Impact of semaglutide use in obese and diabetic patients with hidradenitis suppurativa

Abstract

Hidradenitis suppurativa (HS) is a chronic debilitating inflammatory skin disease with a complex pathogenesis. It is recognized that obesity, which is associated with increased production of proinflammatory adipokines and cytokines is a significant risk factor.1 In addition, a higher prevalence of obesity in patients with HS, ranging from 5.9% to 73.1% has been noted.2 Semaglutide, a glucagon-like peptide-1 (GLP-1) receptor agonist, is one of the FDA-approved treatments for obesity and diabetes.3, 4 Besides benefits of weight and glucose levels management, it has anti-inflammatory properties5 that may impact other comorbidities, such as HS. This retrospective study used a centralized research patient registry (RPDR) to identify patients with HS treated with semaglutide from May 2019 to May 2024. After IRB approval, we reviewed electronic medical records. Eligible patients had HS and dermatology follow-ups within 6 months prior to and after receiving subcutaneous semaglutide. We collected information on body mass index (BMI), and HbA1c results at baseline, 6- and 12-month follow-ups (±2 months). We evaluated differences in baseline clinical and demographic characteristics between patients who achieved improvement of HS while on semaglutide (responders) versus patients who remained stable or worsened while on therapy (non-responders). Information on response was based on changes in lesion count (more than 50% reduction in any inflammatory lesion type and no new lesions of other types), need for rescue therapy (brief course of systemic antibiotics or systemic steroids as well as intralesional steroids for disease flare) or clinical evaluation at dermatology follow-ups (description of improvement or clearance by same dermatologist). A total of 45 patients were included: 36 females and 9 males, mean age was 42 years old and 21 were diabetic (Table 1). Most patients were Caucasian and had Hurley II stage. Semaglutide starting dose was 0.52 ± 0.47 mg/week and increased to 1.11 ± 0.82 mg/week and 1.36 ± 0.86 respectively, at 6 and 12 months, respectively. Most patients experienced weight loss on semaglutide at 6 (5.9 ± 13.6 lb) and 12 months (10.1 ± 15.4 lb). (Table 2). HS improved in 27 patients after semaglutide. There was a higher proportion of men and smokers among patients who improved on semaglutide, although not statistically significant. There were no differences in Hurley stage, prior disease course or duration and comorbidity frequencies between responders and non-responders. Higher semaglutide doses were associated with improvement at 3, 6 and 12 months. In a logistic regression model including male (OR 7.39, 95%CI 0.68–79.86, p = 0.10), current smoking (OR 5.22, 95% CI 0.83–32.81, p = 0.08) and 6-month dose (OR 2.76, 95% CI 1.02–7.48, p = 0.045) as potential predictors, improvement remained significantly associated with semaglutide dose. Like prior studies, we found progressive decreases in weight and BMI on semaglutide. Paradoxically, 20% gained weight during treatment. In STEP 5 trial, the semaglutide group achieved a mean weight loss of 15.2% from baseline.3 There is limited research on semaglutide in HS patients. Our findings suggest that patients taking higher semaglutide doses at any point during treatment, regardless of the presence of diabetes, showed greater improvement. Another retrospective study with 30 patients using semaglutide was associated with improved quality of life and less flares of HS; however, impact of increasing doses was not evaluated.4 Our study is unique as it evaluates factors that may influence HS response in patients taking semaglutide for obesity. Male, current smoking and increased doses seemed to be the most important positive predictors of response to therapy, although only semaglutide had a significant association. Limitations include a small sample size, lack of a control group and simultaneous use of other HS treatments. Long-term, controlled trials to evaluate semaglutide as an adjunct therapy for HS should be encouraged. None. Xinaida Taligare V. Lima, M.D., is a clinical investigator for Amgen, Biogen and Janssen. She is on the speaker's bureau of Abbvie, Boehringer, Janssen and Novartis and a consultant for UCB Biopharma. Maria Beatrice Alora, M.D., is a clinical investigator for Pfizer, Inc. Abbvie, Concert Pharmaceuticals, Sanofi, Eli Lilly and Janssen. Marielos I. Posada Posada declares no conflict of interest. Reviewed and approved by MGB IRB; approval #20233143. The data that support the findings of this study are available from the corresponding author upon reasonable request.

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