Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three patients with chronic urticaria, two of whom also had angioedema, were treated with oral cyclosporine, 6 mg/kg per day. In each patient, complete resolution of symptoms occurred within the first week of therapy; however, all patients eventually had to stop therapy as a result of side effects. On stopping therapy, all side effects resolved and the urticaria and angioedema recurred. Although cyclosporine therapy is not an appropriate treatment of urticaria, the results of this preliminary study suggest that cyclosporine and related drugs should be investigated in the treatment of mast cell-mediated diseases.
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PMID:Oral cyclosporine for severe chronic idiopathic urticaria and angioedema. 143 Mar 81

Urticaria and angioedema are clinical manifestations of various immunologic and inflammatory mechanisms, or they may be idiopathic. The respiratory and gastrointestinal tracts as well as the cardiovascular system may be involved in any combination. Patients with urticaria and/or angioedema can be classified based on pathophysiologic mechanisms into those with IgE-dependent or complement-mediated immunologic disorders, those with nonimmunologic disorders in which there is a direct effect on the mast cell or on arachidonic acid metabolism, and those whose condition is idiopathic. Evaluation of patients should focus on a thorough history. Laboratory tests provide minimal additional information. About one half of patients with urticaria alone and 25% with urticaria and angioedema or angioedema alone are free of lesions within 1 year. With urticaria, angioedema, or both, 20% of patients experience episodes for more than 20 years.
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PMID:Acute and chronic urticaria and angioedema. 186 89

Various cells are associated with inflammatory events characteristic of atopic allergy and asthma. As well as T cells and eosinophils, mast cells, basophils, mononuclear phagocytes and platelets have all to be considered particularly as their mediators have potential for contributing directly to the features of bronchial asthma. Nevertheless, mast cell/T lymphocyte/eosinophil interactions may be of particular significance. For instance, the acute symptoms of allergy and asthma such as sneezing, bronchospasm and hives are believed to be largely the result of mediator release from mast cells whereas chronic symptoms (the result of allergic inflammation) can be explained on the basis of eosinophil-mediated tissue damage. Allergen is recognized directly by T cells. Specialized T cell subsets, possibly the Th2 equivalent, predominate in allergy and elaborate IL-4 (an essential co-factor for IgE production) and IL-5 which brings about terminal differentiation and activation of the eosinophil. Basic proteins derived from the crystalloid granule together with PAF and leukotrienes produce chronic wheeze, bronchial irritability, and might also be involved in permanent nasal blockage in chronic rhinitis. This general hypothesis is continually being tested. It is clearly important to identify precise molecular targets in allergy and asthma in order to construct therapeutic strategies.
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PMID:T lymphocytes and their products in atopic allergy and asthma. 193 73

Pruritus is a common symptom associated with chronic renal failure (CRF). But increased plasma histamine levels and skin mast cell proliferation previously reported in these patients did not correlate with the intensity of the pruritus. Since increased mast cell releasability was described in chronic idiopathic urticaria, we attempted to examine whether this mechanism could explain pruritus in patients with CRF. Twenty-five patients with end stage renal failure were skin tested with histamine, codeine, and compound 48/80. There were nine patients on continuous ambulatory peritoneal dialysis, eight patients on hemodialysis, (tested both before and after dialysis) and eight patients with advanced CRF. Wheal area after intradermal injection of three concentrations of the above substances was measured. In general, the wheal areas in all patients with CRF were either similar to or smaller than those of the control group who were without renal impairment. In conclusion, patients with CRF with or without dialysis therapy demonstrated unchanged or decreased skin test responses to histamine, codeine, and compound 48/80. Increased mast cell releasability cannot explain the pruritus in patients with CRF.
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PMID:Cutaneous responses to histamine, compound 48/80, and codeine in patients with chronic renal failure. 195 8

New therapeutic approaches in urticaria are presented with special respect to chronic and physical types including symptomatic dermographism, cholinergic urticaria, pressure and solar urticaria as well as vibratory angioedema. Clinical efficacies of several antihistamines (clemastine, astemizole, terfenadine, acrivastine, hydroxyzine, cimetidine), of ketotifen as a H1 receptor antagonist and mast cell stabilizer, of tricyclic antidepressant doxepin with H1 and H2 antagonist properties, of the calcium channel antagonist nifedipine, of topical corticosteroids and of the attenuated androgen danazol are presented. The data are specified by a detailed description of the design and particular conditions of the underlying study protocols.
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PMID:[The development of recent strategies in the treatment of urticaria as a result of clinically oriented research]. 197 Feb 7

