Inflammation and coagulation systems are simultaneously activated in autoimmune and immune-mediated skin disorders, and the cross-talk that amplifies and maintains their activation seems to have both local and systemic implications. This interplay occurs in
bullous pemphigoid (BP), the prototype autoimmune blistering disease in which eosinophil recruitment and
thrombin generation locally contribute to the formation of
bullae and inflammatory tissue damage. Moreover, the systemic activation of coagulation may explain the increased thrombotic risk observed in BP patients.
Atopic dermatitis (AD), a chronically relapsing immune-mediated inflammatory
skin disease, also involves the local and systemic activation of coagulation, which means that a prothrombotic state could theoretically develop, although the incidence of
thrombosis is not increased in AD patients probably because of their young age. In
psoriasis, a erythematous-squamous inflammatory immune-mediated skin disorder, the activation of coagulation seems to be mainly systemic and related to systemic
inflammation, thus potentially contributing to the disease-related increase in cardiovascular risk in this disease. The activation of coagulation has also been suggested an additional pathomechanism in
dermatitis herpetiformis (DH), a chronic-relapsing autoimmune
skin disease associated with
gluten sensitivity and
celiac disease, but its precise role has not yet been defined. Taken together, these data provide the rationale for controlled clinical trials aimed at evaluating the usefulness of
anticoagulant treatment in autoimmune skin disorders to counteract the local and systemic effects of coagulation activation.