Abstract
BACKGROUND: The response of atopic dermatitis (AD) to different biologics and JAK inhibitors (JAKibs) is variable due to the varied immunological endotypes of AD. AIM AND OBJECTIVES: To assess the effectiveness and adverse effect profile of tofacitinib in recalcitrant, moderate-to-severe AD patients and to compare the cost of therapy of tofacitinib with dupilumab. PATIENTS AND METHODS: We retrospectively analyzed records of moderate to severe AD treated with tofacitinib monotherapy. The response to tofacitinib was assessed using clinical scores including Numerical Rating Scale (NRS), Scoring Atopic Dermatitis (SCORAD), and Eczema Area and Severity Index (EASI) at 4 weeks and 8 weeks of treatment. We also analyzed the duration of remission and time after which recurrences were seen after stopping tofacitinib. The cost of tofacitinib was compared with dupilumab. RESULTS: Twelve cases of recalcitrant moderate-severe AD who had failed systemic agents [oral corticosteroids (n = 7), cyclosporine (n = 4), and azathioprine (n = 2)] were treated with tofacitinib monotherapy. There was a statistically significant reduction in SCORAD, EASI, and NRS scores at 4 weeks and 8 weeks of tofacitinib therapy [mean at baseline: 4 weeks: 8 weeks = SCORAD- 43.54: 22.74: 11.87 (P = 0.002); EASI-19.5: 6.45: 1.6 (P = 0.002); NRS-5.75: 3.25: 1.08 (P = 0.002)]. EASI 90 was achieved by 66% of patients in 8 weeks with treatment failure in one patient. The mean time to achieve complete/near complete resolution (n = 8) of the disease was 6.1 weeks (3-8 weeks). Relapse of the disease was noted in 4/11 (36.3%) patients. Side effects were observed in 5/12 (41.6%) patients (herpes zoster, dyslipidemia, anemia, impetigo, and thrombocytosis). The cost of therapy with dupilumab is 122 times higher than that of tofacitinib therapy (8 weeks treatment). LIMITATIONS: Small sample size and lack of tissue cytokines analysis pre- and post-treatment. CONCLUSION: Tofacitinib (pan JAK inhibitor) inhibits T helper 2 (Th2), Th1, Th17, and Th22 cell lines, and thus has potential for refractory AD. There is a need to generate tissue-based cytokine expression data in Indian patients with AD.