Cases reported "Drug Hypersensitivity"

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1/16. An infectious mononucleosis-like syndrome induced by minocycline: a third pattern of adverse drug reaction.

    A 22-year-old black man developed fever, chills, fatigue, night sweats, tender lymphadenopathy, and a generalized, pruritic, macular eruption 3 weeks after starting minocycline therapy for acne. His illness was also characterized by a palpable spleen tip, marked lower extremity and scrotal edema, and generalized lymphadenopathy. The patient had leukocytosis with a large percentage of atypical lymphocytes on peripheral smear and liver dysfunction. Titers for Epstein-Barr virus, hepatitis b, toxoplasmosis; and cytomegalovirus were all negative. Human immunodeficiency virus-1 viral load and antibodies were also negative. Marked improvement was noted after the discontinuation of minocycline and the use of systemic corticosteroids. With the negative viral serologies, the clinical picture was most consistent with an infectious mononucleosis-like syndrome produced by the minocycline ingestion.
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2/16. 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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3/16. Rocuronium anaphylaxis and multiple neuromuscular blocking drug sensitivities.

    PURPOSE: To report a case of anaphylaxis to rocuronium and the sensitivities to multiple neuromuscular blocking drugs in a patient with no previous exposure to this group of drugs. We describe the current recommendations for both intraoperative and postoperative testing of these patients. CLINICAL FEATURES: A 36-yr-old man was admitted for repair of a ruptured achilles tendon. Following induction of general anesthesia with fentanyl and propofol, 60 mg of rocuronium were given to facilitate tracheal intubation. He immediately became profoundly hypotensive with impalpable pulses, and blood pressure could not be recorded. Airway pressure increased markedly, and hand ventilation of the lungs became very difficult. His airway was secured and he was successfully resuscitated with 3 mg epinephrine and three litres crystalloid and colloid intravenous fluid therapy. His recovery in the intensive care unit was uneventful and the operation was performed four days later under spinal anesthesia. Subsequent skin prick testing, performed six weeks later, demonstrated strong positive weal and flare reactions to rocuronium, vecuronium and pancuronium, and some cross-reactivity with the benzylisoquinolinium group of muscle relaxants. CONCLUSION: Muscle relaxants are responsible for 61.6% of cases of anaphylaxis during general anesthesia. Cross-reactivity is common, as this group of drugs share a quaternary ammonium group. It is mandatory that patients be tested for both the agent responsible and cross-reactivity following an anaphylactic response. We suggest a protocol for investigation of suspected anaphylaxis.
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4/16. hypersensitivity reaction associated with acute hepatic dysfunction following a single intravenous dose of procainamide.

    Rare cases of hepatotoxicity have been attributed to the antiarrhythmic agent procainamide. We here describe the case of a patient who had a hypersensitivity reaction to procainamide with fever, chills, arthralgia, abdominal pain and acute elevations of serum aminotransferase activities and bilirubin concentration. The reaction occurred after the patient had received a large intravenous dose during cardiac electrophysiological testing. This case should alert physicians to potential hepatotoxic reactions to procainamide, particularly with the increasing popularity of cardiac electrophysiological testing, during which this drug is commonly used.
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5/16. vancomycin-induced thrombocytopenia: a case proven with rechallenge.

    In a rare case of vancomycin-induced thrombocytopenia, a 50-year-old man with culture-negative subacute bacterial endocarditis underwent mitral valve replacement surgery and was treated with vancomycin. His platelet count dropped from 346 x 10(3)/mm3 to 13 x 10(3)/mm3 on postoperative day 4, and a differential diagnosis of heparin- versus drug-induced thrombocytopenia was considered. Antiheparin antibodies were detected in the patient's serum on day 5. He showed no signs of bleeding. His platelet count remained below 5 x 10(3)/mm3 despite two platelet transfusions on day 5. A hemorrhagic pericardial effusion with tamponade developed, requiring drainage. A trial with intravenous immunoglobulin led to fever and chills, and the infusion was not completed. vancomycin was changed to clindamycin on day 9, and methylprednisolone therapy was started on day 11. On day 12, the patient's clinical condition improved, and his platelet count increased from 3 x 10(3)/mm3 to 32 x 10(3)/mm3 with no bleeding. On day 18, his platelet count was 424 x 10(3)/mm3, and he was scheduled for discharge with vancomycin therapy for a total of 6 weeks. He received a single dose of intravenous vancomycin 1 g at the hospital; his platelet count dropped to 160 x 10(3)/mm3 1 hour after the infusion and to 58 x 10(3)/mm3 12 hours later. vancomycin was discontinued and clindamycin and prednisone were restarted. On day 20, the patient's platelet count increased to 105 x 10(3)/mm3 and he was discharged with warfarin, prednisone, and clindamycin therapy. We suspect that our patient's thrombocytopenia was due to vancomycin.
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6/16. Mercaptopurine-induced fever in a patient with Crohn's disease.

