Erythrodermic psoriasis(EP) is a rare, life-threatening variant affecting 75%-90% of the body surface area. Characterized by widespread erythema and potential systemic symptoms like fever and lymphadenopathy, it severely impairs patient quality of life. The pathogenesis of erythrodermic psoriasis is not fully understood. It is a multifactorial, multistep process suspected to result from an abnormal immune response induced by both genetic and environmental factors. Key contributors to erythrodermic psoriasis onset include specific gene polymorphisms, altered expression of adhesion molecules, dysregulated cytokine activity, and abnormal activation of T cell subsets. Additionally, imbalances in the skin microbiota and external factors, such as infections and medications, play important roles in disease onset and progression. Distinct from prior reviews that primarily emphasize clinical features and treatment, this review integrates recent mechanistic advances across genetic, immune, environmental, and microbiome domains to provide an updated, systems-level framework for understanding erythrodermic psoriasis and to highlight potential therapeutic implications.
