Cases reported "Drug Hypersensitivity"

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1/81. Skin eruption with gabapentin in a patient with repeated AED-induced Stevens-Johnson's syndrome.

    Skin eruptions have been reported with the use of all antiepileptic drugs and there is a significant risk of cross-reactivity between these agents in causing serious eruptions such as Stevens-Johnson's syndrome. Gabepentin is usually considered a safe agent for patients with a previous history of drug allergies and there have been no cases of skin eruption reported to the gabapentin post marketing surveillance. We report a patient who had severe Stevens-Johnson's syndrome induced by phenytoin and later by carbamazepine. Subsequent use of gabapentin also resulted in a skin eruption which was limited to the lower extremities but without systemic or mucosal involvement. This case suggests that patients with a strong history of drug-induced idiosyncratic reactions may experience such reactions to gabapentin as well.
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2/81. Anticonvulsant hypersensitivity syndrome occurring as sepsis with multiorgan dysfunction.

    phenytoin is a highly effective and widely prescribed anticonvulsant agent. However, it is associated with both dose-related side effects and hypersensitivity reactions. life-threatening anticonvulsant hypersensitivity syndrome in one patient was characterized by a skin eruption and multisystem organ dysfunction.
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3/81. clindamycin hypersensitivity appears to be rare.

    BACKGROUND: A patient developed a generalized confluent erythematous papular rash after a single injection of clindamycin preoperatively. The literature from two small studies suggested a 10% incidence of cutaneous eruptions to clindamycin which seemed too high. OBJECTIVE: Describe a patient with clindamycin hypersensitivity and determine the incidence of hospital-wide adverse drug reactions from clindamycin from 1995-1997. methods: At a tertiary care center, utilizing the Department of Pharmacy records, the incidence of adverse drug reactions was determined with (1) voluntary physician reporting, (2) health information management chart reviews and adverse drug reaction coding, and (3) chart reviews by the pharmacy and therapeutics committee of adverse drug reactions. RESULTS: (I) A 50-year-old patient developed a generalized raised, erythematous rash that worsened over 3.5 days until hydrocortisone was administered. Immediate skin tests with clindamycin were negative. (2) From 3,896 administrations of clindamycin from April 1995 to October 1997, 14 (0.47%) adverse drug reactions occurred but 7 were confounded by other medications also being administered. CONCLUSION: (1) Adverse drug reactions to clindamycin are much lower than reported 25 years ago with an incidence < 1%. (2) A patient who previously had experienced facial edema and a generalized rash after receiving clindamycin and a cephalosporin 6 years ago and who was considered allergic to cephalosporins, was found to be clindamycin allergic when she received a preoperative dose of clindamycin.
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4/81. Lamotrigine overdose presenting as anticonvulsant hypersensitivity syndrome.

    OBJECTIVE: To describe the laboratory and physical manifestations of lamotrigine toxicity presenting as anticonvulsant hypersensitivity syndrome. CASE SUMMARY: A 49-year-old white man presented to our institution with a two-day history of low-grade fever, erythema, and edema involving the periorbital area. Five days earlier, he had been placed on lamotrigine treatment for bipolar disorder. He inadvertently received four daily doses of lamotrigine 2700 mg each. physical examination was significant for periorbital edema and discrete and confluent blanching red macules and papules involving the face, trunk, and extremities. Laboratory tests revealed leukocytosis, hepatitis, and acute renal failure. With normalization of the laboratory results, the eruptions and edema gradually resolved. DISCUSSION: Lamotrigine toxicity can lead to periorbital edema, rash, and multiorgan system abnormalities. This presentation has clinical and laboratory similarities with anticonvulsant hypersensitivity syndrome, which suggests that at some threshold concentration the amount of lamotrigine may overwhelm the body's ability to metabolize the drug, leading to a similar hypersensitivity reaction. Lamotrigine is a relatively new agent, and this report may provide useful insights on evaluating the clinical toxicology of this agent. CONCLUSIONS: Healthcare providers should be aware that lamotrigine overdose may present with multiorgan involvement, similar to anticonvulsant hypersensitivity syndrome.
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5/81. Photosensitivity with sulfasalazopyridine hypersensitivity syndrome.

    Five weeks after the start of treatment with an association of sulfasalazopyridine and piroxicam, a 30-year-old woman presented with an eczematous eruption in light-exposed areas, hepatomegaly and fever (38 degrees C). Laboratory studies showed leukocytosis, eosinophilia and hepatic cytolysis. Treatment consisted of withdrawing the two drugs and topical steroids. The clinical signs regressed in 6 days. An increase in eosinophilia and hepatic cytolysis was observed until the tenth day, after which the trend reversed. Laboratory parameters were normal on the twentieth day. One month later, photopatch testing was performed. A patch test with sulfanilamide irradiated with UVA was positive. Clinical and laboratory findings were highly suggestive of drug hypersensitivity syndrome. The positive result from the UVA photopatch test with sulfanilamide suggests that sulfasalazopyridine was involved in the occurrence of hypersensitivity syndrome in our patient. We conclude that photodistributed eruptions can be observed in drug hypersensitivity syndrome with photosensitizing drugs.
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6/81. 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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7/81. Hypersensitivity syndrome due to 2 anticonvulsant drugs.

