Cases reported "Drug Hypersensitivity"

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1/25. ceftizoxime-induced hemolysis due to immune complexes: case report and determination of the epitope responsible for immune complex-mediated hemolysis.

    BACKGROUND: Several occurrences of immune complex-mediated, cephalosporin-induced intravascular hemolysis have been reported. This report describes the first case of hemolytic anemia caused by an immune-complex mechanism associated with ceftizoxime and delineates the epitope responsible for hemolysis. CASE REPORT: The patient's serum was tested for antibody that reacted with five penicillins and 30 cephems (all types of cephalosporins) by using protocols to detect drug-adsorption and immune-complex mechanisms. The patient's antibody that formed immune complexes with ceftizoxime reacted with 10 of 30 cephems. These 10 drugs were classified as oxime-type cephalosporins, which have a common structural formula consisting of [(Z)-2-(2-amino-4-thiazolyl)-2-methoxyiminoacetoamido] at the C7 position on 7-aminocephalosporinic acid with or without substitution at the C3 position. CONCLUSION: The patient's antibody recognized a common structure in 10 oxime-type cephalosporins, and immune complexes formed by the antibody specifically or nonspecifically bound to red cell membranes. Therefore, when intermittent antibiotic therapy is required, as in this case, care should be taken in antibiotic selection to avoid drug-induced hemolytic anemia. In addition, when this type of hemolysis is observed, tests for antibody that reacts by adsorption and immune-complex mechanisms should be performed against penicillins and cephems to select antibiotics not showing a cross-reaction.
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2/25. Acute tubulointerstitial nephritis following intravenous immunoglobulin therapy in a male infant with minimal-change nephrotic syndrome.

    A boy aged 4 years with nephrotic syndrome (NS) was referred to our hospital because of the third relapse of NS. Hypogammaglobulinemia associated with massive proteinuria was observed at the presentation. Residual urinary tract infection required intravenous piperacillin and immunoglobulin therapy (IVIG). Soon after IVIG, he complained of high fever with chills, bilateral knee joint pain, dry cough and chest discomfort. Although he did not develop renal insufficiency, a transient increase in the urinary beta2-microglobulin and decrease in the serum complement hemolytic activity were observed. These clinical manifestations spontaneously ceased. A percutaneous renal biopsy for his NS performed 19 days after the episode of allergic reaction revealed tubulointerstitial nephritis (tin) with marked eosinophil infiltrates. Glomeruli showed minor glomerular abnormalities. Renal complications associated with IVIG treatment have been reported to date, however, acute tin has rarely been seen.
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3/25. Immune hemolytic anemia caused by sensitivity to a metabolite of etodolac, a nonsteroidal anti-inflammatory drug.

    BACKGROUND: Immune hemolytic anemia can be caused by sensitivity to many different drugs. In some instances, the sensitizing compound can be identified by in vitro testing, but results are often negative. One reason for this is that a drug metabolite formed in vivo can be the sensitizing agent, but the responsible metabolites have rarely been identified at a chemical level. This report describes a patient who developed severe, Coombs-positive hemolytic anemia on two occasions after taking the nonsteroidal anti-inflammatory drug etodolac. Studies were performed to characterize etodolac metabolites to which this patient was sensitive. CASE REPORT: serum was tested for antibody in the presence and absence of drug using conventional methods and urine from individuals taking etodolac as a source of drug metabolites. Urinary metabolites of etodolac were identified by high-pressure liquid chromatography analysis. Glucuronide conjugates of etodolac and the 6-OH metabolite of etodolac were synthesized in a rat liver microsomal system to obtain reference standards. RESULTS: The patient's serum gave only trace ( /-) reactions with normal RBCs in the presence of etodolac but reacted strongly (4 ) in the presence of urine from an individual taking this drug. The active urinary metabolites were identified as etodolac glucuronide and 6-OH etodolac glucuronide. CONCLUSION: This patient appears to have experienced acute, severe immune hemolytic anemia on two occasions because of sensitivity to the glucuronides of etodolac and 6-OH etodolac. In patients suspected of having drug-induced immune hemolytic anemia, RBC-reactive antibodies can sometimes be detected by using urine from an individual taking the implicated medication as the source of drug metabolites in in vitro reactions. For patients who present with acute immune hemolysis, a careful history of drug exposure should be taken, and, where indicated, confirmatory testing should be performed to identify the sensitizing drug and prevent inadvertent reinduction of hemolysis at a later time.
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4/25. Hypersensitivity syndrome associated with dapsone/pyrimethamine (Maloprim) antimalaria chemoprophylaxis.

