What is the pathogenesis of skin necrosis?

With the accelerating pace of life, people face the pressure of life has also brought about a certain impact on their own health, now many people will suffer from skin necrosis of this disease, especially for many office workers and middle-aged and elderly friends should be alert to the occurrence of skin necrosis, now basically the skin has been injured friends are prone to suffer from skin necrosis of the disease, skin necrosis can be alleviated by way of medication to treatment. For skin necrosis can be alleviated through the use of drugs to treat, the following to explain the pathogenesis of skin necrosis. What is the pathogenesis of skin necrosis? Skin necrosis refers to skin erythema, edema, blisters and skin necrosis, dermal microvascular thrombosis changes. There are two types of skin necrosis, one in the stratum corneum and one in the dermis. There are many causes of skin necrosis and the pathogenesis is not well understood. It is considered to be caused by the adhesion of eosinophils to the vascular endothelium , and the presence of adhesion fractions keeps the eosinophils replenished. Eosinophils bind to cytokine-induced vascular cell adhesion molecule type 1 (VCAM-1) at endothelial cells, and play an important role in the movement of eosinophils to endothelial cells through integrin late reactive antigen type 4 (VLA-4) and intercellular adhesion molecule type 1 (ICAM-1). Increased vascular permeability through the release of leukopentaene, C4 and platelet-activating factor by eosinophils, and through the release of granule proteins, leads to pathological changes in eosinophils and mast cells through the release of histamine. The pathology is primarily a necrotizing vasculitis of small dermal vessels. Pathology reveals fibrin-like necrosis of the vessel walls and eosinophilic infiltration throughout the dermis with mild or leukocyte fragmentation. The dermis is generally normal, with occasional intraepidermal blistering or eosinophilic infiltration.