    OBJECTIVE: To report a case of mercaptopurine-induced fever. CASE SUMMARY: A patient with Crohn's disease was treated with mercaptopurine (6-MP) for an exacerbation of his illness. The patient developed fever and chills. After thorough diagnostic examinations and failure to respond to antimicrobial therapy, symptoms were attributed to an allergic-type reaction to 6-MP. The patient defervesced after 6-MP withdrawal. fever and chills, along with arthralgias, recurred upon rechallenge with a single dose of 6-MP. DISCUSSION: Adverse effects attributable to 6-MP therapy in inflammatory bowel disease were reviewed in the literature. Drug-induced fever has been previously reported; however, it is an uncommon adverse effect and is difficult to diagnose. It is also difficult to predict which patients will have the reaction. It is a diagnosis of exclusion requiring a thorough investigation. CONCLUSIONS: Drug-induced fever should be considered when confronted with fever and chills in patients with inflammatory bowel disease being treated with 6-MP. This case report shows the difficulty in differentiating between an infectious process and an adverse reaction to a medication.
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7/16. ibuprofen-induced fever in sjogren's syndrome.

    A 68-year-old woman with a medical history significant for Sjogren syndrome and leukocytoclastic vasculitis of small vessels presented to the emergency department with chills, malaise, a temperature of 39 degrees C, nausea, vomiting, and hypotension. Fifteen minutes earlier she had taken ibuprofen for flu-like symptoms. She was treated with a perfusion of intravenous saline, paracetamol, and ciprofloxacin with improvement 24 hours later. Three months later, she had a similar episode, without hypotension. An oral challenge test with ibuprofen in the hospital produced the same symptoms 3 hours after the last dose. She was treated with metamizole and paracetamol and was asymptomatic the next day. This is the first report of a febrile reaction to ibuprofen in a patient with sjogren's syndrome.
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8/16. Snake venom or antivenom induced urticaria.

    An amateur herpetologist developed chills, diaphoresis and generalized urticaria 5 h after receiving Antivenin (Crotalidae) Polyvalent (Wyeth) for treatment of rattlesnake (crotalus atrox) envenomation. The patient had been bitten 8 mo earlier by a copperhead (agkistrodon contortrix mokeson) resulting in minimal envenomation. He also had been skin testing himself for 6 mo with both diluted crotalus atrox venom and Antivenin (Crotalidae) Polyvalent (Wyeth) to determine how sensitive he was to antivenom and how resistant he was to the effects of venom. Unusual reactions to antivenom during the treatment of snake-bite victims, such as amateur herpetologists or snake fanciers, with access to both venom and antivenom should raise questions about unusual means of sensitization.
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9/16. Drug-induced fever: a clinical report and challenge test with calcium dobesilate.

    A 54-year-old man was receiving calcium dobesilate for retinopathy and after 8 days he presented fever of more than 39 degrees C, generalized myalgia, chills and headache. Other causes of fever were ruled out. A challenge test was done with a single therapeutic oral dose of calcium dobesilate and fever appeared 20 h later and lasted 8 h. Our patient fulfils Young's stringent criteria for drug fever. To our knowledge drug-induced fever due to calcium dobesilate has not been reported previously.
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10/16. azathioprine induced fever, chills, rash, and hepatotoxicity in rheumatoid arthritis.

    Within one year three of 25 patients with rheumatoid arthritis treated with azathioprine 100 mg daily developed the following adverse reactions less than two weeks after starting treatment: patient one showed fever with chills, rash, and severe liver function abnormalities suggestive of cholestasis; the second patient had fever, nausea, diarrhoea, and moderately raised liver enzymes; the third patient showed very high fever and severe chills. In two patients the drug was rechallenged, with more rapidly arising and more severe symptoms. In one case raised liver enzymes persisted until seven months after discontinuation of azathioprine. hypersensitivity reactions and hepatotoxicity of azathioprine are discussed.
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