    BACKGROUND: dapsone 100 mg/pyrimethamine 12.5 mg (Maloprim; Beacons Chemicals Pte Ltd, singapore) is routinely prescribed for antimalarial chemoprophylaxis in military servicemen in singapore who are not glucose-6-phosphate dehydrogenase-deficient. methods: We report a series of three male National Servicemen with hypersensitivity syndrome from Maloprim. RESULTS: The three patients were diagnosed with hypersensitivity syndrome based on the presence of features of a drug hypersensitivity syndrome including fever, lymphadenopathy, maculopapular exanthema, hepatitis, and definite exposure to weekly Maloprim alone. A mild Coombs positive hemolytic anemia was also observed in one patient. All the clinical, hematologic, and biochemical derangements normalized within 3 months of tapering regimens of moderate-dose prednisolone. CONCLUSIONS: Drug hypersensitivity syndromes can occur even on low-dose, weekly drug regimens. Hypersensitivity syndrome from weekly Maloprim is potentially reversible when recognized and treated early.
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5/25. Two cases of immune haemolytic anaemia, associated with anti-piperacillin, detected by the 'immune complex' method.

    BACKGROUND AND OBJECTIVES: Sera containing antibodies to penicillin and penicillin-related drugs are typically thought to react with drug-coated red blood cells (RBCs) (drug adsorption method), but not when the sera are added to drug and RBCs in the same tube ('immune complex' method). Two cases of immune haemolytic anaemia caused by anti-piperacillin have been previously described. Serological details were given in only one patient. In that subject, the antibody was immunoglobulin (Ig)M IgG and reacted by both the drug adsorption and 'immune complex' methods. MATERIALS AND methods: Two patients with cystic fibrosis developed positive direct antiglobulin tests (DATs) and haemolytic anaemia after 11-12 days of piperacillin therapy. Serological studies were performed with piperacillin, Zosyn (piperacillin tazobactam) and penicillin by using the drug adsorption and 'immune complex' methods. RESULTS: The first patient's serum contained an IgG, complement-activating anti-piperacillin that reacted by the 'immune complex' method only. The second patient's IgM IgG, complement-activating anti-piperacillin reacted by the 'immune complex' method and agglutinated piperacillin-treated RBCs. An eluate from the patient's RBCs reacted weakly with all RBCs tested without the presence of drug. This patient had evidence of intravascular haemolysis and died. CONCLUSIONS: We describe the third and fourth examples of immune haemolytic anaemia caused by anti-piperacillin; one was associated with fatal haemolytic anaemia. As piperacillin is commonly used in the treatment of cystic fibrosis, anti-piperacillin should be considered whenever patients with cystic fibrosis develop haemolytic anaemia and/or positive DATs.
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ranking = 0.67270227185764
keywords = anaemia
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6/25. Case report: acute renal failure, thrombocytopenia and nonhemolytic icterus probably caused by mefenamic acid (Parkemed)-dependent antibodies.

