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)

1 Ultraviolet radiation (UVR)-induced wealing was studied in four patients with solar urticaria, whose measured action spectra were within the range 300 to 700 nm. 2 Elevated histamine levels were found in blood draining wealed skin in all four patients. 3 Histological and electron microscopial studies of the irradiated skin showed evidence of mast cell degranulation. 4 These findings demonstrate an association between histamine release from mast cells and wealing in solar urticaria, and should encourage evaluation of drugs which suppress histamine release in this disorder.
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PMID:Elevated blood histamine levels and mast cell degranulation in solar urticaria. 735 7

Idiopathic acquired cold-induced urticaria has provided a model to study release of mast cell-derived chemical mediators into the blood and alterations of neutrophilic leukocyte motility. A factor chemotactic for neutrophilic leukocytes appeared in the circulation after local experimental challenge with ice. After partial purification by Sephadex G-200 gel filtration and by anion and cation exchange chromatography the neutrophil chemotactic activity was excluded on Sepharose 4B gel filtration, indicating a molecular weight in excess of 750,000. On isoelectric focusing it exhibited a neutral isoelectric point. This chemotactic factor showed preferential chemotactic activity for neutrophils and deactivated these cells in vitro and in vivo. HMW-NCF may prove to be a useful marker of mast cell activation and its release may modulate the capacity for motility of neutrophilic leukocytes in humans.
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PMID:High molecular weight neutrophil chemotactic factor: recognition, characterization, and role in the deactivation of neutrophillic leukocytes. 739 8

The urticarias are a complex group of disorders characterised by transient whealing or swelling of the skin. Understanding the many possible causes is the first step in assessing urticaria. Allergic and drug-induced urticaria respond to removal of the cause. The physical urticarias, particularly delayed pressure urticaria and also urticarial vasculitis, require separate consideration. For the majority of patients with chronic idiopathic urticaria, nonsedating antihistamines are the mainstay of treatment. There are several to choose from, including cetirizine, astemizole, loratadine, terfenadine and acrivastine, each with its own pharmacokinetics and antiallergic properties. When these fail, histamine H2-antagonists may help either alone or in combination with H1-antagonists. Older sedative antihistamines are still useful. Ketotifen, oxatomide and azelastine have mast cell stabilising effects that are considered an advantage in treating these disorders. Second-line therapies include a wide range of drugs such as doxepin, dapsone, attenuated androgens, calcium antagonists, antimalarials, gold and methotrexate. The most effective and regularly used second-line agents are corticosteroids. These are best limited to short term crisis management, except in severe recalcitrant cases, and in patients with pressure urticaria or urticarial vasculitis. Recent work on circulating histamine releasing autoantibodies suggests that there is scope for more aggressive immunosuppression in selected patients. However, effective treatment with immunosuppression often requires plasma exchange and more toxic agents such as cyclosporin. Such treatments are only likely to be entertained in exceptional cases.
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PMID:Urticaria. Recognition, causes and treatment. 753 Jun 29

Mast cells are considered to be the primary effector cells in urticaria but it is possible that lymphocytes contribute to the formation of weals by secreting histamine releasing factors. The aim of this study was to examine the population of mast cells and to quantify the T cell subsets and their activation status in delayed pressure urticaria (DPU), chronic idiopathic urticaria and normal controls. Three biopsies were obtained from each of four patients with chronic idiopathic urticaria but not DPU. Three biopsies were taken from each of 13 patients with DPU, from a combination of unchallenged skin and at 0, 2, 6, 24, 48, and 120 h after weighted steel rods (diameter 1.5 cm) had been applied to the thighs. Three biopsies were similarly obtained from each of four normal controls before an identical pressure challenge and at 6, 24 and 48 h afterwards. The chloracetate esterase stain was used to demonstrate mast cells and an alkaline phosphatase anti-alkaline phosphatase immunohistochemical technique to assess the phenotypic and activation characteristics of the T cell infiltrate. The mast cell count did not differ significantly between unchallenged skin from DPU patients and normal controls. Following a pressure challenge to the DPU patients, the number of stainable mast cells decreased significantly to a level comparable with that in spontaneous weals of chronic idiopathic urticaria. Investigation of T cell subsets showed a preponderance of CD4+ cells over CD8+ cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mast cells and T lymphocytes in chronic urticaria. 760 Mar 77

Anaphylaxis is a life-threatening disease that characteristically presents with multiple arrays of dermatologic, respiratory, cardiovascular, and gastrointestinal derangements, in general, suddenly after exposure to an allergen. It can, however, occur without an identifiable precipitant or event, and this well-defined entity has been called idiopathic anaphylaxis. The diagnosis of idiopathic anaphylaxis is made after an appropriate allergic evaluation and exclusion of a provocative trigger. We report an unusual case of manifesting with gastroenteritis, urticaria, hypotension, and syncope. Measurement of serum tryptase, a mast cell enzyme, was used to substantiate the diagnosis. Tryptase level is a useful test that can be used to help diagnose this potentially fatal disease.
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PMID:Serum tryptase in idiopathic anaphylaxis: a case report and review of the literature. 801 May 39

