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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A major aetiologic role for foods has been demonstrated in urticaria, atopic eczema and dermatitis herpetiformis. In some patients with urticaria, whealing occurs within minutes of the ingestion of a particular food. In most, but not necessarily all cases, this appears to be a consequence of IgE-mediated cutaneous mast cell degranulation, i.e. a classical type I hypersensitivity response. In other patients with recurrent urticaria, the whealing may be provoked by foods by a much slower and more insidious reaction. This type of reaction has been established in the case of several common food additives, notably azo dyes, but other foods may be able to cause urticaria in a similar fashion. Foods appear to play an important provocative role in many patients with atopic eczema. The reaction in such cases appears to be slow and insidious, almost always unrecognized by the patient and not detected by skin testing or tests for IgE antibodies. There can be no real doubt that dietary gluten is responsible for most, if not all dermatitis herpetiformis, though this relationship was revealed only by the finding of concurrent and usually asymptomatic jejunal villous atrophy in affected individuals. The mechanisms responsible for the slow food reactions in urticaria, atopic eczema and dermatitis herpetiformis remain largely unknown, but are likely to be different in each case.
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PMID:Diagnosis and management of skin disorders caused by food allergy. 639 Dec 91

Five individuals with idiopathic cold urticaria but not normal volunteers released platelet factor 4 (PF4) detected by radioimmunoassay into the circulation after cold challenge. In three patients, a biphasic rise in PF4 was noted with increases at 1 and 10 to 20 min after immersion, whereas in two others only the later rise was detected. Peak levels of PF4 were detected in all five patients 20 min after cold immersion, whereas peak levels of other mediators such as histamine and eosinophil and neutrophil chemotactic activity occurred earlier at 10, 3 to 10, and 5 to 10 min, respectively. The identification of PF4 in the circulation of patients with cold urticaria after cold challenge provides further evidence for the activation of platelets in mast cell-dependent disorders and suggests new potential mechanisms for the expression of cold urticaria.
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PMID:Release of platelet factor 4 into the blood after cold challenge of patients with cold urticaria. 647 Mar 62

Three subjects diagnosed as having idiopathic acquired cold urticaria were studied to assess the ability of orally administered tiaramide to inhibit the wheal induced following cold challenge with ice cubes placed in contact with the skin, and to establish the safety of multiple doses of 250 mg, q.i.d., for one week administered after a single oral dose of 500 mg. Two subjects completed the study. One subject was known to be unresponsive to antihistamines for allergy and the second was intolerant of antihistamines due to side effects. A third subject discontinued treatment due to an adverse reaction experienced while on the study medication. The skin of the forearm of each subject was exposed to cold stimuli for 1, 2, 3, 4, and 5 minutes by placing five ice cubes on the ventral surface at one minute intervals, and removing all simultaneously five minutes after contact with the first cube. The challenge sites were observed for ten minutes and the area of the wheal, intensity of edema and the time of contact necessary to induce the skin response were recorded. The results of this provocative test following the single and multiple dosage administration of tiaramide were compared to baseline skin responses. After one week of tiaramide treatment at 250 mg, q.i.d., both subjects who completed the study had a markedly attenuated skin response to cold challenge and no adverse effects. Our results suggest that absorbable compounds that can inhibit mast cell degranulation may be efficacious in cold urticaria and of particular value in treating patients who do not respond to standard therapy.
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PMID:Preliminary report on the effects of tiaramide on the ice cube test in patients with idiopathic cold urticaria. 663 14

Tolerance to artificial ultraviolet radiation (UVR) was induced in three patients with solar urticaria by administering graded whole body exposures to long-wave ultraviolet radiation (UV-A, 320-400 nm) in a phototherapy cabinet. Plasma histamine levels, mast cell ultrastructure and cutaneous responses to intradermally injected codeine and histamine were examined before and after the induction of tolerance. No evidence of serum complement activation could be demonstrated following exposure of serum samples to UVR in vitro. These studies suggest that the state of tolerance is due neither to mediator (histamine) depletion nor to a systemic effect induced by UV-A but may be due to an increase in the mast cell degranulation threshold.
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PMID:Studies on the mechanism of clinical tolerance in solar urticaria. 669 47

Exercise-related anaphylaxis is a novel form of physical allergy that is being recognized with increasing frequency in a society with a growing commitment to health through planned exercise. The clinical manifestations progress from pruritus, erythema, and urticaria to some combination of cutaneous angioedema, gastrointestinal and laryngeal symptoms and signs of angioedema, and vascular collapse. The finding of an elevated serum histamine level during experimentally-induced attenuated attacks indicates mast cell participation, as in a physical allergy, and the signs and symptoms are characteristic of a classic anaphylactic reaction to a foreign substance in an allergic human.
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PMID:Exercise-induced anaphylaxis. 671 33

