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 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

Cutaneous wheal and flare responses to increasing concentrations of calcitonin gene-related peptide, substance P, neurokinin A, vasoactive intestinal polypeptide (VIP), compound 48/80, and phosphate-buffered saline were measured in 10 patients with chronic idiopathic urticaria and 10 healthy controls. A significant increase in VIP-induced wheal, but not flare or cutaneous blood flow, was seen in urticarial patients compared with controls (p less than 0.001). No significant differences in responses to other tested compounds were found between these groups. These data point to an increased sensitivity of microvasculature to VIP in patients with chronic idiopathic urticaria.
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PMID:Cutaneous responses to vasoactive intestinal polypeptide in chronic idiopathic urticaria. 137 Feb 36

C1q, a subcomponent of the first complement component, of a 60-year-old female patient with hypocomplementemic vasculitis-urticaria syndrome (HVUS) was characterized. The C1q-precipitin activity (C1q-p) could not be detected by a routine method with 0.6% agarose in 10 mM Na-phosphate buffer containing 10 mM EDTA (pH 7.2). Hemolytic activity of her serum complement (CH50) and levels of C1 and C4 were significantly reduced at the exacerbation stage, but levels of other complement components were almost within the normal range throughout her clinical course. The specific activity of C1q at her exacerbation stage was significantly low, and its elution position on Sephacryl S-300 column was spread toward the low molecular weight in comparison with that of normal plasma. Molecular weights of the delayed fraction of C1q were estimated to be approximately 300,000 on the Sephacryl and 440,000 by the polyacrylamide gel electrophoresis (PAGE) containing sodium dodecyl sulfate (SDS) followed by immunoblotting, respectively. On reduction of her plasma, two bands with molecular weights equivalent to those of B and C chains of the normal C1q in an approximate molar ratio of 2:1 were immunostained. Plasma at her exacerbation stage showed only one precipitation line against anti-human C1q-antiserum which was completely fused with that formed between purified normal human C1q and the same antiserum. The probable structural change of the hypofunctional C1q in the case of this HVUS is discussed.
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PMID:Characterization of C1q found in a patient with hypocomplementemic vasculitis-urticaria syndrome. 250 5

The ability of drugs to inhibit histamine-induced wheals has been used frequently as a pharmacodynamic index of clinical efficacy. Host response using this model can be predictive of clinical response in atopic diseases such as allergic rhinitis and urticaria. Terfenadine is a widely used nonsedating antihistamine currently approved for use at a dosage of 60 mg every 12 hours. Our clinical trial was designed to determine whether higher dosages of this agent were associated with amplified efficacy in suppressing the wheal response to intradermal histamine phosphate. Twenty-six healthy male Caucasian volunteers were randomized in a double-blind crossover fashion to receive terfenadine 60 mg every 12 hours, 120 mg each day, 120 mg every 12 hours, and placebo. Each dose was given orally for three days followed by a 6-day washout period. Histamine was administered intradermally one hour prior to dosing for baseline measurements. Histamine was given at defined intervals after treatment or placebo on days 1 (acute dosing) and 3 (steady state), and the percent inhibition of histamine-induced wheal area as compared with baseline was determined. Subjects receiving all three active doses exhibited significant wheal inhibition compared with placebo on days 1 and 3 (P less than or equal to .01). Subjects receiving the 60 mg every 12 hours and the 120 mg each day dosages exhibited roughly equivalent mean wheal suppression over the 24-hour period of each testing day (54% versus 60%, respectively, on day 1 and 62% versus 63%, respectively, on day 3, no significant differences).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of inhibition of wheal response to histamine by multiple doses of terfenadine. 257 53

Lucilia Caesar larvae (LCL) are used as live fish bait by anglers. Five cases of asthma and rhinoconjunctivitis following exposure to LCL are reported. Three had work-related asthma as they were working on a fish bait farm or shop and two had asthma when they went fishing. In one subject exposure to LCL caused asthma, rhinoconjunctivitis and contact urticaria. In four subjects peak expiratory flow rate (PEFR) was monitored during exposure to LCL. In three out of four subjects there was evidence of LCL-related asthma. In one subject it was not possible to record PEFR during exposure to LCL, as he had not gone fishing since 1985. Two extracts of LCL were prepared: one was the PBS (phosphate-buffered saline) washing fluid of LCL, the other was the PBS extract of homogenized LCL. Positive cutaneous prick tests to both LCL extracts were detected in three out of four symptomatic subjects. Specific IgE against both LCL extract antigens were found by the RAST method in four out of five subjects with LCL-related asthma. One subject had both negative skin tests and RAST. Specificity and potency of LCL-IgE binding was shown by RAST inhibition method performed on the serum pool of four patients with positive RAST results. Significant inhibition of more than 50% by LCL washing fluid at a dilution extract was found at a dilution of 1:10 and by homogenized LCL extract at a dilution of 1:100. No significant inhibition of LCL-IgE binding by dermatophagoides, parietaria and milk antigens was found. This study demonstrated that LCL emanations are potent sensitizers and elicit IgE-mediated asthma.
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PMID:[Asthma caused by Lucilia Caesar larvae: clinical and immunologic study]. 263 Aug 95