The increase in neutrophil chemotactic activity (NCA) is related to mast cell degranulation. This study was performed in 10 patients in whom aspirin-induced urticaria was connected with increased NCA. A state of tolerance to aspirin (ASA) was achieved by administering incremental doses of acetylsalicylic acid. In none of the examined patients was an increase in NCA observed after 600 mg of ASA given after desensitization. The authors conclude that in patients with ASA-induced urticaria, mast cell degranulation does not occur after ASA desensitization.
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PMID:Aspirin-induced neutrophil chemotactic activity (NCA) in patients with aspirin-sensitive urticaria after desensitization to the drug. 808 38

Exercise induced anaphylaxis (EIA) is a relatively new syndrome described in 1980. It is associated with different kinds of exercise, although jogging is the most frequently reported. 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. In the full-blown phase a differential diagnosis must be done with the following syndromes: exercise-induced asthma, idiopathic anaphylaxis, cardiac arrhythmias, carcinoid syndrome. An elevated serum histamine level during experimentally-induced attacks and cutaneous degranulation of mast cells after attacks proved a mast cell participation in the pathogenesis of the syndrome. As predisposing factors, a specific or even aspecific sensitivity to food has been reported and such cases are called "food-dependent EIA". Another precipitating factor includes drug intake; moreover a familial tendency has been reported in some studies. Although the prognosis of this syndrome is not well defined, a reduction of attacks occurs in 45% of patients by means of elimination diets and behavioural changes. Treatment of attacks should include all the manoeuvres efficacious in the management of conventional anaphylactic syndrome, including the epinephrine administration. Prevention of attacks may be achieved by limitation of the exercise program or interruption of the program at the appearance of the first premonitory symptoms. The use of H1 antihistamine-receptor antagonists in maintenance therapy seems to be useful, although no controlled data are available.
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PMID:[Anaphylaxis induced by exertion]. 809 51

Chronic urticaria can be produced by a number of stimuli that cause mast cell mediator release. Patients with urticaria caused by physical agents account for roughly one-fifth of all cases of chronic urticaria. There are about 20 different types of physical urticaria. Two forms, dermographism and cholinergic urticaria, are quite common and represent more than two-thirds of all cases of physically caused urticaria. More than one agent may precipitate urticaria in a given individual. Urticarial response can be easily reproduced in the sensitive patient and, generally, lasts less than one hour. Systemic features such as flushing, dizziness, headaches, and even hypotension, may occur during severe episodes. Identification of the causative physical agent is necessary for effective therapy.
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PMID:Physical urticarias. 817 38

Tryptase (T), chymase (C), carboxypeptidase A, cathepsin G-like constituent of preformed mediators contained in mastocyte granules, are a group of neutral proteases with proteolytic activity. These enzymes gives differentiation of two groups of mastocytes, MCTC and MCT as a function of the richness of enzymes. Although the functions of these molecules are becoming better and better understood, their exact roles as well as that of their inhibitors, still remain to be explored in urticaria.
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PMID:[Proteolytic enzymes and their inhibitors]. 821 29

We described a case of anaphylaxis diagnosed by the evaluation of plasma mast cell tryptase and a case of anaphylactoid reaction. In a patient undergoing pulmonary lobectomy, anaphylaxis, showing the elevation of plasma tryptase, was provoked by physiological glue for hemostasis during the operation. During the operation, cardiovascular collapse occurred suddenly, at which time the cause was not diagnosed. After completion of the operation and removal of drapes, diffuse urticaria with wide erythema on the torso and the upper extremity was noticed. Suspecting allergic adverse reaction, plasma tryptase was measured 2h and 5h after the start of the episode, showing 34.6 ng.ml-1 at 2h and 15.3 at 5h. Because these elevations of plasma tryptase indicated degranulation of mast cells, evaluation of the causative drugs was performed 7 weeks after the episode. Physiological glue was confirmed to be causative drug. In another patient for total hysterectomy and bilateral oophorectomy, adverse reaction occurred after completion of the operation and extubation. Increase in plasma histamine concentration to 4.94 ng.ml-1 that could induce systemic reaction was noticed; however, concentrations of plasma tryptase 25 min, 3h and 7h after the episode were not elevated. This finding indicated that the adverse reaction was not based on degranulation of mast cell, and was anaphylactoid reaction provoked by nonspecific histamine-release. In conclusion, measurement of plasma tryptase is a useful method for differential diagnosis of anaphylaxis and anaphylactoid reaction.
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PMID:[Usefulness of measurement of mast cell tryptase for differential diagnosis of anaphylaxis and anaphylactoid reaction]. 852 64


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