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)

Fifteen patients with coronary artery spasm completed a double-blind placebo-controlled trial comparing diltiazem and nifedipine. Increasingly, higher daily doses (diltiazem, 90 to 360 mg; nifedipine, 30 to 120 mg) were administered to achieve optimal clinical effects. Daily diaries and ambulatory electrocardiographic recordings were used to assess efficacy and side effects. Both drugs significantly decreased angina frequency compared with that in the preceding placebo period (diltiazem 1.4 +/- 0.4 [mean +/- SEM] to 0.4 +/- 0.2 episodes per day; nifedipine 1.4 +/- 0.3 to 0.4 +/- 0.1 episodes per day; both p less than 0.05). Ambulatory electrocardiographic recordings showed fewer ST shifts than were expected during all treatment periods (0.02/h recorded during placebo, none during diltiazem and 0.02/h during nifedipine therapy). Although some patients responded better to one drug than the other, neither drug resulted in a clearly superior clinical response. Diltiazem was discontinued in one patient because of urticaria, but the total number of side effects was higher with nifedipine (12 of 15 patients) than with diltiazem (5 of 15, p less than 0.01). Nine patients remained symptomatic on single drug treatment and entered open label treatment with the combination of diltiazem and nifedipine. Three patients did not tolerate the combination because of important side effects; the other six also had side effects, but these were relatively minor. Four patients received no more benefit from the combination than from a single agent; the condition of two patients improved. Both diltiazem and nifedipine provide effective antianginal therapy for coronary spasm, but diltiazem has fewer side effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of diltiazem and nifedipine alone and in combination in patients with coronary artery spasm. 354 92

Seven individuals with exercise-induced anaphylaxis under natural circumstances, characterized by the appearance of pruritic cutaneous erythema and urticaria and associated vascular collapse and/or upper respiratory tract symptoms and signs of angioedema, were subjected to a controlled period of exercise in a laboratory. Experimental challenge consisted of running in an occlusive suit on a treadmill of moving grade with maintenance or acceleration of speed for 5 to 17 min. Cutaneous pruritus and erythema without urticaria developed in four of the subjects and progressed to angioedema in two of them; the other three subjects were unaffected. Repeat challenge of three of the abnormal responders elicited a clinical response similar to that of the previous exercise challenge. In those subjects with a clinical response to exercise challenge, mean change from baseline levels of histamine to peak levels was 7.0 +/- 3.0 ng/ml (mean +/- SEM), whereas in the group without clinical symptoms the mean change from baseline was an increase of 0.6 +/- 1.6 ng/ml (mean +/- SEM). The abnormal elevations in serum histamine during the seven exercise-induced symptomatic episodes returned to normal in about 20 min while clinical signs were also subsiding. There were no changes in pulmonary function. Exercise-induced anaphylaxis is clinically separable from cholinergic urticaria and represents a distinct form of physical allergy.
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PMID:Exercise-induced anaphylaxis: a distinct form of physical allergy. 682 91

The single isotopic-enzymatic assay of histamine was modified to increase its sensitivity and to facilitate measurement of plasma histamine levels. The modification involved extracting 3H-1-methylhistamine (generated by the enzyme N-methyltransferase acting on histamine in the presence of S-[methyl-3H]-adenosyl-L-methionine) into chloroform and isolating the 3H-1-methylhistamine by thin-layer chromatography (TLC). The TLC was developed in acetone:ammonium hydroxide (95:10), and the methylhistamine spot (Rf = 0.50) was identified with an o-phthalaldehyde spray, scraped from the plate, and assayed in a scintillation counter. The assay in plasma demonstrated a linear relationship from 200 to 5000 pg histamine/ml. Plasma always had higher readings than buffer, and dialysis of plasma returned these values to the same level as buffer, suggesting that the baseline elevations might be attributable to histamine. However, all histamine standard curves were run in dialyzed plasma to negate any additional influences plasma might exert on the assay. The arithmetic mean (+/- SEM) in normal plasma histamine was 318.4 +/- 25 pg/ml (n = 51), and the geometric mean was 280 +/- 35 pg/ml. Plasma histamine was significantly elevated by infusion of histamine at 0.05 to 1.0 micrograms/kg/min or by cold immersion of the hand of a cold-urticaria patient. Therefore this modified isotopic-enzymatic assay of histamine is extremely sensitive, capable of measuring fluctuations in plasma histamine levels within the normal range, and potentially useful in analysis of the role histamine plays in human physiology.
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PMID:Measurement of plasma histamine: description of an improved method and normal values. 709 24

The effect of topical indomethacin on the weal and flare response was measured in 9 patients with chronic dermographic urticaria. An augmentation of dermographic wealing by topical indomethacin was shown with lowering of the weal threshold from 22.3 +/- 4.7 g/mm2 (mean +/- SEM, n = 9) to 16.4 +/- 3.8 (p < 0.005), but without a change in the shape of the force/response curve. Flare was increased by indomethacin particularly in patients with a greater lowering of the weal threshold. The augmentation of weal and flare by indomethacin in individual patients was not related to the degree of inhibition of UVB erythema in individual patients. These findings indicate that in chronic dermographic urticaria there is an abnormality involving eicosanoid production by a non-cyclo-oxygenase pathway. It is suggested that this acts by augmenting the effect of histamine on a new class of histamine receptor, the definition and antagonism of which should lead to better control of urticarial disease.
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PMID:Topical indomethacin aggravates the weal and flare response in chronic dermographic urticaria: evidence for a new class of histamine receptors. 809 60

