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

This study examined cutaneous mast cell behaviour in 14 patients with chronic urticaria but no dermographism and 11 healthy controls, by measuring cutaneous weal and flare reactions evoked in response to intradermal challenge injections of 0.1 ml isotonic saline, histamine (20 micrograms), codeine phosphate (10 micrograms) and compound 48/80 (10 micrograms). Five minutes after each injection, the area of the resulting weal and flare was calculated by computer-aided planimetry. The process was repeated at 15, 30 and 45 min following the injection. In patients, saline flares were significantly larger than those of the volunteers at 15, 30 and 45 min (p < 0.05). However, histamine and codeine flare areas were significantly smaller in the patients when compared to the controls at 15, 30 and 45 min (p < 0.05). Compound 48/80 produced smaller reactions in the patients without reaching statistical significance.
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PMID:Aberrant cutaneous weal and flare responses in chronic urticaria. 136 42

Treatment of chronic urticaria presents a challenge to both practitioner and patient. Traditional H1 antagonists with good efficacy but substantial side effects are being supplanted in many cases by nonsedating H1 antagonists such as terfenadine and astemizole. Antidepressant medications and combinations of H1 and H2 antagonists offer improved results for selected patients. Further development and investigation of mast cell stabilizers and inhibitors of urticaria mediators other than histamine hold promise. A better understanding of the underlying pathogenesis remains the greatest hope of formulating rational and effective therapy.
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PMID:Pharmacologic therapy for urticaria. 167 97

Circulating histamine-releasing factors have been identified in the serum and plasma of chronic-urticaria patients by in vivo skin testing and in vitro histamine release from heterologous mixed leukocytes. Quantitative mast cell studies of serum skin test biopsies and electron microscopy indicate that the serum factors release histamine by mast cell degranulation. Peripheral blood basophils and total cellular blood histamine are reduced in chronic-urticaria patients suggesting that the circulating serum factors cause sustained degranulation. Histamine-releasing activity has been identified by skin testing in ultrafiltered serum fractions less than 30 kDa and greater than 100 kDa. In vitro histamine-releasing activity was confined to ultrafiltered serum fractions greater than 100 kDa and was present in IgG purified from some chronic-urticaria sera by protein G affinity chromatography. The dose-response relationship and kinetics of histamine release in vitro were similar to those of anti-human IgE. 'Desensitisation' of basophils by prior incubation with anti-IgE in the absence of calcium and competitive inhibition studies with myeloma IgE serum indicated that histamine-releasing autoantibodies in chronic-urticaria sera and purified IgG have the properties of anti-IgE. Plasma exchange in 4 patients with active chronic urticaria refractory to antihistamine therapy showing in vivo and in vitro histamine-releasing activity was followed by temporary remission of disease activity in 2 of them. It is possible that chronic urticaria is an autoimmune disease.
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PMID:Histamine-releasing autoantibodies in chronic urticaria. 172 16

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

Although known for more than 80 years, histamine still remains a fascinating substance for allergy research. Histamine antagonists have been in clinical use since 1942. The classical H1-antagonists with sedative side-effects have been more or less replaced by newer non-sedating H1-antagonists; the role of H2-receptors in allergic diseases is still controversial. There, are however, increasing reports of beneficial effects of H2-antagonists, mostly in combination with H1-antagonists, in a variety of allergic and pseudoallergic conditions such as chronic urticaria, anaphylactoid reactions due to colloid volume substitutes, opioid analgesics and radiographic contrast media. The combined use of H1- and H2-antagonists might not only act as specific histamine antagonism but exert a mast cell stabilizing effect, as demonstrated in animal experiments and some clinical studies. Future research will show whether the combined use of H1- and H2-antagonists will become a routine therapeutic procedure in allergy therapy.
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PMID:H1- and H2-antagonists in allergic and pseudoallergic diseases. 197 7

The wheal-and-flare response to intradermal autologous serum in chronic urticaria offers a model for study of the pathogenesis of the disorder. Serial biopsies of autologous serum induced wheals were performed in 5 chronic urticaria patients to assess the evolution of the cellular inflammatory response and to look for evidence of mast cell degranulation. Perivascular neutrophils and eosinophils were seen as early as 30 min, becoming more intense and diffuse over 2 h. T lymphocyte numbers were increased by 2 h, CD4+ cells outnumbering CD8+ cells at 24 h. By 48 h, the neutrophils were clearing, but eosinophils and lymphocytes persisted. The histology of compound 48/80-induced wheals was similar to serum-induced wheals, but there was little or no response to physiological saline (0.16 M). Stainable mast cells were reduced in compound 48/80- and serum-induced wheals when compared to saline skin tests. Mast cell granules appeared swollen and had lost their characteristic lamellar substructure on electron microscopy of a serum-induced wheal biopsied at 10 min. Eosinophil degranulation was also observed at 2 h. The resemblance of the inflammation to the late phase of IgE-mediated immediate hypersensitivity reactions in atopics supports the concept that a circulating factor causes mast cell degranulation in chronic urticaria and may be important in the pathogenesis of the disorder.
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PMID:The pathology of the autologous serum skin test response in chronic urticaria resembles IgE-mediated late-phase reactions. 209 45

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

Patients with chronic urticaria are more sensitive to codeine skin testing than other allergic individuals. Nonlesional skin in most patients with chronic urticaria was found to contain increased numbers of both total and atypical mast cells. The presence of increased mast cell density was found to correlate with the degree of clinical (dermatographism) and functional (codeine skin test) skin sensitivity.
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PMID:Mast cell heterogeneity in chronic idiopathic urticaria. 224 7

The regulatory effects of various endocrine factors on allergic processes have been widely studied. The clinical importance of hyperthyroidism in asthma and in chronic urticaria has been demonstrated in several cases. These observations may be attributed to modulatory effects of thyroid hormones on mast cell releasability and/or on other target organs as blood vessels. To evaluate the effects of thyroid hormones on mast cell releasability and on the cutaneous vasculature, we analyzed the wheal and flare response to compound 48/80, to codeine, and to histamine in patients with hyperthyroidism and in a control group. No significant difference was found between the two groups. We could not demonstrate any in vivo effect of the thyrotoxic state on the cutaneous response to these substances.
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PMID:Cutaneous responses to histamine, compound 48/80 and codeine in patients with hyperthyroidism. 230 20

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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