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)

Twenty-one patients were entered into a phase I trial to evaluate toxicity, antitumor effects, and biological responses at tumor sites during treatment of R24, an immunoglobulin G3 (IgG3) mouse monoclonal antibody (mAb) against GD3 ganglioside. Toxicity was related to dose of R24. Urticaria and pruritus were the most prominent side effects, with nausea, vomiting, and diarrhea occurring at the highest dose levels. Partial responses were observed in four patients lasting from 6 to 46 weeks, and mixed responses were seen in two patients. Responses occurred as early as 4 weeks and as late as 10 weeks after beginning treatment. Twenty of the 21 patients developed human IgG antibodies against R24. Antimouse Ig antibodies were first detected at a median of 14 days after starting treatment, but three of the four patients who had a partial response developed the antimouse Ig responses later than 20 days. Peak serum levels of R24 were related to dose and ranged from a mean of 0.9 micrograms/mL at the lowest dose level (1 mg/m2/d) to 44 micrograms/mL at the highest dose (50 mg/m2/d). The amount of R24 reaching tumor sites corresponded to the dose administered, and R24 could be detected in tumors as late as 30 days after finishing treatment. Inflammation at tumor sites was observed during treatment. Biopsies of tumors taken before, during, and after treatment revealed that R24 induced deposition of complement components, increased numbers of mast cells with mast cell degranulation, and infiltration of T lymphocytes. These results suggest that treatment with R24 can produce a localized inflammatory response at tumor sites that is capable of producing tumor regression.
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PMID:Phase I trial of a mouse monoclonal antibody against GD3 ganglioside in patients with melanoma: induction of inflammatory responses at tumor sites. 317 29

The manifestations, evaluation, treatment, and course of 123 patients with idiopathic anaphylaxis (IA) are described for a total of 374 patient years of our management. Observation of this group of patients resulted in the description and classification of IA as one or more episodes of generalized IA with multiple systemic manifestations or IA with life-threatening angioedema of the tongue or larynx. Therapy is based on the frequency of episodes. Acute therapy is appropriate for infrequent episodes, but prophylactic therapy is indicated for frequent episodes. In patients with frequent episodes, remissions can be induced and maintained with prednisone. Prolonged remissions may occur after prednisone is stopped. There have been no deaths from IA in patients managed by our service. By definition, there is no identifiable antigen responsible for episodes of IA, and there is no underlying disease in these patients. A mast cell basophil-activation mechanism is suggested. IA may represent the most severe form of a spectrum of diseases that include idiopathic urticaria and angioedema.
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PMID:Idiopathic anaphylaxis: classification, evaluation, and treatment of 123 patients. 232 60

In order to establish the role of mast cells in aspirin-induced urticaria and angioedema, neutrophil chemotactic activity (NCA) in serum was assayed using the method of Nelson before and after aspirin challenge. In 14 (82.4%) persons sensitive to aspirin an increase in NCA during aspirin-induced urticaria and angioedema was observed and in 9 of them (52.9%) it was considerable (index NCA greater than or equal to 2.0). None of the 18 persons from the control group with idiopathic urticaria and/or angioedema but without aspirin-sensitivity exhibit an increase in NCA after aspirin challenge. The author assumes that mast cell degranulation does occur in aspirin-induced urticaria and angioedema.
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PMID:Serum neutrophil chemotactic activity (NCA) during aspirin-induced urticaria and angioedema. 322 43

Anaphylaxis, the most emergent manifestation of allergy, is best described by its clinicopathologic alterations. Sites of involvement include skin (urticaria), upper respiratory tract (laryngeal edema), lower respiratory tract (bronchospasm), and the cardiovascular system (severe hypotension). Ultrastructural analysis of skin biopsy specimens obtained from individuals experiencing exercise-induced anaphylaxis before and immediately after exercise revealed changes indistinguishable from those observed after immunologic challenge of pulmonary mast cells, and included enlargement of the mast cell granules, solubilization (discharge) of mast cell granule contents, and merger of the granule membranes with adjacent granule membranes and the mast cell membranes. Successful reversal of anaphylaxis requires prompt recognition of symptoms and early institution of therapy. Patients prone to exercise-induced anaphylaxis should avoid any foods, drinks, or pharmaceutical agents, particularly acetylsalicylic acid, for 4, and preferably 6, hours before exercise.
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PMID:Anaphylaxis. 337 13

Food-associated, exercise-induced urticaria-angioedema is increasingly being recognized. We studied five atopic individuals in whom ingestion of food was followed by exercise-induced urticaria-angioedema. The combined effect of food and exercise on skin wheal response to compound 48/80 and histamine was studied. Symptoms could be reproduced in only four of the patients who performed strenuous exercise after ingestion of food to which they were skin sensitive. When symptoms appeared, that is, after a combination of food and exercise challenge, there was a marked increase in the wheal response to compound 48/80 (greater than 200%) and not to histamine. Food or exercise challenge alone did not induce any significant change in the skin reactivity to compound 48/80 or to histamine. It was concluded that mast cell releasability could be increased when the patient was subjected to combined factors.
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PMID:The effect of food and exercise on the skin response to compound 48/80 in patients with food-associated exercise-induced urticaria-angioedema. 337 28

