Urticaria - current concepts A . TAAFFE

Histamine This is concentrated in granular depots within both mast cells and circulating basophils. The Type I mast cells found close to the arterioles and venules seem more important in this regard than the larger, regularly shaped, Type II cells scattered in the perivascular supporting tissues (Beaven, 1976a). Histamine release is accompanied by degranulation of the mast cells and basophils and is induced through the influence of tissue trauma, antigenantibody, immediate hypersensitivity reactions, burns and drugs. The release, which is often in phases, may differ with the provoking agent. Compound 48/80 is a polypeptide histamine liberator used in most research studies. The intracellular levels of adenosine-5-monophosphate (cAMP) and guanosine monophosphate (GMP) control the rate of histamine release. Exchange of calcium ion with extra cellular ions is also important. While adrenaline increases the cellular reserve of cAMP and retards histamine release, carbachol and acetylcholine increase the level of GMP and its release. Otherwise the effects of drug action on the mast cells are unknown. Disodium cromoglycate has proved beneficial in allergic asthma but not in urticaria. Its action cannot be attributed to inhibition of antigen antibody reaction on the cell membrane, interference with cAMP or histamine antagonism (Beaven, 1976b). Reduced basophil counts occur in attacks of acute physical urticaria, and particularly during episodes of hereditary angio-oedema (Robinson and Pennington, 1966). In predominantly basophilic leukaemias, high urinary and circulating histamine levels are found (Beaven, 1976b). However, in chronic urticaria, histamine release by IgE adherence to basophils is probably insignificant. Histamine is metabolized through two pathways, each capable of removing the entire histamine load. One pathway can be blocked by an aspirin inhibition of ribose conjugation (Beaven, 1976a). Histamine dilates the peripheral capillaries. It increases the permeability of the venule, perhaps through longitudinal contraction of structures within the endothelial cell (Warin and Champion, 1974a). The fibrin constituents of the basement membrane may also be disturbed (Lennart and Michaelsson, 1970). There may be a constant cycle of changing vascular tone governed by histamine and utilizing histidine from depots throughout the body (Beaven, 1976a).