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Hidradenitis suppurative (HS) is a chronic inflammatory skin disorder characterized by deep-seated nodules, abscesses, sinus tract formation, and scarring. Growing evidence has begun to support the notion that HS not only is a local follicular disorder but also has strong associations with metabolic dysfunction. The metabolic abnormalities seen in patients with HS include obesity, insulin resistance, metabolic syndrome, adipose-mediated inflammation, and altered cytokine signaling. Sodium-glucose cotransporter-2 inhibitors (SGLT2is) are a class of drugs currently used to lower blood glucose in patients with type 2 diabetes mellitus (T2DM). However, recent studies have provided evidence that SGLT2i can alter multiple immunometabolic mediators, including reducing nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome activity, lowering pro-inflammatory cytokine levels, and improving insulin resistance. The purpose of this review was to determine whether SGLT2i can alter mechanisms involved in the development of HS through their anti-inflammatory and metabolic effects. Using Web of Science and PubMed, a literature review was conducted to compile studies on HS, metabolic dysfunction, and the anti-inflammatory effects of SGLT2is. The current evidence indicates that the metabolic and inflammatory pathways targeted by SGLT2is contribute to the development of HS, including the NLRP3 inflammasome, cytokine production, and adipose-related inflammation. The evidence supporting this is largely mechanistic; therefore, future clinical studies are needed to determine whether SGLT2i use in HS can provide significant improvement. However, with current therapies targeting downstream inflammatory mediators, SGLT2i and potentially other metabolic therapies may be promising adjunctive therapies by targeting upstream metabolic drivers that amplify these mediators.