Urticaria, after ingesting ethanol, is rare. A 36-year-old Caucasian male developed multiple, generalized, pruritic urticarial lesions 5 to 15 minutes after drinking alcoholic beverages of any type. A blinded challenge with 5 mL of chemically pure 95% ethanol in concentrated grape juice caused urticaria and an elevation of plasma histamine. Pure grape juice alone was unreactive. Prick skin tests with Brewers' yeast, ethanol, acetaldehyde, and acetic acid were negative. Hydroxyzine (25 mg, p.o., q.i.d.), given for three days prior to challenge, inhibited skin response and histamine release. Biopsy of the urticarial lesions caused by ethanol ingestion showed mast cell degranulation. In this subject, ethanol appeared to directly affect mast cell mediator release by non-IgE mechanisms.
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PMID:Ethanol-induced urticaria: a case report. 338 58

The mechanism(s) by which repeated cold challenge in a patient with idiopathic acquired cold urticaria resulted in the induction of clinical tolerance to cold stimuli was studied. Plasma histamine levels, mast cell ultrastructure, and the cutaneous response to intradermal injections of morphine, histamine, and substance P were examined before and after the induction of tolerance. Plasma histamine levels draining cold-challenged, clinically tolerant skin were markedly diminished compared to histamine levels obtained during cold-induced angioedema. Furthermore, electronmicroscopy of skin samples taken from tolerant skin after cold challenge revealed intact, largely normal appearing mast cells. Intradermal injection of mast cell secretagogues and vasoactive agonists into normal and tolerant skin sites resulted in similar whealing responses. Thus, these studies suggest that the state of clinical tolerance to cold stimuli is due neither to mast cell-mediator depletion or tachyphylaxis of the cutaneous vasculature to vasoactive agonists. It appears likely that tolerance may be due to the induction of a specific state of unresponsiveness of mast cells to cold stimuli or possibly to depletion of a cold-induced cutaneous antigen capable of triggering mast cell degranulation.
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PMID:A case study on the induction of clinical tolerance in cold urticaria. 340 65

Anaphylaxis, the most emergent manifestation of allergy, is best described by its clinical pathologic alterations. Sites of involvement include skin (urticaria), upper respiratory tract (laryngeal edema), lower respiratory tract (bronchospasm), and the cardiovascular system (severe hypotension). Ultrastructural analysis of skin biopsies obtained from individuals experiencing exercise-induced anaphylaxis prior to and immediately after exercise revealed changes indistinguishable from those observed following immunologic challenge of pulmonary mast cells. These alterations included enlargement of the mast cell granules, solubilization (discharge) of mast cell granule contents, merger of the granule membranes with adjacent granule membranes, as well as the mast cell membrane. The successful reversal of anaphylaxis requires the prompt recognition of symptoms and early institution of therapy for anaphylaxis. Patients suffering from exercise-induced anaphylaxis should avoid any foods, drinks, or pharmaceutical agents, particularly acetyl salicylic acid for four and preferably six hours prior to exercise.
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PMID:Exercise-induced anaphylaxis. 341 89

Recent evidence suggests that mast cell derived mediators other than histamine are likely to be involved in the pathogenesis of physical urticarias. Much of the work has been performed in idiopathic cold contact urticaria where the presence of neutrophil and eosinophil chemotactic factors, and platelet activating factor-like lipid substances have been previously demonstrated. Now, an increase in prostaglandin D2 measured by GC-MS has been demonstrated in venous blood draining the cold challenged area. This appeared a few minutes later than histamine, but then both substances paralleled the onset, development and subsidence of the urticarial reaction. There appeared to be no quantitative relationship between histamine and PGD2 release. A similar rise in histamine and PGD2 occurred on heat challenge of a subject with the rare localized form of heat urticaria. This rise of both substances was considerably reduced after combined treatment with induction of tolerance and oral indomethacin. The concentrations of PGD2 measured suggested that it plays an indirect role.
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PMID:[New pharmacologic developments in physical urticaria--therapeutic consequences]. 347 18

Progressively increasing doses of aspirin (acetylsalicylic acid--ASA) were tolerated by 14 out of 15 patients with confirmed aspirin-sensitive urticaria and in 7 out of 9 patients with aspirin-sensitive asthma. Blood levels of histamine and prostaglandin (PG) F2 alpha were significantly raised in these patients before ASA administration. PGF2 alpha levels fell to within the normal range after challenge doses of ASA which were sufficient to cause symptoms. Skin prick testing with histamine and codeine phosphate did not show evidence of abnormal tissue reactivity or mast cell reactivity. A wider spectrum of mediators will need to be considered if the mechanism of symptom production is to be understood.
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PMID:Clinical and biochemical aspects of "aspirin-sensitivity". 347 39


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