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

Urticaria can result from many different stimuli, and numerous factors, both immunologic and nonimmunologic, are involved in its pathogenesis. Most commonly considered of immunologic mechanisms is the type I hypersensitivity state mediated by IgE. Another immunologic mechanism involves the activation of the complement cascade, which produces anaphylatoxins that can release histamine. Immunologic, nonimmunologic, genetic, and modulating factors converge on mast cells and basophils to release mediators capable of producing urticarial lesions. In addition to the clinical and laboratory diagnosis and treatment regimens, we review such mediators as histamine, kinins, serotonin, slow-reacting substance of anaphylaxis, prostaglandins, acetylcholine, fibrin degradation products, and anaphylatoxins that increase vascular permeability and can thereby produce wheals. Special consideration is given to histamine and the factors that regulate is secretory release from mast cells and basophils, including the modulating role of intracellular levels of cyclic adenosine monophosphate.
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PMID:Urticaria. An updated review. 6 29

An immediate-type systemic reaction in a dog following intravenous radiographic contrast media (RCM) manifested by urticaria and wheezing on one occasion and urticaria alone on another occasion is described. This reactivity disappeared spontaneously and plans to study the mechanisms of such a reaction were not possible. If such reactivity is more persistent in certain other dogs, a model for study of immediate type reactivity to RCM would be available.
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PMID:Acute urticaria and bronchospasm following radiographic contrast media in a dog. 6 44

Concanavalin A (Con A)-induced histamine release from cells of subjects with extrinsic asthma, intrinsic asthma or urticaria and normal individuals was examined utilizing a single isotopic enzymatic assay for histamine. Maximum histamine release by Con A occurred with 0.9 to 4.5 microgram/ml. The mean percentage of maximum histamine release by Con A from cells of donors with extrinsic asthma was 36(+/- 19.3)% while that from cells of normal individuals was 21.4(+/- 23.7)%. However, there was no significant difference between the two groups. The higher reactivity to Con A of cells from individuals with intrinsic asthma or urticaria was not observed compared to that of the normal group. The histamine release by Con A was not correlated with IgE level in the plasma (r = 0.35). It was observed that compound 48/80 inhibited the enzymatic reaction in the isotopic, enzymatic assay.
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PMID:A clinical study of concanavalin A-induced histamine release utilizing a single isotopic enzymatic assay of histamine. 7 62

The following in vitro methods are predominantly discussed: Specific IgE determination (RAST). The test can be used to detect allergies of the immediate type such as anaphylactic shock and urticaria. Antibodies can be detected to a limited number of drugs such as penicillin, ACTH, TSH, insulin, asparaginase and proteins of animal sources. Degranulation of basophil leucocytes and histaminliberation have been used for many years. The practical value of the test has been limited but improved methods for analysis have given the tests hopes for a come-back. Cellular tests like lymphocyteproliferation and macrophage inhibition test (MIF) do not yet give such information which make them helpful as practical tests to detect drug allergy.
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PMID:[Methods for the detection of drug allergies]. 7 90

Thirteen patients with cold urticaria were studied to assess the effect of the systemic drug doxantrazole, which has actions resembling disodium cromoglycate, on cold evoked histamine release. The patients, all of whom developed an immediate local whealing response after cooling of the forearm, demonstrated release of histamine into venous blood draining that forearm. Following doxantrazole treatment, significant suppression of histamine release occurred. In some but not all patients this was accompanied by diminution of urtication in response to cooling. A double-blind study was carried out in 3 subjects, all of whom showed diminished cold-stimulated histamine release after doxantrazole. Two of these showed clinical improvement. Doxantrazole had no effect on erythema due to intradermal histamine, but did suppress the erythematous reaction to intradermal injection of compound 48/80. Our results suggest that doxantrazole or related anti-allergic agents might be useful in the treatment of cold urticaria.
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PMID:Cold urticaria: inhibition of cold-induced histamine release by doxantrazole. 8 Dec 44

Among 41 catteries, the majority of which were investigated because of problems of chronic pruritus, 27 proved to be infected by Cheyletiella mites. The skin lesions consisted of small erythematous papules with crusts and some loose hairs. After removal of the loose hairs Cheyletiella mites could be collected with adhesive tape for microscopic examination. Human involvement (papular urticaria) was observed in 20% of the cases. Bathing with Lindane was an effective mode of treatment.
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PMID:Cheyletiellosis in long-haired cats. 8 38

Results of an investigation of 134 subjects with atopic dermatitis and 29 controls are described. The investigation involved: 1) an allergological enquiry into each patient's medical history, with particular reference to consumption of eggs, milk and fish; 2) a total IgE assay; 3) RAST with egg, milk, cod; 4) a challenge test. Recording of medical histories revealed the existence of clinical sensitivity to egg, milk and cod in respectively 21, 17 and 7 of the 134 subjects with atopic dermatitis, but in none of the controls. In the atopic subjects, RAST demonstrated egg, milk and cod antibodies in 37, 28 and 14 cases respectively, while of the controls only 2 had antibodies--and then in minimal amounts. The maximum incidence of egg and milk antibodies was demonstrated in the initial 3 years of life. Clinical sensitization to cod manifests itself in the form of attacks (urticaria, angi-oedema, vomiting) showing significant correlation between clinical history, results of RAST and the response to challenge, while in the case of sensitivity to eggs and, even less evidently, to milk, the symptoms are more often referred to as "exacerbation of the dermatosis" and the results of RAST, of challenging and the clinical history tend to be contradictory.
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PMID:Food allergy in atopic dermatitis: experimental observations. 8 31

Five patients with delayed cold urticaria are described. The urticarial skin response was present between 24 and 72 hours after ice challenge. In two of the patients the cold sensitivity was of clinical relevance. Some of the patients displayed low alpha1-antitrypsin and increased C4 levels in their serum. Our findings may justify the introduction of cold provocation as a routine procedure in the investigation of a patient with chronic urticaria.
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PMID:Delayed cold urticaria. 8 39

A-20-year-old male Army paratrooper presented with a history of inducible urticaria associated with exercise as well as cold exposure. Upon evaluation, he not only had a positive ice cube test, but also had a positive mecholyl skin test with numberous satellite lesions and generalized punctate urticaria following exercise challenge. Thus, he appeared to have combined cold and cholinergic urticaria. When mediator release was examined during cold and exercise challenge, histamine release was observed in each instance; a rapid rise and fall of plasma histamine was seen after cold challenge, while a lag phase followed by sustained elevation of plasma histamine was associated with exercise challenge. This represents the fourth reported case of combined cold and cholinergic urticaria and is the first in whom mediator release was assessed. The time-course of histamine release was characteristic of each disorder.
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PMID:Evaluation of a patient with cold and cholinergic urticaria. 8 66

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


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