Cases reported "Drug Hypersensitivity"

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1/10. Allergic cholestatic hepatitis and exanthema induced by metamizole: verification by lymphocyte transformation test.

    We report about a 66-year-old-male patient who was hospitalized with generalized exanthema and increase of liver enzymes after intake of metamizole because of flue-like symptoms. Despite initial high dose steroids, disease activity persisted, and therefore liver biopsy was performed. histology revealed acute hepatitis with perivenular non-bridging confluent necrosis and granuloma formation consistent with drug-induced hepatitis. A metamizole-induced process was suspected. Lymphocyte transformation test confirmed the sensitization of the patient's lymphocytes to metamizole and three of its four metabolites (4-methylaminoantipyrine, 4-acetylaminoantipyrine and 4-formylaminoantipyrine). Other drugs could be excluded with high probability. In the follow-up, the general condition of the patient improved, and liver enzymes decreased under treatment with steroids. Thus, we conclude that in this patient metamizole has induced an allergic reaction not only of the skin but also of the liver. To our knowledge, an allergic cholestatic hepatitis caused by metamizole has been reported only once in literature.
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2/10. Possible anaphylaxis after propofol in a child with food allergy.

    OBJECTIVE: To report a case of anaphylaxis due to propofol in a child with allergies to egg and peanut oil. CASE SUMMARY: A 14-month-old boy with a history of reactive airway disease was hospitalized for treatment of respiratory symptoms. The patient had documented allergies to egg, peanut oil, and mold. Within the first few hours after admission, acute respiratory decompensation occurred, and arrangements were made to transfer the patient to our tertiary-care hospital. Prior to transfer, he was emergently intubated under sedation and paralysis with propofol and rocuronium. When emergency air transport arrived, the patient was hypotensive and tachycardic. His symptoms of anaphylaxis were managed throughout the flight and, upon arrival at our institution, the patient was admitted to the Pediatric intensive care Unit. He improved over a 5-day hospital course, and his caregivers were instructed to avoid propofol in the future. The patient's anaphylactic reaction following propofol was rated as a possible adverse drug reaction using the Naranjo probability scale. DISCUSSION: The use of propofol in pediatric patients for procedural sedation has gained increased favor. Since the propofol formulation contains both egg lecithin and soybean oil, its use is contraindicated in patients with hypersensitivities to these components. Several other drugs have a food component, resulting in contraindications and warnings in product labeling. CONCLUSIONS: propofol should be avoided in patients with allergies to egg and/or soybean oil, if possible. Clinicians should consider the potential for adverse drug events in patients with select food allergies.
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3/10. Anaphylactoid reaction to ciprofloxacin.

    OBJECTIVE: To report a case of anaphylactoid reaction in an hiv-negative patient associated with the administration of intravenous ciprofloxacin. CASE SUMMARY: A 79-year-old Armenian man developed an anaphylactoid reaction following a first-time exposure to intravenous ciprofloxacin. This reaction was characterized by severe hypotension, wheezing, tachypnea, tachycardia, and pruritus. The patient had complete recovery once ciprofloxacin treatment was terminated and supportive care was provided. DISCUSSION: fluoroquinolones are important therapeutic agents in the management of infectious diseases and are generally safe and well tolerated. Anaphylactoid and anaphylactic reactions have been documented as adverse effects of ciprofloxacin, ofloxacin, norfloxacin, levofloxacin, and moxifloxacin. To date, >33 cases have been reported with ciprofloxacin, of which at least 10 occurred in hiv-positive patients. In europe, 15 cases of anaphylactoid reactions to ofloxacin have been reported and, more recently, with moxifloxacin. Since anaphylactoid reactions are potentially life threatening, the administration of fluoroquinolones to patients who have experienced a prior reaction to any of these agents should be avoided, unless tolerance has been confirmed by oral challenge tests. CONCLUSIONS: The anaphylactoid reaction in our patient was probably induced by ciprofloxacin as validated by the Naranjo probability scale. Although anaphylactoid/anaphylactic reactions are rare adverse effects of ciprofloxacin and other fluoroquinolones, clinicians should be aware of this potentially fatal event.
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4/10. Anticonvulsant hypersensitivity syndrome: lymphocyte toxicity assay for the confirmation of diagnosis and risk assessment.

