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)

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

Histamine, the main amine released during allergic reactions, can provoke coronary arterial spasm manifested as angina pectoris. This has been shown during clinical and laboratory studies. The effects of histamine on cardiac function are mediated via H1- and H2- receptors situated on the four cardiac chambers and coronary arteries. Coronary arteries of cardiac patients are hyperactive and contain stores of histamine which can initiate coronary artery spasm. Clinical observations indicate that angina pectoris or acute myocardial infarction can be provoked by acute allergic reaction. The coincidental occurrence of chest pain and allergic reaction accompanied by clinical and laboratory findings of classical angina pectoris seems to constitute the syndrome of allergic angina. The clinical symptoms of allergic angina include chest discomfort, dyspnoea, faintness, nausea, pruritus and urticaria. They are accompanied by signs such as hypotension, diaphoresis, pallor and bradycardia. There are also electrocardiographic findings indicating myocardial ischaemia, arrhythmias and conduction defects. Thus, in patients undergoing acute allergic reaction, the development of chest pain could be explained by the mechanism of coronary arterial spasm provoked by the release of histamine, which constitutes the syndrome of allergic angina.
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PMID:Histamine-induced coronary artery spasm: the concept of allergic angina. 179 97

The protective efficacy of oral cetirizine, a selective and potent H1-receptor antagonist, against the immediate bronchoconstrictive response to allergen inhalation and exercise challenge was evaluated in 16 subjects with stable, predominantly mild asthma. The subjects underwent double-blind, crossover pretreatments in randomized order in two separate protocols with (1) three daily oral doses of 20 mg of cetirizine and placebo, followed by allergen inhalation, and (2) single oral doses of cetirizine (5, 10, and 20 mg), albuterol (4 mg), and placebo, followed by exercise with cold-air inhalation. Cetirizine failed to decrease bronchial sensitivity to inhaled allergen in eight of 10 subjects. Neither cetirizine nor albuterol uniformly inhibited exercise-induced bronchoconstriction. Serum concentrations of cetirizine were consistent with systemic H1-blocking activity. Modest bronchodilation occurred after administration of cetirizine and albuterol before exercise but not after the third dose of cetirizine in the allergen protocol. One subject developed moderate drowsiness during multiple dosing with cetirizine. Thus, cetirizine, in the doses studied, is not uniformly effective in preventing allergen- or exercise-induced bronchoconstriction. Histamine is one of many mediators participating in immediate asthmatic responses, and selective H1 antagonists do not completely block these airway events. However, cetirizine may still clinically benefit some patients with asthma, such as patients with allergic rhinitis or urticaria.
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PMID:Effects of oral cetirizine, a selective H1 antagonist, on allergen- and exercise-induced bronchoconstriction in subjects with asthma. 196 19

The capacity for ketotifen to prevent mast-cell degranulation in vivo was studied in patients with physical urticarias. Patients were exposed to the appropriate stimulus to elicit their physical urticaria before and during ketotifen therapy. Histamine concentrations in plasma samples, obtained before and serially after the physical provocation, were determined by radioenzymatic thin-layer chromatography. Ketotifen therapy was associated with marked reductions in plasma histamine levels after stimulation and in clinical evidence of urticaria in each patient. A direct correlation of ketotifen therapy and a reduction in histamine release was confirmed in a patient with a cold-induced urticaria who was studied again after discontinuation and again after reinstitution of therapy. Although the mechanism of action is unknown, this report shows that ketotifen is capable of inhibiting cutaneous mast-cell degranulation and its accompanying symptoms. These findings suggest important therapeutic alternatives for patients with mast-cell-mediated diseases.
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PMID:Prevention of mast-cell degranulation by ketotifen in patients with physical urticarias. 242 Feb 46

Histamine release from peripheral blood basophils challenged with C5a, f-met-peptides and calcium ionophore was studied in patients with cold urticaria before and after exposure to low environmental temperatures. Compared to healthy controls, stimulated mediator release before cold exposure was increased in 7 of 11 patients. When challenged by cold exposure mediator release from in vitro-stimulated basophils was decreased. This decrease was more pronounced after stimulation with receptor-mediated stimuli (e.g. C5a) as compared to receptor-unrelated stimuli, e.g. calcium ionophore. In 4 of 11 patients stimulated mediator release before cold exposure was moderately increased. Also after cold exposure only a weak decrease of stimulated histamine release was seen. Levels of activated complement components (C3a) before and after cold exposure failed to provide evidence for complement activation in vivo. Also the number of circulating basophils as well as their cellular histamine content remained normal after cold exposure. The results show that in these patients release of histamine is altered before and after cold exposure. These changes in basophil responsiveness are not due to complement activation in vivo.
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PMID:Decreased releasability of basophils from patients with cold urticaria after cold exposure. 247 11

