Janus-kinase inhibitors in dermatology: A review of their use in psoriasis, vitiligo, systemic lupus erythematosus, hidradenitis suppurativa, dermatomyositis, lichen planus, lichen planopilaris, sarcoidosis and graft-versus-host disease.

Recent studies on molecular pathways have elucidated novel therapeutic approaches in inflammatory and autoimmune skin disorders. Specifically, the dysregulation of the Janus kinase signal transducer and activator of transcription (JAK-STAT) cascade plays a central role in the pathogenesis of many skin conditions. JAK inhibitors, with their ability to selectively target immune responses, are potential treatment options. Using the National Library of Medicine, we provide a comprehensive review of the use of United States Food and Drug Administration (FDA)-approved and emerging JAK or tyrosine kinase 2 (TYK2) inhibitors in a wide range of dermatologic conditions, including psoriasis, vitiligo, systemic lupus erythematosus, hidradenitis suppurativa, dermatomyositis, lichen planus, lichen planopilaris, sarcoidosis and graft-versus-host disease. In patients with psoriasis, oral deucravacitinib (TYK2 inhibitor) has been approved as a once-daily therapy with demonstrated superiority and efficacy over apremilast and placebo and tolerable safety profiles. In patients with vitiligo, topical ruxolitinib (JAK1 inhibitor) is approved as a twice-daily treatment for repigmentation. The efficacy of several other JAK inhibitors has also been demonstrated in several clinical trials and case studies for systemic lupus erythematosus, hidradenitis suppurativa, dermatomyositis, lichen planus, lichen planopilaris, sarcoidosis and graft-versus-host disease. Further investigations with long-term clinical trials are necessary to confirm their utility in treatment and safety for these diseases.

Concomitant psoriasis and hidradenitis suppurativa responsive to adalimumab therapy: A case series.

Psoriasis and hidradenitis suppurativa are inflammatory dermatoses that have been associated with arthritis, metabolic syndrome, obesity, and smoking. They share common pathogenic mechanisms such as elevated levels of several proinflammatory cytokines including tumor necrosis factor (TNF), interleukin-17A, and impaired Notch pathway. Thus, treatments for both diseases are sometimes overlapping. Biological therapy such as adalimumab is effective for patients with hidradenitis suppurativa and psoriasis. Adalimumab is a monoclonal antibody that binds to TNF and inhibits the cytokine interaction with the TNF receptors, thus inhibiting the inflammatory cascade. Currently, data are lacking on the treatment for co-occurrence of psoriasis and hidradenitis suppurativa. This case series describes three patients with a diagnosis of concomitant psoriasis and hidradenitis suppurativa. In these cases, after 12 weeks of treatment with adalimumab 40 mg every other week, the average Psoriasis Area Severity Index score reduced from 21.4 to 2.9 for psoriasis, Hidradenitis Suppurativa-Physician's Global Assessment from 3.3 to 0.7, and pain Visual Analog Scale for hidradenitis suppurativa from 4.6 to 2. The results suggest that adalimumab is a treatment of choice for patients with concomitant hidradenitis suppurativa and psoriasis.