    OBJECTIVE: To report a case of anticonvulsant hypersensitivity syndrome (AHS) precipitated by exposure to phenobarbital. CASE SUMMARY: An 11-year-old girl receiving phenobarbital developed fever, exfoliative skin rash, mucous membrane lesions, alopecia, and hepatic inflammation. Investigations ruled out an infectious etiology; an adverse event following phenobarbital administration was considered. Applying the Naranjo probability scale for objective causality assessment showed the adverse reaction was probably due to phenobarbital. The diagnosis was confirmed by in vitro lymphocyte toxicity assay, which demonstrated increased cell death following exposure to phenobarbital, as well as other aromatic anticonvulsants and lamotrigine. DISCUSSION: AHS is a rare, potentially fatal event with multisystem manifestations. It is reported following exposure to aromatic antiepileptics. The mechanism proposed for AHS is accumulation of toxic arene oxide metabolites due to a defect in epoxide hydrolase-mediated detoxification. Despite the difference in chemical structure of lamotrigine, in vitro susceptibility to AHS was demonstrated in our patient. CONCLUSIONS: Although AHS is a rare event, it should be suspected in patients who develop unexplained systemic manifestations following exposure to aromatic antiepileptics. The potential of lamotrigine to cause AHS should be remembered when this drug is used in subjects who have developed AHS on exposure to phenobarbital and other first-line antiepileptic agents.
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5/10. Successful desensitization to oxaliplatin.

    OBJECTIVE: To report the successful desensitization of a patient to oxaliplatin utilizing an 8-hour desensitization regimen in a controlled environment. CASE SUMMARY: A 53-year-old white woman with metastatic colon cancer was receiving oxaliplatin, bevacizumab, and capecitabine every 2 weeks, with a partial response to therapy. On her fifth cycle of this regimen, she experienced diaphoresis, hypotension, nausea, abdominal cramping, and coryza. According to the Naranjo probability scale, oxaliplatin, and not bevacizumab, was the probable cause of the hypersensitivity reaction. The woman continued therapy with capecitabine and bevacizumab, resulting in stable disease. Due to her initial response to the oxaliplatin-based regimen, it was decided to attempt desensitization to oxaliplatin in a controlled, inpatient environment. An 8-hour desensitization schedule was employed, and the patient successfully completed an additional 3 cycles with full-dose oxaliplatin. DISCUSSION: hypersensitivity reactions to platinum-containing compounds are well described and potentially life threatening. With expanded use of oxaliplatin in various malignancies, an increased number of hypersensitivity reactions will likely be reported. patients with previous hypersensitivity reactions to carboplatin are at risk for similar reactions to oxaliplatin. We achieved successful desensitization for oxaliplatin using increased concentrations of the drug over an 8-hour period concomitant with oral and intravenous corticosteroids and histamine blockers. CONCLUSIONS: hypersensitivity reactions to platinum compounds may result in discontinuation of active therapies in patients with metastatic disease. Desensitization to oxaliplatin is possible utilizing this approach.
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6/10. hypersensitivity reactions to oxaliplatin in two asian patients.

    OBJECTIVE: To report 2 cases of hypersensitivity reactions associated with oxaliplatin treatment in Asian patients. CASE SUMMARIES: A 33-year-old Chinese woman received adjuvant oxaliplatin in combination with fluorouracil and leucovorin. Shortly during her sixth infusion, she developed a severe hypersensitivity reaction. Despite prophylactic measures, she developed another reaction of similar severity during her subsequent infusion and was not further rechallenged with oxaliplatin. The second case involved a 45-year-old Malay woman who received oxaliplatin, fluorouracil, and leucovorin for metastatic colorectal cancer. Shortly during her ninth infusion, she developed a mild hypersensitivity reaction. With prophylactic measures, she developed less marked reactions with her subsequent 3 infusions. DISCUSSION: hypersensitivity reactions to oxaliplatin have been reported to be between 12% and 16% in the Western population. As of April 20, 2005, there are only 2 previously published reports of hypersensitivity reactions to oxaliplatin in 6 Asian patients. The incidence rates of such reactions in different Asian ethnic groups could vary. The cumulative dose, time of exposure to oxaliplatin, and clinical features were variable and unpredictable in all of the reported Asian patients who developed hypersensitivity reactions. An objective causality assessment using the Naranjo probability scale revealed that oxaliplatin was the highly probable cause of hypersensitivity in the 2 Asian patients reported by our center. CONCLUSIONS: patients who develop mild to moderate reactions can be rechallenged with the drug administered as a slow infusion with prophylactic measures. Desensitization may allow patients who experience severe hypersensitivity reactions to oxaliplatin to further receive effective therapy for their colorectal cancer.
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7/10. hypersensitivity syndrome and pure red cell aplasia following allopurinol therapy in a patient with chronic kidney disease.

