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 62 year-old female developed bronchospasm after intravenous vecuronium administration. Vecuronium is reported to have major advantages over pancuronium due to the lack of significant histamine-releasing activity and cardiovascular side effects. However, macular rash, systemic collapse and bronchospasm have been reported before. The patient received cholecystectomy under general anesthesia. She had a history of urticaria when she had had a intravenous pyelography and showed positive skin test to antibiotic, ceftizoxime. During induction with thiopental plus vecuronium and on addition of vecuronium, bronchospasm was induced within five minutes in each time. Both episodes of bronchospasms were relieved with intravenous aminophylline and methylprednisolone. During the operation arterial blood gas samples were taken twice and showed no abnormal findings. Further blood samples were taken for complement C3, C4, plasma IgE and white blood cell counts. Skin test to vecuronium was also performed. In spite of these data, the mechanism of bronchospasm remained obscure. Careful attention should be paid to the use of vecuronium, especially for the patient who showed allergic response to some drugs.
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PMID:[Possible bronchospasm after administration of vecuronium]. 167 99

Forty children (0-5 years old), presented with immediate contact urticaria, rash and often atopic dermatitis (n = 34). Redness or urticaria around the mouth appearing after consuming cow's milk or egg, were the major complaints in all. These symptoms suggested a food-induced immediate contact reaction, which can be immune-mediated or irritative. To reinduce this reaction, a skin provocation test, called SAFT, was performed. SAFT stands for Skin Application Food Test. This test is based on direct skin contact, during a maximum of 30 min with food in its 'ordinary consumptive state'. The SAFT can be regarded as a 'physiological' provocation patch test. If positive, contact urticaria develops most often within a few minutes. The results of SAFT and IgE RAST correlated significantly well. Total IgE values were not informative. The rapid onset of the SAFT reaction, induced by proteins, supported by RAST results, strongly indicates an immune-mediated mechanism. In 52% of the 34 patients with atopic dermatitis, dermatitis was exacerbated following food-to-skin contact. Immune-mediated contact reactions to foods play an important role in (dermal) food allergy.
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PMID:Immediate contact reactions to cow's milk and egg in atopic children. 167 37

An open comparative trial of nizatidine in the treatment of duodenal ulcer (DU) was carried out with cimetidine as control. Forty-three patients with endoscopically proven DU were recruited into the study. Twenty-three patients were assigned to treatment with nizatidine 300 mg daily and 20 patients (controls) were on cimetidine 800 mg daily. Both groups were comparable in age and sex distribution - age range 21 to 74 years; mean 53.4 years and 43 years in the nizatidine and cimetidine groups respectively. Liver function tests, full blood counts, platelets, urea, electrolytes were done together with endoscopy at four, eight, twelve weeks. In the nizatidine group, 16 patients completed the study whilst 17 patients on cimetidine completed the study. Healing rates at four and eight weeks on nizatidine were 9/16 (56%) and 14/16 (87.5%) respectively. On cimetidine, healing rates at four and eight weeks were 14/17 (80%) and 16/17 (94%) respectively. There was no statistical difference in healing rates between the two groups at four and eight weeks (p = 0.1, p = 0.47). One patient on nizatidine developed urticaria rash which resolved on drug withdrawal. No other adverse clinical or biochemical effects were observed in the cohort after twelve weeks of treatment. Nizatidine is as effective as cimetidine in healing DU at four and eight weeks.
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PMID:Nizatidine versus cimetidine in the treatment of duodenal ulcers. 167 16

Reactions to intravenous protamine include rash, urticaria, bronchospasm, hypotension, and/or pulmonary artery pressure elevation. We have previously shown that in diabetic patients receiving daily protamine-insulin injections, the presence of anti-protamine IgE or IgG antibodies are significant risk factors for acute, life-threatening reactions when protamine is given intravenously. To study protamine reactions further, we measured serum anti-protamine IgE and IgG antibody levels, in-vitro basophil histamine release and intracutaneous skin testing to protamine serially in an NPH-insulin dependent diabetic who had a severe, protracted anaphylactic reaction to protamine. At the time of his protamine reaction, his serum contained 8.5 ng/ml of anti-protamine IgE and 1.3 micrograms/ml of anti-protamine IgG antibody. One month following the reaction both anti-protamine IgE and IgG increased to 16 ng/ml (twofold rise) and 90.5 micrograms/ml (70-fold rise), respectively. With time, both anti-protamine IgE and IgG antibody declined. Serial intradermal skin tests using protamine sulphate did not discriminate between the protamine reactor and nine normal control subjects who had no prior exposure nor any demonstrable serum IgE antibody to protamine. In-vitro basophil histamine release to protamine sulphate was inconclusive in discriminating between the protamine reactor and normal control subjects. We postulate that protamine may be an incomplete or univalent antigen that must first combine with a tissue macromolecule or possibly heparin to become a complete multivalent antigen capable of eliciting IgE antibody-dependent mediator release.
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PMID:Serial immunological investigations in a patient who had a life-threatening reaction to intravenous protamine. 170 34

