Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 33-year-old female patient with acquired cold urticaria, together with her 8-year-old healthy daughter, was subjected to a brief period of cold exposure. The effect of this treatment upon a number of key factors of the plasma coagulation, kallikrein and complement systems was investigated. Cold air provocation caused increased fibrinolysis, together with a measurable consumption of the protease inhibitors alpha1-antitrypsin (alpha1AT), alpha2-macroglobulin (alpha2M) and C1Inactivator (C1INA). Kaolin activation of the patient's plasma elaborated exceptionally high levels of esterolytic activity, both before and after cold exposure, indicating pre-enzyme lability. Both subjects had abnormally high serum ratios alpha2M/alpha AT. Impressive leucocytosis was observed in the symptomless child.
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PMID:Enzyme activation and inhibition induced by cold provocation in a patient with cold urticaria. 4 15

The erythema and wealing resulting from the application of thurfyl nicotinate ointment (Trafuril) and from the inoculation of kallikrein has been studied in patients with chronic urticaria and normal controls. Polyphloretin phosphate (PPP) suppressed the reaction in controls but in patients with urticaria it increased the reactions to Trafuril and had little effect on the kallikrein reaction. PPP also suppressed the PGE2-induced erythma in normal controls but not in urticaria patients. In a separate study using fibrinolysis autography, prostaglandin (PG) E2 and PGF2alpha depressed fibrinolysis in the skin of two pigs and both kallikrein and Trafuril suppressed fibrinolysis in human skin. It is suggested that the inflammatory reaction induced by thurfyl nicotinate and kallikrein is mediated in part by a prostaglandin-like action. Several anomalies in the action of Trafuril in skin diseases can be explained if such prostaglandin-like activity is mediated in part through inhibition of fibrinolysis.
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PMID:The cutaneous reactions to kallikrein, prostaglandin and thurfyl nicotinate in chronic urticaria and the effect of polyphloretin phosphate. 5 6

The hypothesis that deficiencies of plasma protease inhibitors might play a role in the pathogenesis of chronic urticaria was evaluated. Plasma levels were measured in patients with urticaria and a matched control group for alpha1-antitrypsin, alpha2-macroglobulin, total trypsin-inhibiting capacity, kallikrein-inhibiting capacity, and the complement factors C1 esterase inhibitor, C3, and C4. A total of 92 patients with chronic urticaria or more than three months' duration was studied. Patients with acquired cold urticaria had significantly decreased levels of alpha1-antitrypsin and total antitrypsin activity. In patients with acquired angioneurotic edema, alpha1-antitrypsin levels and antichymotrypsin activities were lowered, with less significant decreases in anti-trypsin and antikallikrein activities. Levels of C1 esterase inhibitor , C3, and C4 were normal in all groups. There was no correlation between the increased sensitivity to intracutaneously administered kallikrein injection and deficiencies of of protease inhibitors.
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PMID:Protease inhibitors in plasma of patients with chronic urticaria. 6 Sep 15

Oral administration of 50 mg tartrazine to 122 patients with a variety of allergic disorders caused the following reactions: general weakness, heatwaves, palpitations, blurred vision, rhinorrhoea, feeling of suffocation, pruritus and urticaria. There was activation of the fibrinolytic pathway as shown by reduction of plasminogen with high pre-kallikrein and low kallikrein values. Reduction in complement activity (CH50) was seen in three out of sixteen reactions.
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PMID:The danger of "yellow dyes" (tartrazine) to allergic subjects. 62 44

Insignificant variation was noted in the mean levels of the complement components CIQ, C4, C2, C3, C5 and C3PA between various groups of sera from patients with urticaria, angio-oedema, dermatitis herpetiformis, alopecia areata, or hay fever. No deficiencies were found. Elevated C9 levels in chronic urticaria and angio-oedema reflected its nature as an acute phase protein. The assessment of C components in single or sequential serum samples revealed only marginal variations. Similar results were recorded for plasminogen the immunoglobulins, G, A and M. Some evidence is provided for the primary involvement of the kallikrein-kinin system in urticaria.
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PMID:Complement component profiles in urticaria, dermatitis herpetiformis, and alopecia areata. 95 50

The effects of oral cetirizine on spontaneous and provoked urticaria were evaluated in two studies. In a double-blind crossover trial, 30 patients with idiopathic urticaria received 10 or 20 mg of cetirizine or placebo. Cetirizine was significantly more effective than placebo in reducing the incidence of erythema, wheals, and pruritus. No serious side effects were reported. In the second study of ten patients with chronic urticaria, immediate and delayed reactions to injected autologous serum, histamine, kallikrein, and synthetic platelet-activating factor (PAF)-acether were inhibited by 10 mg of cetirizine. These results suggest that the mechanism of action of cetirizine may involve inhibition of PAF-induced influx of eosinophils.
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PMID:Cetirizine in the treatment of chronic urticaria. 182 14

