Chronic urticaria includes several different subsets with distinct pathophysiologies, and with important implications for investigation and treatment. Chronic 'idiopathic' urticaria represents a special challenge, which, until recently, was not taken up by dermatological or immunological investigators. However, it has now emerged that at least 30% of patients possess histamine-releasing autoantibodies against Fc epsilon R1, or less commonly IgE itself. These autoantibodies are causative. Recent work implicates complement activation in most cases. Functional (i.e. histamine releasing) autoantibodies are specific to chronic urticaria. However, immunoreactive (non-histamine-releasing) anti-Fc epsilon R1 autoantibodies can be found in sera of patients with physical urticarias and with autoimmune connective tissue and bullous diseases. The reason for the occurrence of this disease type in some individuals but not others is unclear. One possibility is the development, in genetically predisposed persons, of autoantibodies by molecular mimicry - perhaps against lipopolysaccharide of Helicobacter pylori, an organism frequently infecting the upper gastrointestinal tract of chronic urticaria patients.
A careful drug history should be obtained from all patients with acute or chronic urticaria/angioedema, especially in the elderly. Although strictly comparable data are lacking, drug-induced urticaria appears to be more common in developed countries than in Malaysia, at least in a Hospital setting. Culprit drugs include antibiotics, analgesics and contrast media. Pseudoallergic drug-induced urticaria mimicks true allergic urticaria, but without an evident immunological basis, and is at least as common as the allergic type. In Malaysia, and in many other countries compulsory, ingredient labelling of 'traditional' medicines would do much to reduce the frequency of drug-induced urticaria.