    A 65-year-old, previously healthy man developed acute renal failure, severe thrombocytopenia and hepatic icterus after a small dose of mefenamic acid (Parkemed). Drug-dependent antibodies reacting against platelets could be identified as the most probable cause for this acute and rapidly reversible disorder. A concomitant hemolytic reaction was not observed and accordingly no drug-dependent red cell antibodies could be demonstrated. The drug-specific antibodies were found only during the acute phase using the platelet immunofluorescence test and a solid-phase immunoassay but not with the monoclonal antibody specific immobilization of platelet antigens assay. After discontinuation of the drug the patient steadily improved and fully recovered until day 22 after admission and drug removal. The clinical course strongly suggests that drug-dependent antibodies against mefenamic acid and/or its metabolites reacting by immune complex mechanism were responsible not only for the thrombocytopenia but also for the renal and hepatic failure.
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7/25. dapsone induced cholangitis as a part of dapsone syndrome: a case report.

    BACKGROUND: dapsone can rarely cause a hypersensitivity reaction called dapsone syndrome, consisting of fever, hepatitis, exfoliative dermatitis, lymphadenopathy and hemolytic anemia. dapsone syndrome is a manifestation of the DRESS (drug rash with eosinophilia and systemic symptoms) syndrome which is a serious condition that has been reported in association with various drugs. cholangitis in dapsone syndrome has not been reported so far in the world literature. CASE PRESENTATION: We report a patient who presented with fever, exfoliative dermatitis, jaundice and anemia within three weeks of starting of dapsone therapy. These features are typical of dapsone syndrome, which is due to dapsone hypersensitivity and is potentially fatal. Unlike previous reports of hepatitic or cholestatic injury in dapsone syndrome we report here a case that had cholangitic liver injury. It responded to corticosteroids. CONCLUSION: We conclude that cholangitis, though unusual, can also form a part of dapsone syndrome. physicians should be aware of this unusual picture of potentially fatal dapsone syndrome.
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8/25. A near fatal case of the dapsone hypersensitivity syndrome in a patient with urticarial vasculitis.

    dapsone (4,4'-diaminodiphenyl sulphone) is used for a variety of dermatological conditions including immunobullous diseases and urticarial vasculitis. Side-effects are common and include lethargy, headaches, methaemoglobinaemia and haemolysis. Severe adverse effects are rare but the dapsone hypersensitivity syndrome is well recognized. Symptoms include fever, haemolytic anaemia, lymphocytosis and hepatitis. We report a near fatal case of the dapsone hypersensitivity syndrome in a patient with urticarial vasculitis. This diagnosis should be remembered in any patient who becomes unwell whilst taking dapsone.
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ranking = 0.074744696873072
keywords = anaemia
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9/25. cefotetan-induced immune hemolytic anemia.

    Immune hemolytic anemia due to a drug-adsorption mechanism has been described primarily in patients receiving penicillins and first-generation cephalosporins. We describe a patient who developed anemia while receiving intravenous cefotetan. cefotetan-dependent antibodies were detected in the patient's serum and in an eluate prepared from his red blood cells. The eluate also reacted weakly with red blood cells in the absence of cefotetan, suggesting the concomitant formation of warm-reactive autoantibodies. These observations, in conjunction with clinical and laboratory evidence of extravascular hemolysis, are consistent with drug-induced hemolytic anemia, possibly involving both drug-adsorption and autoantibody formation mechanisms. This case emphasizes the need for increased awareness of hemolytic reactions to all cephalosporins.
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keywords = hemolytic
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10/25. A case of acute hemolysis after ceftriaxone: immune complex mechanism demonstrated by flow cytometry.

    An immune complex mechanism for ceftriaxone sodium- induced severe autoimmune hemolytic anemia has previously been demonstrated using routine blood bank techniques. We describe herein a patient with severe hemolysis that subsided once the drug was discontinued. Serologic techniques demonstrated immune complex-mediated ceftriaxone-dependent red cell antibodies. These findings were further supported by the results of flow cytometry, in which a change in basal red cell autofluorescence was seen in the presence of the antibody and the drug. Our case illustrates the adjunctive value of flow cytometry in the diagnosis of ceftriaxone-dependent red cell antibody.
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