Two studies of the additional effect of an H2 receptor antagonist when given in combination with an H1 antagonist were undertaken in dermographic urticaria. Using a randomized, double-blind, crossover design in 19 patients, a combination of cetirizine (10 mg at night) and ranitidine (150 mg twice daily) was compared with a combination of cetirizine (10 mg at night) and placebo. The addition of ranitidine did not produce any significant difference in linear analogue scores for weal, itch or sleep disturbance. There was a significant depression of the frictional force/wealing response curve with an increase in wealing threshold (P < 0.0001) following the addition of H2 blockade. The wealing threshold was 54.7 +/- 4.4 (mean +/- SEM) g/mm2 for the H1 antagonist alone, and 73.2 +/- 5.7 for the combination of H1 and H2 antagonists. In a second similar study involving nine different patients, comparing terfenadine (120 mg twice daily) with a combination of terfenadine and ranitidine (150 mg twice daily), the weal threshold was 59.8 +/- 6.6 for the H1 antagonist alone, and 73.0 +/- 6.4 for the combination of H1 and H2 antagonists. Thus, in dermographic urticaria, adding an H2 antagonist to treatment with a potent H1 antagonist gives a small, significant reduction in wealing response, but no symptomatic benefit. We conclude that involvement of the H2 receptor in this urticarial disease is minimal, and does not justify the use of H2 receptor antagonists.
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PMID:In dermographic urticaria H2 receptor antagonists have a small but therapeutically irrelevant additional effect compared with H1 antagonists alone. 825 54

The effect of cetirizine, 10 mg at night, on dermographic urticaria, was studied in 19 patients. The study design was a randomized, double-blind, crossover comparison with placebo, each treatment being given for 7 days. Patients kept a daily diary of itch and weal severity (100-mm linear analogue scale), and recorded sleep disturbance. The dermographic weal response was measured objectively with a spring-loaded stylus, and the weal threshold calculated from the force/response curve. There was a small, insignificant subjective response to placebo, but no objective response. On cetirizine, the subjective assessment of wealing was reduced from 34.3 +/- 6.7 (mean +/- SEM, 0-100 scale) to 16.8 +/- 4.1 (P = 0.02), itch was reduced from 43.2 +/- 6.6 to 19.4 +/- 4.1 (P = 0.001), and nights disturbed from 46.2 to 8.8% (P = 0.03). There was a shift to the right in the position of the force/response curve, and the wealing threshold increased from 24.6 +/- 3.2 to 54.7 +/- 4.4 g/mm2 (P = 0.00001), but there was no correlation between change in itch scores and wealing threshold. Cetirizine 10 mg daily is an effective treatment in dermographic urticaria, and its usefulness will depend on the prevalence of unwanted effects.
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PMID:The effect of cetirizine on symptoms and wealing in dermographic urticaria. 825 55

Cosmetics are a frequent cause of contact dermatitis, not only in females but also in males. Men use cosmetics in the form of deodorant, hair dye and aftershave lotions. U.S.A men spent more than 6,000,000,000 million dollars in cosmetic products. Responsible substances of contact dermatitis are unidentified in many occasions, what impedes the estimation of morbidity data. It is calculated that 2-4% of dermatological consultations are due to contact dermatitis caused by cosmetics. The Spanish industry manufactures each year articles valued in several thousands of million pesetas, 14% of which are exported. Annual manufacturing is raising between 10 and 11%. The French journal Cosmetology (IMS) pointed as an example the fact that in the third trimester of 1978, the number of sold products was as follows: 87,880 units of cleansing milk; 128,020 creams; 237,200 tonics; 10,228 lip protectors. The Committee of European Unions for Perfumery and Cosmetology (COLIPA) reported in 1978 a yearly sale in Europe of 225,000,000 units of hair dyes, exclusively. Adverse reactions to cosmetics affect not only the skin in the form of irritant or contact dermatitis, but cases of conjunctivitis, asthma, urticaria, rhinitis, angioedema, pneumonitis and anaphylaxis-like reactions due to cosmetic products, mainly hair bleaching agents, perm liquids and hair spray, have been also reported. The present work studied the prevalence of sensitizations to cosmetic products on the professional staff of a beauty salon in our city of Las Palmas (SEM). Twenty people came to our Unit of Allergology to fill a questionnaire and undergo a skin test.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prevalence of cosmetic sensitivity among beauticians]. 855 88

Background Acquired cold urticaria (ACU) is a physical urticaria characterized by local skin reactions after cold exposure. Objective markers of disease severity and activity would be helpful. Unfortunately, such markers are not yet available, even though stimulation time and temperature thresholds are promising candidates. Objectives We assessed and correlated critical temperature thresholds (CTTs) with disease severity and activity in patients with ACU. Methods CTTs were determined in 45 patients with ACU by TempTest-based cold contact stimulation tests (Emo Systems GmbH, Berlin, Germany), and ACU severity and activity were assessed using Likert scales. Results Patients with ACU exhibited mean +/- SEM CTTs of 17 +/- 6 degrees C (range 4-27 degrees C). These thresholds and their changes correlated with the severity (r = 0.53, P < 0.05) and activity of disease (r = 0.64, P < 0.05), respectively. Conclusions These findings indicate that temperature threshold measurements may be used for assessing disease severity and activity as well as the efficacy of therapeutic measures including novel treatment approaches for cold urticaria.
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PMID:Results and relevance of critical temperature threshold testing in patients with acquired cold urticaria. 1978 1