INTRODUCTION
Hidradenitis suppurativa (HS) is a chronic inflammatory skin condition associated with significant physical, economic, and psychosocial burdens.1 It is characterized by painful follicular occlusions, primarily at intertriginous locations, which can further manifest as nodules, abscesses, skin tunnels, and fibrosis.2 HS is frequently associated with comorbidities such as obesity, diabetes, and metabolic syndrome3, which can exacerbate systemic inflammation.4 Despite the multitude of existing treatments for HS–including topicals, oral antibiotics, and biologics–many patients are dissatisfied with available therapies5, underscoring the need for innovative treatments.
Glucagon-like peptide-1 Receptor Agonists (GLP-1RA) medications have emerged as a novel treatment opportunity for HS patients. Initially implemented as a type 2 diabetes mellitus (T2DM) medication, GLP-1RAs have demonstrated efficacy for weight loss and are used off-label for their systemic anti-inflammatory effects.6 Preliminary studies have suggested that GLP-1RA may improve HS morbidity by reducing mechanical stress and systemic inflammation, while simultaneously addressing multiple comorbidities that often present with HS.7
The pathogenesis of HS is complex and not fully understood. Lesions generally begin with defective hair follicle maturation, resulting in occlusion and rupture. This leads to exaggerated proliferation of both keratinocytes and the immune system, with neutrophilic and lymphocytic predominance. HS is strongly associated with immune abnormalities, oxidative damage,8 and elevated cytokine pathways, including tumor necrosis factor-alpha (TNF-α), interleukin-17A (IL-17A), interleukin-17F (IL-17F), interleukin-1 beta (IL-1β), interleukin-23 (IL-23), and interleukin-26 (IL-26).2,7
Glucagon-like peptide-1 Receptor Agonists (GLP-1RA) medications have emerged as a novel treatment opportunity for HS patients. Initially implemented as a type 2 diabetes mellitus (T2DM) medication, GLP-1RAs have demonstrated efficacy for weight loss and are used off-label for their systemic anti-inflammatory effects.6 Preliminary studies have suggested that GLP-1RA may improve HS morbidity by reducing mechanical stress and systemic inflammation, while simultaneously addressing multiple comorbidities that often present with HS.7
The pathogenesis of HS is complex and not fully understood. Lesions generally begin with defective hair follicle maturation, resulting in occlusion and rupture. This leads to exaggerated proliferation of both keratinocytes and the immune system, with neutrophilic and lymphocytic predominance. HS is strongly associated with immune abnormalities, oxidative damage,8 and elevated cytokine pathways, including tumor necrosis factor-alpha (TNF-α), interleukin-17A (IL-17A), interleukin-17F (IL-17F), interleukin-1 beta (IL-1β), interleukin-23 (IL-23), and interleukin-26 (IL-26).2,7
