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)

A 27-year-old woman experienced pruritus, eye and throat irritation, hoarseness, shortness of breath, and fatigue within half and hour of exposure to carbonless copy paper. On two separate occasions, she was purposely challenged in a controlled-blinded fashion with portions of the carbonless copy paper. This resulted on both occasions in contact urticaria of the hand that held the paper and changes in pulmonary function flow-volume loops characteristic of upper airway obstruction. To determine if alterations in prostaglandin (PG) metabolism might explain these findings, plasma PGF2 alpha and thromboxane B2 (both capable of causing these symptoms) were measured before and during the second exposure period. Both PGF2 alpha and thromboxane B2 increased substantially. We conclude that the cutaneous and respiratory symptoms induced by carbonless copy paper were probably related to PG release.
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PMID:Contact urticaria and airway obstruction from carbonless copy paper. 623 81

The nonsedating histamine H1 receptor antagonist fexofenadine is the active metabolite of terfenadine. It reduced the allergic response in animal models of allergy and did not prolong the QT interval (QTc) in dogs or rabbits at plasma concentrations many times higher than those seen after administration of therapeutic dosages. Similarly, relative to placebo, fexofenadine did not affect mean QTc in patients given dosages of up to 480 mg/day for 2 weeks or in volunteers who received up to 800 mg/day for 6 days or 240 mg/day for 12 months. In a double-blind clinical trial, oral fexofenadine 120 or 180mg once daily controlled symptoms in patients with seasonal allergic rhinitis as effectively as cetirizine. Other double-blind clinical trials showed that fexofenadine 40 to 240mg twice daily was significantly more effective than placebo. Fexofenadine 180 or 240mg once daily was significantly more effective than placebo in patients with chronic idiopathic urticaria. The drug was well tolerated in these clinical trials, with an adverse event profile similar to that seen with placebo. The most common adverse events were headache, throat irritation, viral infection, nausea, dysmenorrhoea, drowsiness, dyspepsia and fatigue.
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PMID:Fexofenadine. 950 46

Introduction. The objective was to evaluate the toxicity of poisoning by metam sodium, a dithiocarbamate fumigant, the breakdown products of which are methyl isothiocyanate (MITC), carbon disulphide (CS2), and dihydrogen sulphide (H2S). Methods. This is a retrospective, observational case series of metam sodium exposure cases reported to the Angers Poison and Toxicovigilance Centre from 1992 through 2009. Results. A total of 106 cases of metam sodium exposure were recorded and 102 cases were included in this study. All cases of exposure were unintentional. Occupational poisoning occurred in eight cases. The most common route of exposure was inhalation (n = 96). In 79 cases, the patients were people living near fields where metam sodium had recently been applied. Most of the reported symptoms involved irritation of the eyes (n = 76), throat and nose (n = 65), attributable to MITC. Cough and dyspnoea occurred in four cases but no persistent, irritant-induced asthma or persistent exacerbation of asthma was observed. Sixteen patients at two different sites of pollution were exposed to emanations from the drainage system in their homes following the illicit discharge of metam sodium into the sewers. Most presented with nausea and headaches, but only four experienced eye or throat irritation. A breakdown product other than MITC was involved: air analysis at one site revealed the presence of CS2 (337 mg/m(3)) and no H2S. Two of these patients, who had consumed some alcohol, experienced dysgeusia but no disulfiram-like reaction. The only lethal case recorded was a truck driver who was found dead of acute lung injury after falling into a tank that had previously contained metam sodium. Two patients who ingested a dilute solution, presented with mild epigastric pain. Four skin exposures caused erythema (n = 2), moderate burns (n = 1), and urticaria (n = 1). According to the poisoning severity score, their symptoms were minor in 99% of cases. Conclusion. Acute metam sodium exposure usually causes minor symptoms. They vary as a function of the circumstances of exposure, which determine the degradation product that forms. On contact with moist soil, metam sodium decomposes into MITC and causes irritant symptoms. Under specific conditions, such as a spillage in the drainage system, metam sodium can degrade into CS2 and cause neurological signs.
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PMID:Metam sodium intoxication: the specific role of degradation products--methyl isothiocyanate and carbon disulphide--as a function of exposure. 2174 Jan 40