Treatment with topical Ruxolitinib is associated with reduced Staphylococcus aureus burden in chronic hand dermatitis
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Presented at: Society for Investigative Dermatology 2025
Date: 2025-05-07 00:00:00
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Summary: Abstract Body: Chronic hand dermatitis (CHD) is a common debilitating skin condition with complex pathophysiology. Studies have linked CHD severity to increased Staphylococcus aureus (Sa) colonization. Our previous open-label study (NCT05293717) showed significant clinical improvement with topical 1.5% Ruxolitinib (RUX; Jak1/2 inhibitor) in moderate to severe CHD. Here, we examine changes in Sa burden/abundance in this cohort. Participants (n=15) applied RUX twice daily for 12 weeks, with a 4-week post treatment follow-up. Every 4 weeks, skin swabs were taken from a dorsal, non-lesional (NL; 4x4 cm) area, along with assessments of disease severity (e.g. Hand Eczema Severity Index/HECSI and ItchyQuant). Sa abundance was measured by quantitative PCR of the femA gene (rCFU). Analysis used 0.05 significance level (Prism) and data reported as medians [IQR]. Sa abundance was significantly reduced from baseline after 8 weeks of RUX treatment (p<0.01, 255.1 [81.1, 2655] vs 42.1 [23.2, 72.3] rCFU) and maintained at week 12 (p<0.01, 50.2 [19.6, 85] rCFU). A greater baseline Sa abundance was found in the atopic (n=7) versus the non-atopic (n=8) subtype (p=0.02, 2,342 [122.6, 31718] & 161 [0, 756.2] rCFU); the RUX response did not differ between them. Sa abundance moderately correlated with HECSI during RUX treatment (r=0.41, p<0.01). Notably, there was increased Sa abundance (p<0.01, 50 [20, 85] & 72 [25, 1427]), increased itch (p<0.01, 1 [0, 2] & 3 [1, 6]), increased HECSI (p<0.05, 6 [2, 9] & 12 [6, 32]) at 4-weeks post-RUX compared to week 12. This study highlights the promising role of RUX in CHD management, with clinical improvement associated to reduced Sa burden and a reversed trend after stopping RUX. Further studies are needed to investigate the contribution of Sa burden in CHD as well as the direct or indirect (e.g. inflammatory mediated) mechanism of RUX. Sumeetha Swaminathan<sup>1</sup>, Kimberly A. Arnold<sup>2</sup>, Hannah Smith<sup>1</sup>, Takeshi Yoshida<sup>2</sup>, Calla Fahey<sup>2</sup>, Julie Ryan Wolf<sup>2</sup>, Anna De Benedetto<sup>2</sup> 1. School of Medicine, University of Rochester, Rochester, NY, United States. 2. Dermatology, University of Rochester, Rochester, NY, United States. Clinical Research: Interventional Research