Physiopathology of urticaria.

Urticaria is a common disorder that affects as many of 20% of all people at sometime during their lives. It is a cutaneous reaction pattern for which there are multiple potential causes. Its physiopathology is poorly defined. The vascular changes observed in urticarial lesions can be attributed to the release of mediators: histamine plays an essential role but others mediators, such as serotonin, eicosanoids, kinins, neuropeptides. may also be involved. These mediators are synthetized by mast cells which are the major effector cell type. However, other cells, basophils, mononuclear cells, platelets, endothelial cells have also been implicated. During immediate hypersensitivity reaction, mast cells and basophils are activated by allergens through cross linking of cell-surface-bound IgE. However, more often than not, these cells are stimulated by non-immunological mechanisms. At present, some data are better understood: in urticaria, there is a late phase reaction which involves cytokines and cell adhesion molecules. Recent work has also demonstrated the role of circulating functional histamine - releasing auto antibodies that bind to the high affinity IgE receptor (FcepsilonRI) or, less commonly, to IgE. As the pathophysiological mechanisms responsible for urticaria are better defined, therapeutic agents other than H1 histamines, should be available.