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There is a growing need for up-to-date information on the pathogenesis, clinical features, and potential treatment options of COVID-19. Researchers all around the world are trying to understand the exact mechanism related to immunopathogenesis and role of the host response in the development of the clinical features of the infection. COVID-19 infection has been linked with several mucocutaneous manifestations, including acral edema, chilblain-like lesions in mild forms, and retiform purpura in severe cases.
Acral chilblain-like lesions are a functional vascular disorder characterized by erythematous, edematous lesions; their clinical and histopathological findings are almost superimposable to cold-induced idiopathic chilblains. Livedo reticularis is a functional and reversible disorder of deeper skin vessels due to the action of various factors, including cold (2). Retiform purpura is an irreversible vascular disorder characterized by central necrosis and/or ulceration (2); it was observed in severe, often fatal COVID-19 patients (4).
When factors of various types, for example cold, act on the lumen and/or walls of deeper and wider vessels, they are capable of causing the functional disturbance known as livedo reticularis. When the action of the same factors is more intense, the same vessels are persistently occluded and there are ischemia and necrosis, i.e. retiform purpura. Therefore, livedo reticularis and retiform purpura are different aspects of the same disease spectrum. The host response to SARS-CoV-2 could be responsible for vascular damage with consequent ischemia leading in mild cases to chilblains and/or livedo reticularis, in severe cases to retiform purpura (1, 3, 5).