A 35-year-old woman had since early childhood suffered from recurrent urticaria-like rash, intermittent fever, arthralgia and pancochlear inner-ear deafness. At the age of 17 years she also developed a steroid-resistant nephrotic syndrome, found to be due to renal amyloidosis (type AA). The triad of renal amyloidosis, inner-ear deafness and recurrent urticaria is characteristic of Muckle-Wells syndrome, which has a hereditary basis. Rapidly progressive renal failure necessitated long-term haemodialysis and two renal transplantations. The accompanying immunosuppressive treatment with corticosteroids, azathioprin and, later, cyclophosphamide brought about a remission of the joint and skin abnormalities. After removal of the first donor kidney and termination of immunosuppressive treatment the syndrome recurred with subacute growth of an amyloid goitre as well as amyloidosis of the optic nerve. A few weeks before death a malignant non-Hodgkin lymphoma of the stomach was demonstrated. It was presumably a complication of long-term immunosuppression and not of the Muckle-Wells syndrome. The patient died of the complications of combination chemotherapy. Necropsy revealed generalized amyloidosis.
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PMID:[Complications in the course of the Muckle-Wells syndrome]. 173 60

Recent advances in medicine, such as cardiac catheterization, phoresis, dialysis, and cardiopulmonary bypass technology, have increased the need for heparin anticoagulation. To antagonize heparin's effect and prevent hemorrhagic complications after the procedure, protamine has likewise been used more frequently. With its increased use have come increased reports of adverse protamine reactions consisting of rash, urticaria, elevation of pulmonary artery pressure, systemic hypotension, and, at times, death. The elevation of pulmonary artery pressure, which appears to be a rather common occurrence in animals, may be an isolated finding without clinical consequences in humans. However, this pulmonary vasoconstriction may, when severe, lead to acute right-sided heart failure and systemic hypotension. Other protamine reactions involve a decrease in systemic vascular resistance and systemic hypotension without changes in pulmonary artery pressure. Causes of acute protamine reactions may involve the generation of anaphyatoxins and prostanoids either from protamine-heparin complexes or complement-fixing antiprotamine IgG antibodies, from inhibition of plasma Carboxypeptidase N, from crosslinking of cell-surface antiprotamine IgE on mast cells and basophils with subsequent mediator release, or from potentiation of IgE-mediated release of histamine through a polycationin-recognition site. Although we have come a long way in understanding the mechanisms by which protamine can cause its ill effects in humans, more work is clearly needed to define, in prospective studies, the incidence of and risk factors for protamine reactions in various patient groups, and to delineate more clearly which mechanisms are involved in each clinical type of acute protamine reaction. Hopefully, this will lead to strategies and protamine alternatives that will prevent or diminish, in frequency or severity, adverse protamine reactions. Alternatively, a clearer picture of the risk factors important for protamine reactions and the predictive value of diagnostic tests (e.g., protamine IgE antibody) can also minimize the clinical impact of this increasingly common adverse event.
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PMID:Allergy to protamine. 178 26

The paper comprises 63 patients with diagnosed vasculitis of the skin who had abnormal findings in the urine. Thirteen of these patients had positive skin findings and abnormal findings in the urine, with concomitant attacks of dyspnea as seen in bronchial asthma. These patients account for 20% of the entire group, while there was an incidence of 37% of systemic manifestations. Skin findings: 45% had a maculopapular rash, 36% had urticarial findings, 13% had urticaria and angioedema and 6% had angioedema alone. Nonspecific biologic syndrome of evolution was statistically significant while no significant changes were found in the number of white blood cells and eosinophils. The degree of proteinuria ranged from 0.1 g/L to 1.16 g/L. Most patients with proteinuria above 0.25 g/L had microhematuria. Slightly over 50% of the patients had signs of complement activation by the alternative pathway, along with the presence of cryoglobulins. Increased histamine in the serum was found in over 50% of the patients although the values of histamine did not correlate with the degree of proteinuria. Proteinuria was not detected in patients with very high values of histamine (and without signs of vasculitis), which indicates that histamine itself responsible for changes in the glomeruli. There is a possibility that local tissue hyperhistaminemia is responsible for the increased permeability of the basal membrane of the glomeruli. According to the obtained results, the etiology of proteinuria and microhematuria should be pursued in the pathogenesis of vasculitis as signs of complement activation indicate. Other possible causes for proteinuria were excluded. The proteinuria was selective, benign according to its course and degree, occurred concomitantly with skin findings and was absent during remission of the disease.
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PMID:[Proteinuria in dermal vasculitis (incidence, degree and possible mechanisms of onset)]. 191 47

