Dermatomyositis (DM) is an idiopathic inflammatory myopathy (IIM) characterized by distinctive chronic cutaneous manifestations. Although immune-mediated and microvascular mechanisms are well established, the role of metabolic dysfunction, particularly hyperglycemia, is underexplored in dermatological conditions. This review synthesizes mechanistic, clinical, and translational evidence to explore the relationship between dysglycemia and cutaneous disease severity in DM. Hyperglycemia is associated with oxidative stress, advanced glycation end-product formation, endothelial injury, and proinflammatory cytokine signaling. These processes may plausibly amplify DM-associated vasculopathy, impair wound healing, and worsen cutaneous inflammation. Limited DM-specific studies demonstrate increased insulin resistance and a higher prevalence of diabetes compared with healthy controls. Meanwhile, case reports suggest that poor glycemic control can exacerbate cutaneous disease. Evidence from other inflammatory dermatoses supports a biologically plausible role for dysglycemia in increasing flare frequency, infection risk, and delayed tissue repair. Dietary patterns characterized by high glycemic index and coexisting metabolic syndrome may further intensify systemic and cutaneous inflammation. Collectively, these findings suggest hyperglycemia as a biologically plausible contributor to cutaneous disease severity in DM that warrants further investigation. These observations highlight the need for future studies to evaluate whether metabolic screening, dietary patterns, and interdisciplinary care influence cutaneous disease activity and wound healing in DM. Prospective clinical investigation is needed to determine whether targeted glycemic optimization is associated with changes in cutaneous and systemic outcomes in DM.