    OBJECTIVE: To report a rare case of combined hypersensitivity syndrome and pure red cell aplasia (PRCA) following allopurinol therapy. CASE SUMMARY: A 43-year-old woman with underlying mesangioproliferative glomerulonephritis developed fever, generalized morbilliform rash, leukocytosis with marked eosinophilia, and hepatic dysfunction 3 weeks after starting allopurinol therapy (300 mg/day for 3 days followed by 200 mg/day) for hyperuricemia and arthritis. The clinical findings were judged to be a probable drug reaction according to the Naranjo probability scale. The drug-induced hypersensitivity syndrome (DHS) resolved after withdrawal of allopurinol and initiation of systemic corticosteroid therapy. However, there was progressive worsening of anemia with reticulocytopenia; PRCA was suspected. PRCA was judged to be a possible drug reaction according to the Naranjo probability scale. The patient refused blood transfusion and bone marrow biopsy. Recombinant human erythropoietin was initiated in addition to prednisolone 15 mg daily. Eleven days later (approximately 7 wk after allopurinol withdrawal), both the hemoglobin level and reticulocyte count began to rise. The patient consented to a bone marrow study at that time, which confirmed the presence of dysplasia involving only the erythroid lineage. DISCUSSION: allopurinol may induce DHS, aplastic anemia, and, in rare instances, PRCA. We report the first case of PRCA concurrent with allopurinol-induced DHS in a patient with chronic kidney disease. Discontinuation of allopurinol is the first step in the treatment of such cases. The slow recovery of PRCA might be partly attributed to her underlying chronic kidney disease. CONCLUSIONS: To minimize serious DHS, proper indications for treatment and dosage adjustment should be closely observed when starting allopurinol therapy in patients with chronic kidney disease.
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8/10. Acute hypersensitivity reaction to ferric gluconate in a premedicated patient.

    OBJECTIVE: To report a case of an acute hypersensitivity reaction to ferric gluconate in a patient premedicated with dexamethasone, diphenhydramine, and prochlorperazine. CASE SUMMARY: A 38-year-old female with persistent iron deficiency anemia was initiated on parenteral iron therapy with ferric gluconate 125 mg intravenously over 10 minutes. The patient initially tolerated this first dose well; however, she later experienced nausea, dizziness, and minor tongue swelling. On her second course of therapy, the woman was premedicated with dexamethasone, diphenhydramine, and prochlorperazine prior to the same dose of ferric gluconate infused over 30 minutes. Subsequently, the patient developed epigastric pain, nausea, swelling of her lips and tongue, and hypotension. The symptoms abated after administration of diphenhydramine, dexamethasone, morphine, cimetidine, intravenous fluids, and oxygen. She was discharged after a short stay in the emergency department observation unit. DISCUSSION: Data are limited on the relative safety of ferric gluconate compared with iron dextran. Ferric gluconate does not appear to be associated with severe life-threatening events; however, the possibility of an acute hypersensitivity reaction with this product does exist. In this case, use of the Naranjo probability scale indicated a probable relationship between the hypersensitivity reaction and ferric gluconate. CONCLUSIONS: Healthcare professionals should be aware of this serious but rare event and encouraged to further document and report these events.
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9/10. Probable loop diuretic-induced pancreatitis in a sulfonamide-allergic patient.

    OBJECTIVE: To report the case of a patient with a prior allergy to a sulfonamide antibiotic who subsequently developed the same reaction when administered various loop diuretics. CASE SUMMARY: A 57-year-old female with cardiomyopathy and "sulfa" (trimethoprim/sulfamethoxazole) allergy documented as pancreatitis presented with symptoms consistent with pancreatitis after use of furosemide. She subsequently developed similar symptoms after multiple rechallenges with various loop diuretics including furosemide, bumetanide, and torsemide. The patient was placed on ethacrynic acid until she was desensitized to furosemide. She had been receiving oral furosemide for 5 months at the time of this report, with no complications. According to the Naranjo probability scale, this reaction was probable. DISCUSSION: Reactions associated with arylamine sulfonamide-containing antibiotics have been commonly reported; however, cross-reactions with non-arylamine sulfonamide-containing medications have been rare. The time delay by which symptoms of pancreatitis presented following administration of loop diuretics suggests an immunologic pathway. In addition, while cases of loop diuretic-induced pancreatitis, including furosemide, have been published, the allergic manifestations with both sulfonamide antibiotics and non-antibiotics in our patient suggest possible cross-reactivity between these 2 drug classes. CONCLUSIONS: The mechanism by which loop diuretics induce pancreatitis appears to be via an immunologic pathway. While the true correlation remains unknown, allergic cross-reactivity may occur between sulfonamide antibiotics and non-antibiotics, such as loop diuretics. Torsemide appears to also be a part of a long list of agents that can cause pancreatitis.
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10/10. Chronic urticaria due to dental eugenol.

    A case is reported of a patient with chronic urticaria. The correlation between the symptoms and dental treatment gave rise to the supposition that a root canal cement was causing the trouble. A causal relationship with eugenol, a cement constituent, could only be established through provocative oral ingestion. There is a high probability that the oral provocation tests to eugenol are relevant. Nevertheless, caution is needed when dealing with chronic urticaria.
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