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)

The blood histamine levels, basophil and eosinophil counts and the percentage of vacuolated eosinophils were observed in 30 controls and 15 patients of urticaria. There was a definite rise in eosinophil and basophil count during the acute stage of the disease which decreased in the quiescent or the symptom-free stage. The behavior of blood histamine level was similar. The mechanisms involved are discussed.
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PMID:Blood histamine levels and eosinophil, basophil counts in urticaria. 4 60

During the routine screening of 152 patients with urticaria or angio-oedema for hypocomplementaemia, 4 patients were found to have low serum levels of the third component of complement (C). These patients were noteworthy and differed from previous reports of patients with urticaria-like skin lesions and hypocomplementaemia because of the absence of immune-complex disease. In addition to the low C3, 2 of these patients were unique on the basis of low serum levels of haemolytic C1, C1q, C1s, and properdin factor B, but normal concentrations of C4 and C2. These C abnormalities may reflect a new clinical entity, and these cases form the first description in man of the C1-bypass complement-activation pathway.
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PMID:C1-bypass complement-activation pathway in patients with chronic urticaria and angio-oedema. 4 98

Patients with idiopathic acquired cold-induced urticaria were evaluated for the release of the preformed mast-cell mediators of immediate-type hypersensitivity during a study in which one arm was immersed in ice water while the other arm remained as a control. Blood specimens were obtained from each arm serially over a one-hour interval, and serum speciments were assessed for histamine, eosinophil chemotactic factor of anaphylaxis, and complement components. Levels of histamine and eosinophil chemotactic factor rose in the arm subjected to cold immersion for three minutes, with peak values occurring between two and five minutes and returning to base line by 30 minutes. No changes occurred in the control arm or in the immersed arm of normal subjects. Assessment of the classical and alternative complement pathways showed no abnormalities. This initial observation of release of eosinophil chemotactic factor of anaphylaxis in vivo along with histamine assigns the mast cell a central role in cold urticaria.
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PMID:Cold urticaria: release into the circulation of histamine and eosinophil chemotactic factor of anaphylaxis during cold challenge. 5 69

Histamine release from peripheral blood leukocytes challenged with anti-human IgE was studied in patients with chronic urticaria and nonatopic controls. 19 of 23 controls, but only 6 of 20 patients, released over 20% of the total available leukocyte histamine. The response to anti-IgE concentrations of 1.66, 0.33, 0.066, and 0.013 mug antibody N/ml was significantly lower in patients than in controls. Serum IgE levels were significantly higher in the patients but total histamine content of about 10(7) leukocytes was not. Deuterium oxide (D2O) greatly increased histamine release (in both groups), indicating that the anti-IgE interacted with the basophils of urticaria patients. Passive sensitization of leukocytes with biologically active IgE was achieved in both patients and control subjects whose cells responded to anti-IgE, but was not achieved in either patients or control subjects whose cells were nonresponsive to anti-IgE challenge. 125I-anti-IgE autoradiographic studies revealed no obvious quantitative abnormality in the amount of basophil-bound IgE in chronic urticaria patients. Ionophore stimulation of aliquots of the same leukocytes used for anti-IgE challenge demonstrated that the urticaria patients' basophils were capable of releasing normal amounts of histamine. Leukocyte cyclic AMP levels in the two groups were not significantly different either in base-line levels or in responsiveness to stimulation with isoproterenol. These data indicate that chronic urticaria patients have a (acquired?) defect in leukocyte histamine release that occurs after the anti-IgE-IgE interaction, but before the actual (second-stage) release process, and that is comparable to the phenomenon of desensitization.
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PMID:Defective histamine release in chronic urticaria. 5 21

The interrelations between cold sensitivity and release of histamine and other mediators in five patients with cold urticaria undergoing cold tolerance treatment were studied. Tolerance to cold was produced in all patients by repeated cold exposure. In four patients tolerance was maintained by once daily exposures. In the fifth patient 4-hourly exposures were necessary. Cold sensitivity was associated with histamine release in venous blood draining urticated skin. No prostaglandin activity was detected, and low concentrations of kinin activity were found in blood draining the normal and exposed skin of healthy subjects as well as in patients with cold urticaria. After induction of tolerance, no histamine release occurred on challenge by cold. Relapse of sensitivity was associated with reappearance of histamine release on challenge. The conclusion that tolerance is due to depletion of histamine stores in skin after repeated cold exposure was supported by diminished wealing in response to injection of a histamine liberator (compound 48/80) in cold-tolerant skin.
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PMID:Induced tolerance in cold urticaria caused by cold-evoked histamine release. 5 49

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 pathogenesis of type I disorders, particularly allergic asthma and urticaria, requires a critical review in the light of recent findings which indicate a second pathway for the release of granulocyte mediators. The isolation of enzyme activity of some of these released mediator establishes a direct link between the immunological system and bradykinin, as well as a system of self modulation of kinin activity. These findings open the door for a broader understanding of the asthmatic process and lay the foundation for integrating extrinsic and intrinsic asthma.
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PMID:A new look at type I immediate hypersensitivity immune reactions. 5 57

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

A double blind crossover trial of levamisole has been carried out in 47 patients with recurrent oral ulceration. Significant decreases in the number of ulcers and ulcer days were found after 2 months of intermittent administration of levamisole. About 64% of patients responded to the drug by a decrease in the number of ulcers of more than 50%, for two or more months. The remaining 36% of patients failed to respond to levamisole and 23% of these had an increased number of ulcers. The side-effects recorded in patients taking levamisole were comparable with those in patients on placebo, except for a flu-like syndrome in 1 patient and urticaria in another, necessitating withdrawal of the drug. The mechanism of action of levamisole in recurrent oral ulceration is not known, but it is suggested that levamisole may correct a deficiency of suppressor cells, or potentiate the cellular responses to crossreacting microbial agents.
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PMID:Double blind crossover trial of levamisole in recurrent aphthous ulceration. 6 61

The authors report the complications associated with the administration of some anaesthetics using propanidide. In one of the controls, premedication using an antihistamine was sufficient to avoid, during a third administration of propanidide, complications which included a fall in blood pressure and which had occurred when the second anaesthetic had been given. In one patient with high plasma histamine concentrations, circulatory arrest occurred during the second and third anaesthetic, despite meclastinum. Only the addition of a glucocorticoid to the premedication made possible an anaesthetic without problems. During a third propanidide anaesthetic given to this same patient, we were able to confirm our hypothesis by a premedication combining meclastinum and a glucocorticoid, despite the high plasma histamine level found. In certain other cases, however, plasma histimine concentration did not increase despite the development of erythema and urticaria of the face and neck. Serious complications were successfully dealt with using a combination of glucocorticoids, adrenaline derivatives and an antihistamine.
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PMID:[Interference between histamine liberation and drugs used in anesthesiology. Prevention and treatment of the complications of histamine liberation]. 6 43


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