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

Histamine poisoning results from the consumption of foods, typically certain types of fish and cheeses, that contain unusually high levels of histamine. Spoiled fish of the families, Scombridae and Scomberesocidae (e.g. tuna, mackerel, bonito), are commonly implicated in incidents of histamine poisoning, which leads to the common usage of the term, "scombroid fish poisoning", to describe this illness. However, certain non-scombroid fish, most notably mahi-mahi, bluefish, and sardines, when spoiled are also commonly implicated in histamine poisoning. Also, on rare occasions, cheeses especially Swiss cheese, can be implicated in histamine poisoning. The symptoms of histamine poisoning generally resemble the symptoms encountered with IgE-mediated food allergies. The symptoms include nausea, vomiting, diarrhea, an oral burning sensation or peppery taste, hives, itching, red rash, and hypotension. The onset of the symptoms usually occurs within a few minutes after ingestion of the implicated food, and the duration of symptoms ranges from a few hours to 24 h. Antihistamines can be used effectively to treat this intoxication. Histamine is formed in foods by certain bacteria that are able to decarboxylate the amino acid, histidine. However, foods containing unusually high levels of histamine may not appear to be outwardly spoiled. Foods with histamine concentrations exceeding 50 mg per 100 g of food are generally considered to be hazardous. Histamine formation in fish can be prevented by proper handling and refrigerated storage while the control of histamine formation in cheese seems dependent on insuring that histamine-producing bacteria are not present in significant numbers in the raw milk.
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PMID:Histamine poisoning (scombroid fish poisoning): an allergy-like intoxication. 268 58

In the present study we examined the effects of chlorpheniramine and ranitidine, indomethacin, BW755C (an inhibitor of cyclo-oxygenase and lipo-oxygenase enzymes of arachidonic acid metabolism), dexamethasone, and capsaicin on nonimmunologic contact urticaria (NICU) induced in the guinea pig ear by benzoic, acid cinnamic acid, cinnamic aldehyde, methyl nicotinate, diethyl fumarate, or dimethyl sulfoxide. The intensity of edema in the urticarial reaction was quantified by measuring the ear thickness. Antihistamines inhibited reactions to intradermal histamine but not to agents causing NICU. Indomethacin and dexamethasone inhibited reactions to cinnamic acid and cinnamic aldehyde but not to other NICU agents. BW755C and capsaicin had no effect on reactions to any of the NICU agents. Mast cell degranulation during the reaction was not seen in histologic sections. Histamine and capsaicin-sensitive nerves did not seem to be essential for the development of NICU in the guinea pig ear. The details of the inhibitory effects of indomethacin and dexamethasone are not clear, but it seems probable that more than one mechanism is involved in NICU due to different agents.
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PMID:Pharmacological studies on nonimmunologic contact urticaria in guinea pigs. 310 19

One hundred and twenty patients with chronic idiopathic urticaria, who entered a study at five centres (Sheffield, London, Bristol, Cardiff and Leeds) were treated with therapeutic doses of the H1 antagonist chlorpheniramine for 6 weeks. Histamine H1 non-responders (40 patients) were entered into a double-blind study and received chlorpheniramine plus cimetidine 400 mg q.d.s. (21 patients) or chlorpheniramine plus placebo (19 patients) for a further 8 weeks. The most important response measure was the change from baseline of the total symptom score: an assessment of the number and duration of new weals and degree of itching. There was a statistically significant difference between the average response in the two treatment groups in favour of chlorpheniramine plus cimetidine after 4 and 8 weeks' treatment (P less than 0.05 and P less than 0.01, respectively). No significant side-effects related to treatment were noted.
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PMID:Cimetidine and chlorpheniramine in the treatment of chronic idiopathic urticaria: a multi-centre randomized double-blind study. 330 90

Bronchial hyperreactivity was studied in 79 patients who gave a history of allergic symptoms. Twenty-nine of them suffered from rhinitis, 28 from eczema, 21 from urticaria and one from gastrointestinal allergy. Forced expiration in the first second (FEV1) was measured in each. If FEV1 was greater than 1 l a histamine challenge was done. Histamine (0.6 mg/ml) was inhaled by tidal breathing for one minute. FEV1 was measured before the inhalation and two min after cessation of the inhalation. If FEV1 dropped greater than 20% the inhalation was assessed as positive and the provocation was stopped. If the challenge was not positive another inhalation with histamine (2.4 mg/ml, l min) was done. If FEV1 dropped greater than 20% when measured two min after the inhalation the provocation was called positive. Twenty-two patients with rhinitis had a negative bronchial challenge, six had a positive. One of them had asthma, three suffered also from cough and/or serous sputum production, and two had hay fever. Out of 28 with eczema, 20 had negative histamine challenge and five a positive. Four of these suffered from daily cough and/or serous sputum production, one had no airway symptoms. Fifteen out of 21 suffering from urticaria had a negative histamine challenge, three had a positive. Two of them suffered from asthma and one complained of daily cough and/or serous sputum production. It is concluded that allergic subjects without symptoms from the airways, have a bronchial reactivity to inhaled histamine similar to the general population.
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PMID:Bronchial hyperreactivity in allergic subjects. 346 10


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