Progressively increasing doses of aspirin (acetylsalicylic acid--ASA) were tolerated by 14 out of 15 patients with confirmed aspirin-sensitive urticaria and in 7 out of 9 patients with aspirin-sensitive asthma. Blood levels of histamine and prostaglandin (PG) F2 alpha were significantly raised in these patients before ASA administration. PGF2 alpha levels fell to within the normal range after challenge doses of ASA which were sufficient to cause symptoms. Skin prick testing with histamine and codeine phosphate did not show evidence of abnormal tissue reactivity or mast cell reactivity. A wider spectrum of mediators will need to be considered if the mechanism of symptom production is to be understood.
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PMID:Clinical and biochemical aspects of "aspirin-sensitivity". 347 39

We examined the antibody response to a rabies vaccine doubly inactivated with 0.025% beta-propiolactone and 0.1% tri(n)butyl phosphate and stabilized with 2.5% human serum albumin. Antibodies were measured by using the following four antigen preparations: complete doubly inactivated rabies vaccine, rabies vaccine inactivated only with tri(n)butyl phosphate, beta-propiolactone and human serum albumin, and human serum albumin alone. The fluid phase of the preparation of beta-propiolactone and human serum albumin completely inhibited IgE binding to solid-phase vaccine. Of 21 subjects with urticarial reactions to a booster, 19 had IgE to doubly inactivated vaccine and to beta-propiolactone and human serum albumin. None of 27 immunized subjects without urticaria had detectable IgE. In paired pre- and postimmunization sera, IgE appeared in six of seven of the subjects with urticaria and in one of seven nonreactors. These sera did not contain a significant level of IgE to singly inactivated vaccine or to human serum albumin alone.
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PMID:IgE and IgG antibodies to beta-propiolactone and human serum albumin associated with urticarial reactions to rabies vaccine. 355 91

Mizolastine is a new, nonsedating antihistamine providing satisfactory symptom relief in allergic rhinitis and urticaria. The purpose of this study was to use the wheal and flare skin reactions model to assess the maintenance of the pharmacodynamic effect of mizolastine, administered for 2 months. This double-blind, parallel-group study involved 60 atopic patients randomly allocated, after a 1-week placebo run-in, to once-daily 10 mg mizolastine (n = 29) or placebo (n = 31) groups. Treatment continued for 8 weeks. Prick tests were performed in duplicate with histamine chlorhydrate (10 mg/ml), codeine phosphate (9%), and five increasing concentrations (1-500 reactivity index/ml) of standardized allergen extracts (grass pollen or mites) at days 0, 7, 28, 42, and 56. After 7 days of treatment, inhibition of histamine-induced wheal was -76% and +20%, respectively, with mizolastine and placebo (P = 0.0001), in comparison with baseline; inhibition of flare was -86% and +5%, respectively, with mizolastine and placebo (P = 0.0001). Suppression was maintained to a similar extent throughout the study. Results were consistent between histamine-, codeine-, and allergen-induced tests. Safety was satisfactory in both groups. The study confirms mizolastine as a potent antihistamine which does not induce subsensitivity when taken for 8 weeks, and which can be safely recommended in allergic conditions.
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PMID:Lack of subsensitivity to mizolastine over 8-week treatment. 879 22

To evaluate the skin reactivity and the mast cell releasibility in the acquired immunodeficiency syndrome (AIDS), 24 patients with AIDS were skin tested with histamine (1 mg/ml) and codeine phosphate (0.9, 0.09, and 0.009 mg/ml), a mast cell degranulating agent. They were compared to 12 HIV-negative healthy volunteers and 16 urticaria-prone subjects. Reactivity to codeine phosphate was lower in patients with AIDS than in HIV-negative subjects. This difference in skin reactivity was the more significant when the AIDS group was compared to the urticaria-prone group. There was no correlation between the reactivity to codeine and the IgE levels. Possible explanations to the decreased skin reacting to codeine in patients with AIDS include a decrease of local mast cell density or releasibility. This suggests that a mechanism related to urticaria and involving mast cells is quite unlikely to be at the origin of the hypersensitivity reactions observed in AIDS.
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PMID:Decreased skin reactivity to codeine in patients with the acquired immunodeficiency syndrome. 880 35

Solar urticaria is characterized by itching weals that occur a few minutes after exposure to visible or ultraviolet light. The symptoms may sometimes restrict normal daily life. Treatment is difficult in more severe cases. We describe one patient with solar urticaria who was successfully treated with cyclosporin A. The patient had first been treated with antihistamine, PUVA and chloroquine phosphate without effect. Cyclosporin was given in a dose of 4.5 mg/kg body weight/day. Phototesting before, during and after treatment showed a decreased light sensitivity to UVA, UVB and visible light during cyclosporin treatment compared with phototesting before therapy. The patient could be out in the sun for at least 1 h with minimal urticaria during cyclosporin therapy compared with only a few minutes previously. However, 1-2 weeks after cyclosporin therapy was discontinued, skin symptoms returned. Cyclosporin therapy is a possible treatment in severe cases of solar urticaria where other treatments have failed, especially in countries where treatment is necessary only for a few months during summer.
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PMID:Cyclosporin A therapy for severe solar urticaria. 936 Nov 30


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