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)

Among all the known drug intolerances, adverse reactions to heparin are not very common. No desensitization in patients with heparin hypersensitivity has ever been attempted. We report the case of a 55-year-old female patient with mitral stenosis and insufficiency, and tricuspid and aortic insufficiency. The patient underwent heparin treatment, and urticaria occurred with either s.c. calcium heparin or i.v. sodium heparin. Allergy testing (skin tests and patch tests) was negative. A pseudoallergic intolerance was diagnosed. Mitral valve replacement with the extracorporeal circulation method was necessary; therefore, heparin treatment was administered. A heparin rush desensitization together with antihistamine drugs (4 mg clorpheniramine maleate for 3 d) was started: 50 UI (0.5 mg) s.c. sodium heparin were first administered; within 4 d, 5000 UI (50 mg) sodium heparin was administered i.v. with no side-effects. A full-dosage heparin treatment was then administered and heart surgery was easily performed. During the postsurgical course, i.v. sodium heparin was smoothly replaced with s.c. calcium heparin (25,000 UI s.c. per day) and with oral anticoagulants (sodium warfarin).
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PMID:Rush desensitization in heparin hypersensitivity: a case report. 803 62

Sequential skin testing including immediate patch test (IPT), skin prick test (SPT), and intradermal test (IT) with sodium benzylpenicillin G (Pen G), and SPT with benzylpenicilloyl human serum albumin (BPO-HSA) was done in 58 subjects with a history of probable anaphylactic reaction or shock of unknown cause. Based on positive skin tests, the diagnosis of penicillin anaphylaxis was confirmed in 30 patients. The average age of onset of penicillin allergy was 42 years ranging from 20-70 years. The sex ratio was 2:28 with marked female predominance. Anaphylactic shock, wheezing and urticaria occurred in 21, 20, 19 patients, respectively. Most symptoms were induced by skin tests and inhalation. The results of skin tests in these patients showed that IPT with 500 U/ml of Pen G was not only reliable but also safe. It is suggested that patients suspected of penicillin anaphylaxis should received IPT with 500 U/ml of Pen G as the initial diagnostic step; if a negative reaction occurred, then SPT and IT should be applied with the same concentration of Pen G, until a positive reaction developed or all the skin testing showed negative results. SPT to BPO-HSA was safe, but its positive rate was only 47.8% in our study; it seems to be less important than skin test to Pen G. As a whole, the skin testing procedure we recommend is relatively reliable, safe and practical even in individuals extremely sensitive to penicillin. In addition, once the patient develops a positive IPT, Pen G residue on the testing site should be wiped away rapidly and washed out with cool water thoroughly to disrupt further violent reaction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Skin testing in patients with high risk of anaphylactic reactions to penicillin. 821 54

Since the introduction of sodium metabisulfite as a food preservative, it has been associated with several idiosyncratic reactions (eg, bronchospasm, oculonasal symptoms, and urticaria/angioedema) in sulfite-sensitive individuals. The pathogenic mechanism of these reactions is not yet understood. We report the case of two crewmen on a shrimp trawler who were found dead in the ship's hold. Their deaths had occurred while they were applying dry sodium metabisulfite, referred to as "shrimp dip" in the shrimping industry. Postmortem examinations showed diffuse pulmonary edema consistent with death secondary to asphyxia. Associated findings were visceral congestion. Although it is possible to measure death from sodium metabisulfite with available records, its potential morbidity cannot be estimated. It is known that sodium metabisulfite can react with acids and water, releasing toxic sulfur dioxide (SO2) gas. In addition, SO2 gas reacts with respiratory tissue forming sulfureous acid, and inducing a pulmonary reaction causing hypoxemia. Furthermore, sodium metabisulfite, compared with sodium bisulfite, has a much greater propensity to release SO2 gas. We conclude that there is a need for improved education regarding the potential side effects of sodium metabisulfite, thus eliminating needless occupational morbidity and mortality.
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PMID:Sodium metabisulfite and SO2 release: an under-recognized hazard among shrimp fishermen. 826 51

Recognition of sulfite sensitivity by the practicing dermatologist has become increasingly important. A wide spectrum of anaphylactoid reactions can occur after ingestion of sulfite additives in foods and medications. We report the case of a 47-year-old man with severe acute intermittent urticaria. A placebo-controlled oral challenge test with 50 mg sodium disulfite resulted in an acute urticaria attack. A biopsy taken 5 h after the appearance of the urticaria demonstrated a leukocytoclastic vasculitis with eosinophilia. Avoiding foods and drugs containing sulfites is often difficult due to its widespread use. Therefore, the patient should be equipped with a medical emergency kit.
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PMID:Disulfite-induced acute intermittent urticaria with vasculitis. 827 92

Metabisulfite sensitivity is being described with growing frequency. Sulfites are used in food, drinks, and drugs. Adverse reactions to apparently nontoxic doses have been described. Exposure of sensitive persons to sulfites has produced asthma, and occasionally other adverse reactions in nonasthmatic patients. We present a case of urticaria induced by metabisulfites. During the previous 2 years the patient had suffered episodes of urticaria and angioedema limited to the face, neck, upper thorax, and dysphonia without asthma after the ingestion of food and drinks containing sulfites. Oral challenge with 25 mg of potassium metabisulfite elicited urticaria on the face and neck, nasal itching, rhinorrhea, and dysphonia. Prick and intradermal tests were negative. Two further challenges with the same doses were also positive. One of these was controlled with placebo, 30 minutes after oral administration of 400 mg sodium cromolyn; the second was carried out 90 minutes after oral administration of 5000 micrograms cyanocobalamin. We have been unable to identify a pathogenic mechanism.
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PMID:Sulfite-induced urticaria. 837 95

