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)

Urtica is characterized by an erythematous wheal surrounded by a flare and is frequently caused by physical agents (e.g. cold). The exact mechanism and mediators involved in the mechanism of physical urticaria are not known. This study of the role of the neurogenic factors in cold urticaria showed, that local capsaicin treatment (desensitization) of the skin in patients with cold urticaria resulted in the abolition of whealing in response to cold. This result suggests that C-fibers might play an important role in the pathomechanism of idiopathic contact cold urticaria.
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PMID:A possible pathomechanism of the idiopathic cold contact urticaria. 175 25

Topical application of a clioquinol and Bacitracin powder resulted in contact urticaria and an anaphylactoid reaction. Prick tests with clioquinol and bacitracin solution produced a wheal and flare response. This problem is unusual, but has been reported and previous reports are summarized.
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PMID:Contact urticaria syndrome and anaphylactoid reaction from topical clioquinol and bacitracin (Banocin): a case report. 182 91

A 34-year-old Japanese female with solar urticaria is described, who had an episode of urticarial response when she was exposed to indoor fluorescent light first and sunlight later. The action spectrum was found to range from 480 to 520 nm with an inhibition spectrum above 650 nm in the visible light by both postirradiation and preirradiation. Injection of in vitro-irradiated serum did not produce an urticarial wheal on the patient. In the Japanese literature, 17 cases of solar urticaria with inhibition spectra have been reported. The wavelength of the inhibition spectrum was longer than that of the action spectrum in each case.
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PMID:Inhibition spectra of solar urticaria: a case report and a review of the Japanese cases. 193 65

Pruritus is a common symptom associated with chronic renal failure (CRF). But increased plasma histamine levels and skin mast cell proliferation previously reported in these patients did not correlate with the intensity of the pruritus. Since increased mast cell releasability was described in chronic idiopathic urticaria, we attempted to examine whether this mechanism could explain pruritus in patients with CRF. Twenty-five patients with end stage renal failure were skin tested with histamine, codeine, and compound 48/80. There were nine patients on continuous ambulatory peritoneal dialysis, eight patients on hemodialysis, (tested both before and after dialysis) and eight patients with advanced CRF. Wheal area after intradermal injection of three concentrations of the above substances was measured. In general, the wheal areas in all patients with CRF were either similar to or smaller than those of the control group who were without renal impairment. In conclusion, patients with CRF with or without dialysis therapy demonstrated unchanged or decreased skin test responses to histamine, codeine, and compound 48/80. Increased mast cell releasability cannot explain the pruritus in patients with CRF.
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PMID:Cutaneous responses to histamine, compound 48/80, and codeine in patients with chronic renal failure. 195 8

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

1. The kinetics of weal formation and disappearance following intradermal injection of histamine, compound 48/80 and antigen were measured in indomethacin and inert geltreated human forearm skin. 2. Rates of formation went in descending order for histamine, 48/80 and antigen; rate constants of disappearance for equal sized weals were the same for histamine and 48/80 but were much less for antigen. The corresponding half-lives were 77, 73 and 160 min for histamine, 48/80 and antigen weal disappearance respectively. 3. Cyclo-oxygenase inhibition by topical indomethacin had no effect either on the immediate weal and flare responses or on the rates of formation and disappearance of the weals. 4. These findings together with previous studies using H1-receptor antagonists indicate that 48/80 acts by histamine release but that antigen releases both histamine and an additional material or materials which are not related to cyclo-oxygenase activity. 5. Exacerbation of chronic idiopathic urticaria by cyclo-oxygenase inhibitors is therefore likely to be part of the urticarial disease process.
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PMID:The effect of indomethacin on the kinetics of histamine, 48/80 and antigen wealing. 210 36

Mast cell inflammatory mediators, such as histamine, and newly formed compounds, such as the leukotrienes, cause wheal and flare when they are injected intradermally into normal subjects and may therefore play a role in the formation of urticaria. The effects of intradermal injections (50 microliters) of six different concentrations of histamine (range, 3.3 x 10(-4) to 3.3 x 10(-9) mol/L) and the leukotrienes C4, D4, and E4 (range, 2 x 10(-4) to 2 x 10(-9) mol/L) have been compared in 10 normal subjects and in 10 patients with chronic idiopathic urticaria. Wheal-and-flare sizes were measured at timed intervals up to 4 hours, and area under the curve for each response over time was calculated. There were no significant differences in leukotriene-induced responses between groups. Maximum sizes of histamine-induced wheal and flare were similar in each group of subjects. There were, however, significant increases in mean areas under the response curve of histamine wheal and flare in the patients with urticaria (wheal, p less than 0.001; flare, p less than 0.001; analysis of variance). These findings demonstrate a prolongation of skin responses to histamine in patients with urticaria and suggest an impaired clearance of histamine (or other vasoactive agents released by histamine) from the skin of these patients.
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PMID:Skin responses to intradermal histamine and leukotrienes C4, D4, and E4 in patients with chronic idiopathic urticaria and in normal subjects. 217 51

