• Riccardo Asero, Piersandro Riboldi, Alberto Tedeschi, Massimo Cugno, and Pierluigi Meroni.
• Ambulatorio di Allergologia, Clinica San Carlo, Paderno Dugnano (MI), Italy. Electronic address: r.asero@libero.it.
• Autoimmun Rev. 2007 Nov 1; 7 (1): 71-76.

AbstractChronic urticaria (CU), defined as recurrence of wheals with or without angioedema for more than 6 weeks, is a quite common disease that may severely worsen the quality of life. Studies carried out during the last 2 decades have demonstrated an autoimmune pathogenesis mediated by functionally active autoantibodies to the high affinity IgE receptor (FcepsilonRI) or to IgE which are able to induce histamine release from basophils and mast cells. However, such mechanism can be detected in less than 50% of patients only. The present article reviews recent findings showing an additional pathogenic mechanisms in CU patients: activation of the coagulation cascade resulting in thrombin production. Thrombin is a serine protease which may play a key role in urticaria, being able to induce edema through an increase in vascular permeability, mast cell activation and degranulation, and to induce the production of the anaphylotoxin C5a. Such mechanism seems to be active in the majority of CU patients, however their relationship with anti-FcepsilonRI or anti-IgE autoantibodies is still matter of research.

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