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 use of the urine histamine metabolite, N-methylhistamine (N-MH), as a parameter of histamine release in immediate allergic reactions was investigated. Baseline levels were determined in 34 normal control subjects and 29 atopic patients. Increases of urine N-MH values were measured during histamine infusions and in venom-allergic patients receiving bee-sting challenges. N-MH was determined by a newly developed radioimmunoassay. Baseline levels in control subjects and atopic patients demonstrated no significant differences. With regard to challenge tests, fluctuation of N-MH levels during a 6-hour period was measured. Random 6-hour increases in healthy and atopic subjects ranged from 5% to 41%. Before infusion of histamine (0.25 micrograms/kg/min for 30 minutes), baseline values were 137 +/- 11.4 micrograms N-MH per gram of creatinine and 9 +/- 1.1 micrograms N-MH per hour (n = 9). Levels peaked 1 hour after infusion at 275 +/- 45 micrograms/gm of creatinine and 44 +/- 5.6 micrograms/hr and decreased to resting levels after 2 hours. Metabolization by N-MH accounted for 9.5% +/- 4.9% (range, 2.4% to 18.4%) of infused histamine in the urine of the nine subjects. Bee-sting challenges were performed in 12 patients and three control subjects. Only in three patients experiencing generalized urticaria, nausea, dyspnea, and hypotension were significant increases of urine N-MH levels (138%, 144%, and 238%) observed. All other patients and three normal control subjects demonstrated normal local reactions without increase of N-MH values.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Determination of N-methylhistamine in urine as an indicator of histamine release in immediate allergic reactions. 170 26

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

Histamine plays a key role in the pathogenesis of chronic urticaria (CU). The authors of this paper have studied the effects of ingested histamine in 25 patients with CU. A 120 mg dose of histamine, well-tolerated in the healthy subject, was instillated into the duodenum. Concomitantly, plasma histamine (H) levels and plasma and urinary methylhistamine (MH) levels were measured. Intraduodenal administration of histamine was responsible for the development of an attack of urticaria in 64% of patients, while control subjects were asymptomatic. Plasma histamine levels were significantly higher after digestive histamine challenge (DHC) in patients with CU compared with controls. An abnormal increase in plasma histamine was observed in 72% of them. Plasma MH exhibited the same kinetic behaviour with a usually delayed time-pattern. Urinary MH concentration was higher in patients presenting with early-onset urticaria during the first hour than in those with the late-onset type between 1 and 12 hr after DHC. The coefficient of methylation (plasma MH/MH+H) was not significantly different in patients presenting with an attack of urticaria following DHC and in other subjects. Urinary excretion of MH and urinary flow increased significantly in patients presenting with an attack of urticaria following DHC which corresponds to increased absorption of histamine during the 5-hr period following DHC and its role on excretion by the kidney via vasodilation which it induces. This study demonstrates the abnormal frequency of disturbances in the metabolism of exogenous histamine in patients with CU. Increased plasma H accounts for the abnormal passage of H across the intestinal barrier which can result either from intestinal hyperpermeability and/or a deficit in the enzymatic catabolism of histamine. The systems of methylation and urinary clearance of MH appear to be effective. It is thus postulated that there is a deficit in diamine oxidase (DAO) in the enterocyte. The lack of correlation between the kinetic behaviour of plasma H and the onset of urticaria draws attention to the extent of individual variability in skin reactivity to histamine.
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PMID:Abnormalities in histamine pharmacodynamics in chronic urticaria. 1077 95

Adverse reactions to antibacterial agents are not uncommon in children. They are classified as 'immediate' or 'nonimmediate' according to the time interval between drug administration and onset. Immediate reactions occur within 1 hour and are manifested by urticaria and/or angioedema, bronchospasm and anaphylactic shock; immunological reactions are mediated by IgE antibodies. The main nonimmediate reactions (occuring after more than 1 hour) are maculopapular rash, urticaria and serum sickness; T lymphocytes may participate in maculopapular rash. Clinical assessment of such reactions is complex. The patient's history is fundamental; the allergological examination includes in vivo and in vitro tests selected on the basis of the clinical features and the phase of reaction. In the late phase, prick and intradermal tests are sensitive in evaluating beta-lactam allergy. Together with delayed-reading intradermal testing, patch testing seems to be useful in diagnosing maculopapular reactions to systemically administered aminopenicillins. Determination of specific IgE levels is the most common in vitro method for diagnosing immediate reactions. In the acute phase, serum tryptase and urinary N-methylhistamine assays are reliable in diagnosing type I pathogenic mechanisms in immediate reactions. Unfortunately, there are few in vitro tests for evaluating other reactions, and most are not fully validated. In selected cases, provocation tests should be performed.
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PMID:Recognising antibacterial hypersensitivity in children. 1093 62