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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histamine release from peripheral blood leukocytes challenged with anti-human IgE was studied in patients with chronic urticaria and nonatopic controls. 19 of 23 controls, but only 6 of 20 patients, released over 20% of the total available leukocyte histamine. The response to anti-IgE concentrations of 1.66, 0.33, 0.066, and 0.013 mug antibody N/ml was significantly lower in patients than in controls. Serum IgE levels were significantly higher in the patients but total histamine content of about 10(7) leukocytes was not. Deuterium oxide (D2O) greatly increased histamine release (in both groups), indicating that the anti-IgE interacted with the basophils of urticaria patients. Passive sensitization of leukocytes with biologically active IgE was achieved in both patients and control subjects whose cells responded to anti-IgE, but was not achieved in either patients or control subjects whose cells were nonresponsive to anti-IgE challenge. 125I-anti-IgE autoradiographic studies revealed no obvious quantitative abnormality in the amount of basophil-bound IgE in chronic urticaria patients. Ionophore stimulation of aliquots of the same leukocytes used for anti-IgE challenge demonstrated that the urticaria patients' basophils were capable of releasing normal amounts of histamine. Leukocyte cyclic AMP levels in the two groups were not significantly different either in base-line levels or in responsiveness to stimulation with isoproterenol. These data indicate that chronic urticaria patients have a (acquired?) defect in leukocyte histamine release that occurs after the anti-IgE-IgE interaction, but before the actual (second-stage) release process, and that is comparable to the phenomenon of desensitization.
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PMID:Defective histamine release in chronic urticaria. 5 21

IgE is a homocytotropic antibody which binds to the surface of the mast cell. Antigen with affinity for IgE triggers conformational change at the cell surface, resulting in the release of chemical mediators from the mast cell granules. The mediators histamine, slow reacting substance of anaphylaxis and eosinophil chemotactic factor cause smooth muscle contraction, increased capillary permeability, eosinophil attraction and increased glandular secretions. The release of mediators from the mast cell granules is controlled by intracellular levels of cyclic nucleotides. In particular, elevated cyclic AMP inhibits mediator release. Adrenergic, cholinergic and prostaglandin receptors all influence mediator release. The characteristic immunopathology of immediate hypersensitivity reactions is a result of local or systemic mediator release. Such reactions include anaphylaxis, asthma, allergic rhinitis, urticaria and angioedema. Similar immunopathology may sometimes result from mechanisms not involving IgE or histamine mediators. Routine investigation of patients with immediate hypersensitivity should include eosinophil counts and IgE levels in blood and secretions, and immediate hypersensitivity skin tests. RAST testing is not routine. Therapeutic principles of these reactions include restoration of inhibitory levels of cyclic nucleotides, antagonism of mediator effects and immunological manipulation of the IgE mediated allergic reaction.
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PMID:The immunological basis of immediate hypersensitivity. 8 47

Use of differential effects of agonists and antagonists has provided an experimental basis for subdivision of histamine receptors into H1 and H2. This has enabled classification of the responses to histamine in a wide range of organs and tissues. In human skin the vascular and sensory effects of histamine have been studied, and the influence of histamine on epidermal cell growth has been evaluated in vitro. The direct vasodilator and vascular permeability actions of histamine appear to involve both H1 and H2 receptors. However, the axon reflex flare due to histamine appears to be predominantly an H1 effect. Histamine itch involves H1 receptors. These findings have prompted clinical evaluation of combined therapy with H1 and H2 antagonists in patients with urticaria. Initial results have been encouraging in patients with factitious urticaria. Histamine exerts an inhibitory action on epidermopoiesis in vitro in a number of mammalian epidermal cell outgrowth systems including human explants. The pathophysiological relevance of this effect, which involves epidermal H2 receptors and which may be cyclic AMP dependent, is unknown.
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PMID:Histamine receptors in human skin: indirect evidence. 713 77

We report a patient with chronic urticaria which was closely associated with elevated levels of thyroxine. The urticaria responded poorly to antihistamines and only partially to systemic steroids, but resolved consistently when the thyroxine level was reduced to normal. The mechanism for the association may involve modulation of the cyclic AMP levels within mast cells.
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PMID:Urticaria associated with thyrotoxicosis. 856 60