Side-effects of proguanil reported to the Swedish Adverse Drug Reaction (ADR) register from 1981 to 1988 are described and related to sales figures of the drug in Sweden during the same period. One serious reaction, thrombocytopenia, and 7 minor reactions, mainly urticaria and exanthema were believed to be causally related to proguanil intake in an estimated 60,000 users of the drug. Proguanil can be considered a very safe drug but rare hematological side-effects may possibly occur.
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PMID:How safe is proguanil? A post-marketing investigation of side-effects. 195 33

Multiple antibiotic sensitivity (MAS), a common but complex clinical problem, has not been reviewed in the pediatric population. We evaluated 120 children with a history of MAS. The offending antibiotics were beta lactam (186 adverse reactions), sulfonamide (86 adverse reactions), macrolide (32 adverse reactions), erythromycin/sulfisoxazole (26 adverse reactions), aminoglycoside (2 adverse reactions), and tetracycline (2 adverse reactions). Urticaria occurred in 183 reactions, followed by polymorphous rash (n = 71), angioedema (n = 19), erythema multiform (n = 9), bronchospasm (n = 8), arthralgia (n = 7), serum sickness (n = 4), and laryngeal edema (n = 3), the mean age for the first reaction was 3 years (range 1 month to 13 years). Adverse reaction to three classes of antibiotics were noted in 22 patients, and two patients were noted to have adverse reactions to four or more antibiotic classes. Skin tests (ST) were performed in 98 children using penicillin G, a commercial benzyl penicilloyl polylysine, a minor determinant mixture, and a beta lactam analog. Positive ST were noted in 26% (31/120) of the MAS patients. Children with a history of MAS are likely to have true IgE-mediated reactions as documented by positive immediate hypersensitivity reactions to penicillin and/or its minor determinants. Therefore, MAS patients should be carefully evaluated for antibiotic sensitivity and not be assumed to have sensitivity to drug formulation as a basis for MAS.
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PMID:Multiple antibiotic sensitivity in a pediatric population. 195 73

The clinical efficacy of cefodizime has been tested in several open and comparative studies, above all in lower respiratory tract infections (LRTI) and uncomplicated urinary tract infections (UTI), performed in 151 centres in Europe, Latin America, South-Eastern Asia and South Africa. Of 3791 patients, 2260 could be evaluated for efficacy and safety. Comparative studies in LRTI were carried out vs cefotaxime and cefuroxime (301 vs 299 patients); both clinical and bacteriological results were superimposable (range of satisfactory clinical outcomes from 86% to 95%; bacteriological eradication 95% to 100%). In open studies (533 evaluable patients) the percentage of clinical successes ranged from 79.1% to 91.8% and the bacteriological eradication from about 87% to 90%, according to the type of infections. Comparative studies (cefodizime vs cefuroxime or ceftizoxime) in UTI again demonstrated the equivalence of treatment. In open studies (374 evaluable patients) the percentage of satisfactory clinical outcomes ranged from 84.6% in complicated upper UTI to 95.9% in lower uncomplicated UTI, with overall bacteriological eradication of 92.7%. Side effects could be evaluated in 5801 patients (Western and Japanese clinical studies); 3.79% of patients showed side effects (1.99% gastrointestinal disturbances, 0.9% rash or urticaria, 0.9% other effects); 1.13% of patients required discontinuation of treatment. No relevant changes in laboratory parameters were observed. Cefodizime has been shown to be an effective and safe agent in the treatment of LRTI and UTI caused by susceptible pathogens. A dosage regimen of 1 g every 12 h seems to be the most suitable schedule for the treatment of LRTI while 1 g every 12 h or 2 g every 24 h can equally well be adopted for treatment of UTI.
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PMID:Cefodizime in clinical use: a review of the clinical trial reports. 207 46


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