The effects of oral administration of the antihistamine cetirizine on the weal and flare caused by intradermal injection of platelet activating factor (PAF-acether), kallikrein, histamine and the patient's own serum were investigated in 10 patients with chronic urticaria. Cetirizine markedly reduced the weal and flare induced by all these agents as measured 12 min after the injections. The delayed reactions observed after injection of PAF, kallikrein and serum were also inhibited by cetirizine at 6 hours. In addition, reactions which were present 20 h after injection of the agent before administration of cetirizine were found to be inhibited at the same point in time after cetirizine treatment. These effects might explain the good inhibitory clinical effect of cetirizine on the patients' urticaria. No side-effects were noted during the treatment.
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PMID:Effect of cetirizine on cutaneous reactions to PAF, kallikrein and serum in patients with chronic urticaria. 196 2

Erythema multiforme (EM) is an inflammatory disorder of the skin, which may include mucous membrane involvement, that features target (iris) lesions. Mediators specifically involved in EM are not well characterized; its pathogenesis remains enigmatic. In this study, evidence for participation of kinins in the pathophysiology of inflammation in EM was investigated by assessing cleavage of high-molecular-weight kininogen (HMWK) in plasma. These data were compared with analyses of plasmas from patients with serum sickness, chronic idiopathic urticaria/angioedema, and from normal control subjects. Patients with EM demonstrated significant levels of circulating cleaved HMWK in plasma during active disease (p less than 0.01), which declined during remission/recovery. Plasmas from patients with EM obtained during active disease also demonstrated significant levels of 94 kd C1 inhibitor (p less than 0.01) and C1 inhibitor-kallikrein complexes. Patients with serum sickness and chronic idiopathic urticaria/angioedema did not demonstrate these findings and did not differ from normal control subjects (p = not significant). Although the kininogenase responsible for HMWK cleavage in EM has not been conclusively demonstrated, these findings suggest that HMWK cleavage resulted from activation of the contact system and that some of the manifestations of EM in selected patients may in part be accounted for by inflammatory and proinflammatory actions of kinins. Based on these preliminary findings, it will be important to establish whether or not HMWK cleavage in EM is a general finding in patients with this disorder. Further investigation is needed to characterize more clearly kininogenase activity and elucidate the possible role of kinin generation in EM.
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PMID:High-molecular-weight kininogen is cleaved in active erythema multiforme. 270 41

Data early obtained on activation of the kallikrein-kinin system in acute forms of pollinosis and urticaria were corroborated in vitro. These experiments exhibited enzymatic activation of Hageman factor and prekallikrein using "liberator", obtained after incubation of the leukocyte fraction enriched with basophils and specific allergen. I ml of the "liberator" containing 10(7) cells activated Hageman factor up to 12-20 mU per min (evaluated by BAEE-esterase activity of the kallikrein developed) as well as kallikrein activity was increased up to 80-130 mU within 1.5-2 hrs of incubation. The Hageman factor was distinctly inactivated after long-term incubation with the "liberator".
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PMID:[The mechanism of activation of kallikrein-kinin system in the plasma of patients with atopic allergic diseases]. 323 45

Activity of kallikrein and content of prekallikrein were estimated in blood serum of 34 patients with atopy and of 17 patients with urticaria by means of the chromatographic procedure. In these patients activity of alpha 1-proteolytic inhibitor (alpha 1-PI) and alpha 2-macroglobulin (alpha 2-MG) was studied. At the acute period of pollinosis activation of the kallikrein-kinin system was found, which correlated with the disease aggravation. During specific immunotherapy of the patients with atopy activation of the kallikrein-kinin system occurred, which depended on the total concentration of allergen administered. At the same time, activation of the kallikrein-kinin system, observed under conditions of urticaria, was most distinct in the patients with chronic relapsing urticaria and was related to the degree of the disease aggravation. Preparations of proteinase inhibitors analogous to contrical were only short-term effective in chronic relapsing urticaria. In the patients with distinct aggravation of pollinosis inhibitory activity of alpha 2-MG was markedly increased which occurred apparently as a result of blood pachyemia simultaneously with activation of the kallikrein-kinin system. Distinct increase in the alpha 1-PI activity was not found in the patients with pollinosis and urticaria even at the step of pronounced aggravation. Phenotyping of the inhibitor in 10 patients with a marked decrease in its activity enabled to find 6 persons exhibiting the heterozygous genotype with a defect allele.
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PMID:[Activity of the prekallikrein-kallikrein system and characteristics of its regulation in various allergies]. 364 May 71


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