Skin autoimmunity and blood coagulation

Evidence exists that the immune and coagulation systems are simultaneously activated in some systemic autoimmune disorders. Although proinflammatory mediators induce tissue factor (TF) expression, the main initiator of blood coagulation, activated proteases of coagulation may act on protease-activated receptors (PAR) triggering inflammation. Such a cross-talk amplifies and maintains the activation of both systems. This review focuses on the involvement of immune and coagulation system in two skin disorders as chronic urticaria (CU), autoimmune in about 45% of cases, and bullous pemphigoid (BP), the prototype of autoimmune blistering diseases. Several investigators demonstrated the activation of coagulation in CU through the involvement of eosinophils, of TF pathway with thrombin generation and increased vascular permeability. Preliminary data indicate that anticoagulant treatment with heparin and warfarin may be effective in reducing the symptoms of this disorder. The activation of coagulation seems to display local and systemic implications in BP. Eosinophils' recruitment and thrombin generation locally contribute to the bulla formation and tissue damage. The systemic activation of coagulation may explain the increased thrombotic risk observed in these patients. Taken together, these data provide the rationale for proposing clinical trials on the anticoagulant treatment in both CU and BP patients.