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 55-year-old woman with rheumatoid arthritis in overlap with polymyositis received sulfasalazine for control of synovitis. Cholestatic jaundice, fever, urticaria and agranulocytosis developed after 20 days of treatment and culminated in fatal adult respiratory distress syndrome secondary to Legionella pneumophila. The increasing use of sulfasalazine in the therapy of rheumatoid arthritis mandates that the clinician be aware of this idiosyncratic drug reaction.
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PMID:Cholestasis and fatal agranulocytosis complicating sulfasalazine therapy: case report and review of the literature. 288 Sep 97

Excluding the most frequent kinds of problems seen with the nonsteroidal antiinflammatory drugs (NSAID)--gastritis, peptic ulceration and renal effects--published reports indicate that these drugs may cause a wide variety of rare adverse reactions. The most serious of these are hypersensitivity reactions: blood dyscrasias (aplastic anemia, thrombocytopenia, agranulocytosis, hemolytic anemia), erythema multiforme and hepatitis. Aseptic meningitis and anaphylactoid reactions may strike patients with underlying immunologic abnormalities; urticaria, bronchospasm and proctocolitis may affect aspirin-sensitive patients. Other unusual reactions include several kinds of bullous dermatitis, febrile reactions, pneumonitis, esophageal ulceration, parotitis, pancreatitis and neurological or psychological effects.
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PMID:Rare adverse reactions to nonsteroidal antiinflammatory drugs. 398 96

We report our experience with 8 patients with Felty's syndrome who were treated with D-penicillamine for a mean of one year. Six of the 8 patients experienced improvement in their neutropenia. Cutaneous ulcers healed in 4 of 6, while recurrent infections cleared in 3 of 5 patients. The drug was withdrawn in 6 patients--lack of response in one, thrombocytopenia in one, urticaria in one, rash in one, and granulocytopenia in 2. One of the latter 2 patients developed pancytopenia and died. Although D-penicillamine is effective in treatment of Felty's syndrome, its side effects can be serious and potentially lethal. Its use should be limited to patients who have failed other treatments.
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PMID:D-penicillamine in Felty's syndrome. 405 91

Between 1969 and 1979 a course of either propylthiouracil or carbimazole was given to 102 patients with Graves' disease. Ten of the patients discontinued the therapy because of adverse reactions or persisting symptoms, and 40 relapsed at some time after cessation of the therapy, giving a proportion of total failures of 49%. The proportion of such failures increased from 45% in 1969-72 to 57% in 1973-79. The probability of relapse was significantly higher in 1973-79 than in the earlier period (p less than 0.01). Patients aged 30-39 years had the highest proportion of failures (55%), but the mean time until relapse (6 months) was shortest in patients older than that. Adverse reactions--agranulocytosis, leukopenia, urticaria and elevated serum levels of liver enzymes--were seen in 12 patients. Six patients developed hypothyroidism after a mean time of 3.5 years after termination of thionamide therapy.
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PMID:Relapses after thionamide therapy for Graves' disease. 689 89

Aclacinomycin A (ACM-A), an anthracycline analog, was given to 17 patients with solid tumors and to one patient with multiple myeloma, in a phase I clinical trial. A single dose of 60-120 mg/m2 was given every 3 weeks. Dose-limiting toxicity was myelosuppression, especially thrombocytopenia. Granulocytopenia was variable and did not always recover by Day 21 in time for the next ACM-A treatment. Other toxic effects were nausea, vomiting, urticaria, and elevation of hepatic enzymes. Alopecia was not a side effect, even in patients receiving multiple courses of ACM-A. Nine patients were monitored with 24-hour continuous ECG recordings (Holter) on 19 ACM-A treatment days. The incidence of premature atrial and ventricular beats was significantly increased following ACM-A administration. In addition, one patient developed episodes of high-degree atrioventricular block and complete heart block after each of four ACM-A doses, necessitating the insertion of a pacemaker. No antitumor responses were seen in the ten patients who had measurable disease and who had received two or more courses of ACM-A. The recommended doses for solid tumor phase II studies are 100 mg/m2 as a single dose every 4 weeks for patients with high performance status and minimal prior chemotherapy and 60 mg/m2 every 4 weeks for all other patients. Until the acute cardiac effects of ACM-A are further understood, we recommend that all patients receiving ACM-A be monitored by ECG recordings.
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PMID:Phase I trial of aclacinomycin A. 695 61