We have experienced two cases of anaphylactoid reactions following intravenous methylprednisolone sodium succinate administration. They had neither asthmatic nor other allergic histories. The first case was a 45-yr-old man. In addition to the antigenicity of hydrocortisone itself, it is suggested that administration speed was so fast that its side effects were intensified. The second case was a 10-yr old girl. Succinate ester was thought to be the cause of her allergic reaction (urticaria). It is also possible that her hypersensitivity to steroids was dose-dependent.
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PMID:[Two cases of anaphylactoid reactions after intravenous methylprednisolone sodium succinate administration]. 843 80

Occupationally induced hypersensitive reactions towards chemical compounds are increasingly observed. In this regard ammonium persulfate (APS) is reported as an inducer of erythema, urticaria, eczema, rhinitis and bronchial asthma. On the basis of these reactions, persulfates obviously show some characteristics of skin-sensitizing as well as respiratory allergens. We measured the effect of APS on the release of inflammatory mediators, i.e. leukotriene B4 (LTB4), from human polymorphonuclear neutrophils (PMN). The effect of the persulfate was analyzed in comparison of the corresponding sulfate. After different cellular activation either with the Ca ionophore A23187, the tripeptide formyl-methionyl-leucyl-phenylalanine (fMLP) or sodium fluoride (NaF) coincubation of PMN with APS led to a diminished generation of LTB4. In addition it was demonstrated that APS decreased the stability of leukotrienes in cell-free systems. However, cells which were preactivated with APS and subsequently washed showed an increase in leukotriene formation after stimulation with fMLP or NaF but not with the Ca ionophore. Thus, the concentration of APS at local tissue sites as well as the occurrence and nature of a secondary cell-activating stimulus finally determine to what extent persulfates will interfere with cellular functions, e.g. mediator suppression or induction, which are then responsible for clinical disease processes.
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PMID:Dual effect of ammonium persulfate on the generation of leukotrienes from human neutrophil granulocytes. 876 98

Sulfite is commonly used in pharmaceuticals as a preservative. We report a unique clinical presentation of localized periorbital edema on the left eye after administration of sulfite-containing dexamethasone. The patient's sulfite sensitivity was confirmed by sulfite oral provocation test: periorbital edema on the same site developed after ingestion of 200 mg sodium bisulfite. She was non-atopic and did not complain of any respiratory symptoms. Allergy skin prick test with 100 mg/ml sodium bisulfite showed a negative result. She also has aspirin-sensitive urticaria which was confirmed by oral provocation test. In conclusion, sulfite can induce a localized periorbital edema, an uncommon manifestation in sensitive patients. Further investigations are needed to clarify the pathogenetic mechanisms.
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PMID:Localized periorbital edema as a clinical manifestation of sulfite sensitivity. 887 7

In a retrospective analysis, 79 allogeneic bone marrow recipients treated with AmBisome prophylactically or because of proven or suspected invasive fungal infection (IFI) were evaluated in 92 episodes. The median duration of treatment was 14 (range 1-112) days. The mean maximum dose given was 1.64 +/- 0.8 mg kg-1 day-1 and the mean total dose was 1.29 +/- 2.28 g. The overall incidence of reported adverse events was 194, of which none had a serious outcome. In six cases, the drug was withdrawn as a result of toxic or allergic reactions: dyspnoea and flush (3), urticaria (1), cholecystitis (1) and disorientation (one case, probably not related to AmBisome). No anaphylactoid reactions were seen. Laboratory findings, including low serum potassium (48% of the episodes), increased serum creatinine (38%) and increased serum sodium levels (7%), caused no major clinical problems. Thirteen cases of verified IFI were evaluated regarding the efficacy of AmBisome. Survival or cure of the mycotic infection occurred in 5/13 patients (38%). Two patients were treated with AmBisome (3.6 and 3.3 mg kg-1 day-1) because of verified IFI before BMT. One died of IFI. The other died of venoocclusive disease of the liver (VOD) without histological evidence of active IFI. We found a significant (P < 0.05) reduction in autopsy-proven IFI, 12/199 (6%) compared to the period when only conventional doses of amphotericin B were used, 26/227 (11%).
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PMID:Safety and efficacy of liposomal amphotericin B in allogeneic bone marrow transplant recipients. 890 28

We report two cases of vasospastic angina associated with anaphylactic reaction caused by nonsteroidal anti-inflammatory drugs (NSAIDs). Both patients exhibited anaphylactic manifestations, such as general rash and urticaria, along with angina pectoris with electrocardiographic ST-segment elevations after suppository administration of diclofenac sodium or indomethacin, the most commonly used NSAIDs. Although these patients had normal coronary arteriograms, intracoronary administration of ergonovine or acetylcholine provoked diffuse coronary artery spasms accompanied by chest pain and ischemic ST-segment changes. It is therefore suggested that an allergic mechanism may be involved as a causative factor of the coronary artery spasm induced by NSAIDs.
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PMID:Vasospastic angina induced by nonsteroidal anti-inflammatory drugs. 922 Jan 83


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