroblasts. Results Our results revealed that the increased expressions of transforming growth factor-β receptor I ( TGF-β RI) and TGF-β RII in TGF-β1-treated fibroblasts were suppressed by tacrolimus treatment. In addition, tacrolimus significantly inhibited fibroblast proliferation enhanced by TGF-β1. TGF-β1 increased type I collagen production, and this enhancing effect was suppressed by tacrolimus. The down-regulation of MMP-1 and up-regulation of TIMP-1 induced by TGF-β1 were reversed by tacrolimus. The increase in phosphorylated p38 mitogen-activated protein kinase (p38 MAPK) expression stimulated by TGF-β1 was down-regulated by tacrolimus. Moreover, the fibroblasts treated with p38 MAPK inhibitor significantly reduced type I collagen expression induced by TGF-β1. Conclusions The present results demonstrated that tacrolimus significantly inhibited physiological functions of fibroblasts enhanced by TGF-β1 in vitro. Clinically, we propose that topical tacrolimus may not only reduce AD recurrence but also ameliorate dermal fibrosis often seen in chronic AD lesions. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented regarding the case of a 40-year-old woman with symmetrical vitiligo over bilateral periocular areas treated with combined helium-neon laser and topical tacrolimus therapy.