Skin biopsy specimens were obtained from 43 consecutive patients with chronic idiopathic urticaria and from seven normal controls. Of 43 patients, 42 had a non-necrotizing perivascular infiltrate composed primarily of mononuclear cells. There was no evidence of damage to vessel walls, of nuclear debris, or of extravasation of red blood cells, and most cells were seen around vessels rather than within the vessel wall. One patient had vasculitis with a neutrophilic infiltrate, nuclear debris, and positive immunofluorescence. Quantitative cell counts revealed four times the number of mononuclear cells and 10 times the number of mast cells in urticaria biopsy sites vs normal skin. Thus chronic urticaria is characterized by an accumulation of mononuclear cells and mast cells with mast cell degranulation presumably associated with hive formation. In our series, the characteristic lesion is not vasculitic. The stimulus responsible for the infiltration of skin with these cells is unknown.
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PMID:Histologic studies of chronic idiopathic urticaria. 682 93

Mast cells in skin are distributed around dermal and subcutaneous blood vessels. Activation of tissue mast cells produces secretion and/or generation and secretion of a variety of biologically active molecules. Mast-cell-dependent mediators may be classified as smooth-muscle-contracting and vasoactive activities, chemotactic factors, enzymes, and proteoglycans. These mediators alter the microenvironment to produce a biphasic response. The initial or humoral phase of the response is mediated by materials that alter vascular permeability; peripheral blood leukocytes attracted by chemotactic factors establish the cellular phase. Failure to limit the humoral phase creates a pharmacologic state that may be recognized in skin as urticaria/angioedema. The inability to control the cellular phase permits progression to a local inflammatory state with subacute and chronic tissue injury recognized in skin, for example, as necrotizing vasculitis. As an example of the former, certain forms of physical urticaria have provided experimental models in humans to allow observation of the clinical manifestations, study of tissue alterations by histologic analysis, measurement of mediators released into the circulation, and assessment of motility of peripheral blood leukocytes. An example of the role of the mast cell in the production of subacute and chronic inflammatory cutaneous disease is suggested by studies in a patient in whom exposure to the physical stimuli of cold and trauma was followed by initial mast cell degranulation, subsequent tissue deposition of circulating immune complexes, and the development of a necrotizing vasculitis.
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PMID:Mast cells in cutaneous inflammatory disorders. 685 53

Urticaria and angioedema may occur in skin and mucus membranes when mast cells are activated by various physical stimuli, including trauma, pressure, vibration, light, cold, heat, and (in rare cases) water. Experimental challenge of patients with cold-induced and cholinergic urticaria/angioedema in particular provides an in vivo model of mast cell activation in humans. This model synthesizes observations of the evolution of clinical manifestations, histologic analysis of tissue alterations, measurement of mediators released into the circulation, and assessment of leukocyte motility. The model in turn allows a characterization of mediators that exist preformed in mast cell granules or that are generated through interactions with other cell types. Release of these mediators produces a variety of biologic effects, including elaboration of certain enzymes and alterations in venular permeability, smooth muscle contraction, leukocyte motility, and the release of substances from other cell types.
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PMID:Physical urticaria/angioedema: an experimental model of mast cell activation in humans. 700 77

The eosinophilic activity appearing in the venous effluent of the cold-induced angioedematous extremity of patients with cold urticaria has been resolved into three fractions by gel filtration and Dowex-1 chromatography. The low molecular weight activity, 300-700 mw, is highly acidic while the activity of 1000-3000 mw is composed of highly acidic and less acidic moieties. Each of the three activities has a different retention time on high pressure liquid chromatography, indicating that they represent distinct fractions which differ in size, charge, and hydrophobicity. Each fraction requires a gradient to attract eosinophils in a dose-response fashion and each deactivates eosinophils at subchemotactic concentrations. The more acidic 1000-3000 mw fractions also attract human monocytes in a chemotactic gradient at concentrations identical to those which attract human eosinophils. These three classes of eosinophil chemotactic activities and the activity for monocytes appear and disappear from the venous effluent with essentially the same time course as a distinct neutrophil chemotactic factor and histamine with cold induction of angioedema in patients with cold urticaria. The elaboration of these diverse chemoattractants in experimentally induced physical allergy provides potential pathways for mast cell-mediated infiltrative reactions.
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PMID:The functional and physicochemical characterization of three eosinophilotactic activities released into the circulation by cold challenge of patients with cold urticaria. 708 32

We described the sixteenth reported case of local heat urticaria, in a 59-yr-old woman with erythema and angioedema upon contact with hot water or outdoor heat exposure. Immersing her hand in 39 degrees to 40 degrees C heated water resulted in an erythematous, angioedematous response sharply demarcated by the line of immersion and was associated with immediate increases in histamine concentration (18 to 135 ng/ml) and high molecular weight neutrophil chemotactic activity (two to five times prechallenge levels) in venous blood draining the challenge site. We suggest that the local heat urticarial response in this woman was a form of physical urticaria associated with release of mast cell-derived mediators, akin to cold and cholinergic urticaria.
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PMID:Mediator release in local heat urticaria. 728 47


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