The pathogenesis of urticaria.
The underlying pathophysiology of chronic urticaria is mast cell activation, with release of histamine and other mast cell mediators. A weal producing factor has been identified in the serum of 60% of patients with chronic idiopathic urticaria. In half of these patients there is evidence for functional autoantibodies against the high affinity IgE receptor or IgE, or both. These autoantibodies release histamine from basophils and mast cells. It is therefore likely that there is an autoimmune basis for up to 30% of patients with idiopathic urticaria. In the other half of patients whose serum causes weals, the factor releases histamine from mast cells only and is as yet unidentified. So far no clinical difference has been associated with presence/absence or type of weal producing factor. Exacerbating factors in chronic urticaria such as aspirin, food additives, febrile illness and psychological stress should be identified and avoided. Treatment is symptomatic with the low sedation antihistamines. In the most severe cases not responding to conventional therapy and which may have the weal producing factor, treatments with non specific immune therapy such as cyclosporin, and intravenous gammaglobulin and also plasmapheresis have been promising.
Black
A K
AK
St John's Institute of Dermatology, St Thomas Hospital, London, UK.
D001323:Autoantibodies / Q000097:blood; D006633:Histamine Antagonists / Q000627:therapeutic use; D006636:Histamine Release; D006801:Humans; D008407:Mast Cells / Q000276:immunology / Q000378:metabolism; D017455:Receptors, IgE; D014581:Urticaria / Q000175:diagnosis / Q000209:etiology* / Q000628:therapy
D001323:Autoantibodies; D006633:Histamine Antagonists; D017455:Receptors, IgE