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 erythematoussquamous
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.
Keywords: Eosinophil, tissue factor, bullous pemphigoid, atopic dermatitis, psoriasis, dermatitis herpetiformis, inflammation, coagulation, ELISA, innate immunity
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