The general features of allergic drug reactions in man have recently been reviewed by Parker (85). By definition allergic drug reactions are produced by specific immunologic processes. Allergic drug reactions must be distinguished from adverse reactions due to overdosage, normal pharmacologic action, toxic metabolite formation, idiosyncrasy, nonspecific release of pharmacologic effector molecules, or drug interactions. The clinical manifestations of drug allergy are quite protean. In addition to classical manifestations of allergy such as serum sickness, anaphylaxis, contact dermatitis or urticaria, drug allergy may produce hemolytic anemia, thrombocytopenia, granulocytopenia, hepatitis, nephritis, pneumonitis, vasculitis, or neuritis where a single organ or cell type is affected. While many drugs produce reactions with suggestive of allergy, definitive experimental evidence either for or against mechanism is usually not available. Some of these reactions may involve allergic mediators released or produced nonimmunologically through pharmacologic, osmotic, or toxic effects on cells involved in immune inflammation (mast cells, basophils, phagocytes, and lymphocytes) or through nonspecific activation of effector molecules in extracellular fluid such as the complement proteins. Drugs may also induce the formation of autoantibodies through mechanisms that are largely obscure, but may in some instances involve the direct participation of the drug as a hapten and in other instances occur indirectly through a pharmacologic or toxic action on the cells responsible for immune homeostasis.
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PMID:Allergic reactions in man. 704 Nov 44

Omeprazole has been marketed in France since 1989, for the healing of peptic ulcers, erosive reflux esophagitis and the Zollinger Ellison syndrome. It is a proton pump inhibitor which inhibits the acid secretion in the stomach. In the majority of the clinical trials, omeprazole has been found to be well tolerated: headache, dizziness, skin rash, constipation have just been noted. Since September 1989, 143 adverse reactions have been reported to pharmacovigilance centres and Astra France: 37 neurological and psychiatric side effects, especially confusion in patients with hepatic diseases and/or advanced age; 35 cutaneous reactions, generally rash and urticaria; 22 hematological effects: leucopenia and agranulocytosis have been reported but the relation with omeprazole is very uncertain; 10 gastrointestinal effects, generally diarrhoea, nausea, vomiting and abdominal pain; 8 hepatic disorders, especially moderate elevation of aminotransferases. This study confirms the safety of this drug, during short treatment; the frequency of notified adverse effects is about 1/12 200 treatments of 4 weeks. The ministry of health, has decided, in november 1991, to inform the prescribers of this potential toxicity of omeprazole, particularly, of the risk of confusion, hepatotoxicity and leucopenia.
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PMID:[Evaluation of unexpected and toxic effects of omeprazole (Mopral) reported to the regional centers of pharmacovigilance during the first 22 postmarketing months]. 814 27

Propylthiouracil (PTU) is usually the first choice for the treatment of hyperthyroidism, but it has serious side effects such as hepatitis, cholestatic jaundice, splenomegaly and lupus-like syndrome, in addition to mild and common side effects like granulocytopenia, pruritus, urticaria and maculopapular or papular eruption. Antineutrophil cytoplasmic antibody (ANCA)-positive vasculitis is another serious side effect. A 14-year-old female receiving PTU treatment for hyperthyroidism was referred to our clinic with fever, cough and dyspnea. The PTU dosage was first decreased but pericardial, dermal and joint involvement ascribed to PTU developed later and the drug was discontinued. ANCA-positive vasculitis due to PTU was considered when tests revealed an ANCA-positive state. We suggest that severe multisystemic vasculitis due to PTU should be considered during PTU usage.
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PMID:Propylthiouracil-induced hypersensitivity syndrome. 1684 20

Antithyroid drugs have been widely used in the treatment of hyperthyroidism. However, these drugs are known to have significant side effects. There are minor side effects such as skin rash or urticaria and major side effects. Especially, agranulocytosis and MPO-ANCA related vasculitis syndrome are the most serious, and although it occurs infrequently, it is clinically important, and clinicians must be alert to it when using antithyroid arugs. The author describes about the issues of side effects induced by antithyroid drugs.
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PMID:[Issues of side effects induced by antithyroid drugs]. 1715 87

Acquired agranulocytosis is a rare, life-threatening disorder. The few known causes/associations usually are readily identifiable (e.g., drug reaction, Felty syndrome, megaloblastosis, large granular lymphocytic leukemia, etc.). We report a novel association with mast cell disease. A 61-year-old morbidly obese man developed rheumatoid arthritis unresponsive to several medications. Agranulocytosis developed shortly after sulfasalazine was started but did not improve when the drug was soon stopped. Other symptoms across many systems developed including hives and presyncope. Marrow aspiration and biopsy showed only neutropenia. Serum tryptase was mildly elevated; urinary prostaglandin D2 was markedly elevated. Other causes were not found. Mast cell activation syndrome (MCAS) was diagnosed. Oral antihistamines, montelukast, and cromolyn were unhelpful; aspirin was initially felt contraindicated. Imatinib immediately increased neutrophils from 0% to 25% but did not help symptoms; subsequent addition of aspirin increased neutrophils further and abated symptoms. Different presentations of different MCAS patients reflect elaboration of different mediators likely consequent to different Kit mutations. Mast cells (MCs) help regulate adipocytes, and adipocytes can inhibit granulopoiesis; thus, a Kit-mutated MC clone may have directly and/or indirectly driven agranulocytosis. MCAS should be considered in otherwise idiopathic agranulocytosis presenting with comorbidities best explained by MC mediator release.
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PMID:Mast cell activation syndrome masquerading as agranulocytosis. 2233 92


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