The mechanisms by which tolerance is induced in solar urticaria were investigated in two patients whose eruptions were induced by wavelengths in the range 320-455 nm in one patient and 400-495 nm in another. Tolerance to radiation was induced by repeated exposures of the skin to the eliciting wavelengths of light. Weal and flare responses to intradermal injections of histamine and the histamine-releasing agent (codeine) were unaltered in the tolerant skin when compared with adjacent normal skin. Intradermal injection of in vitro irradiated serum or plasma from the patients induced an urticarial reaction in the unexposed skin but not in tolerant skin and repeated injections induced tolerance to the eliciting radiation. The results suggest that tolerance is not due to exhaustion of the photoallergen in the skin, or to an increase of the mast-cell degranulation threshold caused by exposure to ultraviolet radiation, or mast-cell mediator depletion, or histamine tachyphylaxis. It is likely that binding sites of IgE on mast cells remain occupied by the photoallergen during the state of tolerance, and that histamine release from mast cells is blocked.
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PMID:Solar urticaria: studies on mechanisms of tolerance. 235 12

Recent case reports have suggested that H2-antihistamines used alone may be effective in the treatment of acute urticaria, a common complaint of patients presenting to the emergency department. This contradicts accepted doctrine on the treatment of acute urticaria. Based on theories of H1- and H2-receptor interaction at the cellular level, it has been stated that H2-blockade before H1-blockade may exacerbate symptoms. The purpose of our study was to compare diphenhydramine, an H1-blocker, with cimetidine, an H2-blocker, in a randomized, prospective, double-blind clinical trial. Ninety-three patients presenting to the ED with clinical evidence of acute urticaria were treated with either 50 mg diphenhydramine IM or 300 mg cimetidine IM. Patients' signs and symptoms were quantitated on a numeric scale before receiving medications and 30 minutes after treatment. Parameters measured included degree of itching, intensity and extent of wheals, degree of sedation, and perception of overall improvement. Each medication provided significant relief of itching and wheal intensity (P less than .0001). Sedation was caused by both diphenhydramine (P less than .0001) and cimetidine (P less than .0006). However, the degree of sedation caused by diphenhydramine was significantly greater than that caused by cimetidine (P = .0001). The perception of overall improvement was greater with cimetidine, with 87% of patients reporting improvement, whereas 76% of diphenhydramine-treated patients reported improvement. Our results indicate that cimetidine is efficacious as the initial treatment of acute urticaria and has less tendency toward sedation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of cimetidine and diphenhydramine in the treatment of acute urticaria. 240 34

Cell-mediated immunity is generally considered as the principal immunological response to dermatophyte infection. However, certain clinical manifestations associated with a humoral antibody response occasionally occur as complications to dermatophytosis (e.g. vasculitis, urticaria). Immediate wheal reaction to intradermal application of "trichophytin" is frequent in patients with chronic T. rubrum infection and can be passively transferred with serum, which demonstrates the presence of specific IgE antibodies in these patients. Crossed immunoelectrophoresis and modifications thereof were applied for studies of (i) the antigenic structure of dermatophytes in sera from patients with dermatophytosis. The antigenic composition was found to differ between species but was characteristic and constant for different strains of the same species. Partial cross reactivity between different species, especially T. rubrum and T. mentagrophytes was noted. The presence of specific IgG antibodies towards corresponding dermatophytes was associated with tinea capitis (100%), tinea pedis with dermatophytid eruption (62%) and chronic T. rubrum infection (25%). Sera from 50 healthy persons were all negative. Specific IgE antibodies toward T. rubrum were demonstrated in serum from eight patients with chronic T. rubrum infection while specific IgE antibodies were not present in sera from ten patients with tinea capitis and four controls. The possible role of IgG and IgE antibodies in inflammatory and non-inflammatory dermatophyte infections is discussed.
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PMID:Humoral antibody responses in the immunopathogenesis of dermatophytosis. 242 54


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