A frequent cause of contact urticaria is skin exposure to the common stinging nettle (Urtica dioica). The urticaria is accompanied by a stinging sensation lasting longer than 12 h. Little is known of the cellular and molecular mechanism of stinging-nettle urticaria. After preliminary pharmacological analysis of pro-inflammatory activity in nettle stings, the cellular response of mononuclear cells, polymorphonuclear cells and mast cells was examined in six people 5 min and 12 h after nettle contact. Only mast cell numbers were significantly increased at 12 h. Ultrastructurally, some mast cells showed evidence of degranulation at 5 min and 12 h. At 12 h mast cells were closely associated with dermal dendritic cells and lymphocytes suggesting a functional unit. The mean histamine and serotonin contents of a nettle hair were found to be 6.1 ng and 33.25 pg, respectively. Nettle-sting extracts did not demonstrate histamine release from dispersed rat mast cells in vitro. These results suggest that part of the immediate reaction to nettle stings is due to histamine introduced by the nettle. However, the persistence of the stinging sensation might suggest the presence of substances in nettle fluid directly toxic to nerves or capable of secondary release of other mediators.
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PMID:Contact urticaria due to the common stinging nettle (Urtica dioica)--histological, ultrastructural and pharmacological studies. 202 24

It appears that when hives are fleeting, as is seen in physically induced hives, they are caused by a rapid burst of local mast cell degranulation. There is no tissue infiltration with cells, no late-phase component to the reaction, and therapy is dependent on antihistaminics or mast cell stabilizing agents. The nonsustained mediator release may be a result of the absence of a defined antigen, a very brief encounter with the initiating physical stimulus, and rapid removal of vasoactive substances and chemotactic factors so that the hive disappears quickly and a chemotactic factor gradient is not sustained so as to attract cells. Chronic urticaria differs in that the hive forms slowly, disappears over many hours, and is due to a perivascular accumulation of mononuclear cells and mast cells. These mononuclear cells appear to be critical for development of the lesion. Indirect evidence in support of this is the efficacy of corticosteroids in abrogating this type of hive and new concepts regarding mast cell proliferation and stimulation that are mononuclear cell-dependent.
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PMID:Urticaria: the relationship of duration of lesion to pathogenesis. 2838 90

Mast cells are the repository for histamine in the body. They influence the pathophysiology of allergic diseases, such as rhinitis, urticaria, and asthma; regulate bone formation and integrity; help repair and maintain connective tissue; promote wound healing; and probably contribute to the development and preservation of the endothelium and small blood vessels. Although they are found in all human tissue, mast cells are most prevalent at the interface between the host and its environment, that is, in the skin and in the mucosa of the upper and lower respiratory tracts and the gastrointestinal tract. Recent evidence suggests that two types of mast cells exist: (1) the connective tissue type, found primarily but not exclusively in loose connective tissue and skin, and (2) the mucosal type, found primarily in gastrointestinal mucosa and peripheral airways. The factors that produce this differentiation are not fully known. Although both mast cell types have IgE receptors that can be activated by allergens, differences between the two types exist in their responses to nonallergic signals, the mediators they release, their proteoglycan constituents, and the makeup of their granular enzymes. The importance of these biochemical differences to cellular functioning remains to be investigated.
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PMID:Mast cell biology. 222 21

A randomized study in a group of 87 patients with drug-allergic-type reactions (DAtR) manifested by urticaria and or angioedema, revealed in 55 patients (63.2%) the presence of chronic urinary infections (CUI), significantly different (p less than 0.001) from the control group (80 patients without DAtR) in which the incidence of CUI was only 20% (16 patients). Among the drugs observed to induce allergic-type reactions were substances such as penicillins and aspirin which are not used in CUI. It was therefore assumed that it is not their frequent use in CUI (as is the case with antibacterial drugs and contrast iodide substances) that leads to DAtR but rather more the CUI proper. The assumption that CUI are risk factors for the occurrence of DAtR is discussed and the following mechanisms are suggested in support of this assumption: enhancement of IgE secretion (by the drugs as allergens--complete or haptens--or by the inhibiting effects of some antibiotics on the T suppressor cells): nonimmunological mast cell degranulation (by the bacterial wall products--lectins and proteoglycans--or by the endotoxines with complement activation generating anaphylatoxines C3a and C5a): neurovegetative changes induced by infectious diseases.
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PMID:Contributions to the study of the favouring role of chronic urinary infections in inducing and starting drug-allergic-type reactions. 228 68

Biopsy specimens from lesional and uninvolved skin of nine patients with delayed pressure urticaria, three patients with acute urticaria, six patients with chronic recurrent urticaria, and four patients with urticaria pigmentosa were analyzed by routine histology and by immunochemistry for their reactivity with monoclonal antibodies to three different subsets of macrophages. Skin from 12 healthy volunteers served as control. Uninvolved skin of patients did not differ from that of healthy volunteers. An antibody against activated macrophages (27E10) was reactive to a marked extent with macrophages in wheals of pressure urticaria, more variably in acute and chronic urticaria, and practically not at all in urticaria pigmentosa. Antibodies with specificities for macrophages in healing (RM3/1) and normal (25F9) tissue reacted more markedly in all but pressure urticaria lesions, compared with normal skin. These findings indicate an active involvement of inflammatory macrophages in whealing reactions while these cells play apparently no role in cutaneous mast cell proliferation (urticaria pigmentosa).
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PMID:Macrophage subsets in different types of urticaria. 235 29


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