ArticleClinical, cosmetic and investigational dermatology2025
Tofacitinib as a Novel Therapeutic Option for Pemphigus Vulgaris: A Case Report and Mechanistic Insights.
Article in Clinical, cosmetic and investigational dermatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Pemphigus Erythematosus Treated with JAK1 Inhibitor Upadacitinib: A Case Report and Brief Literature Review.Clinical, cosmetic and investigational dermatology · 2026Article
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Authors and funding
6 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Pemphigus vulgaris (PV), a life-threatening autoimmune blistering disorder mediated by pathogenic anti-desmoglein antibodies, manifests clinically with extensive cutaneous and mucosal vesicles, bullae, and erosions. While corticosteroids remain first-line therapy, a substantial subset of patients develop refractory disease requiring advanced therapies. Tofacitinib, an oral Janus kinase (JAK) 1/3 inhibitor, demonstrates broad immunomodulatory effects through interference with cytokine signaling pathways. We report the case of a 50-year-old male with recalcitrant PV who achieved sustained remission following adjunctive tofacitinib therapy. Combination therapy with tofacitinib (5 mg twice daily) and prednisone (60 mg/day) enabled successful corticosteroids withdrawal within 5 months, achieving complete clinical remission (PDAI=0) and serological improvement (Dsg1/Dsg3 antibodies reduced by 64.5%/75.8%). Longitudinal immunohistochemistry (IHC) revealed attenuated phospho-STAT3 and phospho-STAT6 in post-treatment lesional skin compared to baseline. Proteomic profiling of PV lesions (n=3) versus healthy controls (n=3) identified 198 differentially expressed proteins (fold change >1.5, p<0.05), with KEGG pathway analysis revealing predominant enrichment in JAK-STAT signaling, IL-17-mediated inflammation, and lymphocyte differentiation pathways. Independent validation in an expanded cohort (5 PV vs 5 controls) confirmed constitutive JAK-STAT hyperactivation: phospho-STAT3 (7.2±1.64 vs 1±0, p<0.001) and phospho-STAT6 (9.6±1.34 vs 1.2±0.45, p<0.001) were markedly elevated in untreated PV lesions. These findings posit tofacitinib as a promising steroid-sparing agent in PV management, potentially through multimodal inhibition of pathogenic cytokine networks. Large-scale randomized controlled trials are warranted to validate these observations.
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