    Drug-induced hypersensitivity syndrome is a multiorgan-system reaction characterized by fever, pleomorphic eruption, lymphadenopathy, eosinophilia, lymphocytosis and hepatitis. We report a drug hypersensitivity syndrome in a 6-year-old Tunisian child treated for epileptic absences with sodium valproate and ethosuximide. Imputability of these 2 drugs is probable because of the chronological and clinical features. Positive rechallenge with ethosuximide confirmed the toxicity of this drug. sodium valproate was also responsible because patch testing was positive and followed by a generalized eruption. Human herpesvirus 6 (HHV6) antibody titers increased significantly within 15 days. There was a favourable outcome after discontinuation of the drugs and corticosteroid therapy. Our case is interesting because this drug hypersensitivity syndrome occurred with non-aromatic anticonvulsant drugs. It is the 1st case with ethosuximide and the 2nd with sodium valproate. We also observed a reactivation of HHV6 infection that may contribute to the development of this hypersensitivity syndrome.
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8/81. Sequential assessment of an antidrug antibody response in a patient with a systemic delayed-onset sulphonamide hypersensitivity syndrome reaction.

    A 19-year-old man was treated with trimethoprim-sulphamethoxazole intermittently over 4 weeks. He developed a rash and fever. Despite treatment with low-dose methylprednisolone, his condition worsened. He developed a confluent erythematous macular eruption, elevated liver enzymes, lymphadenopathy, polyserositis and eosinophilia. A tentative diagnosis of sulphonamide hypersensitivity syndrome reaction (SHSR) was made and a serum sample (acute) was obtained to screen for antibodies associated with SHSR. Intravenous methylprednisolone sodium succinate (250 mg every 6 h for 48 h) was administered. The patient's condition improved, and he was discharged with oral prednisone. A convalescent serum sample was obtained 14 weeks later. By Western blotting and enzyme-linked immunosorbent assay (ELISA), antisulphamethoxazole IgG antibodies were detected in the acute serum sample, supporting the clinical diagnosis of SHSR. Contrary to expectations, antibodies were not detected in the convalescent serum sample by immunoblotting. Antisulphamethoxazole antibodies were detected by ELISA in the convalescent serum, but the titre was decreased approximately 45-fold. One possible explanation for the decrease in antibody concentration in the convalescent sample was the administration of high-dose glucocorticoids to the patient following collection of the acute serum sample.
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9/81. Localized pustulosis induced by betalactams.

    Localized forms of pustular drug eruptions related to antibiotics are uncommon and their mechanism is still unknown. We describe herein a patient who developed numerous pin-head pustules without erythema in the peribuccal area after ingestion of ceftibuten and amoxicillin. The relationship with these drugs was confirmed by single-blind oral challenges. The following tests were performed: prick and intradermal tests with benzylpenicilloyl polylysine, minor determinant mixture, benzylpenicillin and amoxicillin; patch tests were also carried out with benzylpenicillin, amoxicillin, cloxacillin, cefuroxime, ceftriaxone, cefazolin, ceftibuten and cefaclor. All cutaneous tests were negative. Controlled single-blind challenge tests were performed with amoxicillin, cefadroxil, ceftibuten, cefuroxime, cefaclor, erythromycin and ciprofloxacin. All betalactam antibiotics tested gave a positive reaction, with good tolerance of other antibiotics; this would appear to indicate a specific mechanism of hypersensitivity and not an unspecific reaction to wide spectrum antibiotics.
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10/81. A case report of olanzapine-induced hypersensitivity syndrome.

    Hypersensitivity syndrome is defined as a drug-induced complex of symptoms consisting of fever, rash, and internal organ involvement. The hypersensitivity syndrome is well recognized as being caused by anticonvulsants. Olanzapine is an atypical antipsychotic agent whose side effects include sedation, weight gain, and increased creatinine kinase and transaminase levels. To date, there have been no reports of hypersensitivity syndrome related to this drug. A 34-year-old man developed a severe generalized pruritic skin eruption, fever, eosinophilia, and toxic hepatitis 60 days after ingestion of olanzapine. After termination of olanzapine treatment, the fever resolved, the skin rash was reduced, eosinophil count was reduced to normal, and the transaminase levels were markedly reduced. Clinical features and the results of skin and liver biopsies indicated that the patient developed hypersensitivity syndrome caused by olanzapine.
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