Cases reported "stevens-johnson syndrome"

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1/231. Infectious crystalline keratopathy and endophthalmitis secondary to mycobacterium abscessus in a monocular patient with stevens-johnson syndrome.

    PURPOSE: To describe the clinical and laboratory features of infectious crystalline keratopathy and endophthalmitis secondary to mycobacterium abscessus in a patient with stevens-johnson syndrome. METHOD: Case report. A 19-year-old man with a history of stevens-johnson syndrome and multiple corneal transplants developed white crystalline corneal infiltrates. RESULTS: anterior chamber aspirate disclosed acid-fast bacilli. A repeat corneal transplant was performed and antibiotic therapy begun. Histopathology showed focal acute inflammation surrounding collections of acid-fast bacilli, which were speciated as M. abscessus. CONCLUSIONS: M. abscessus is a cause of infectious crystalline keratopathy and endophthalmitis. risk factors include ocular surface disease, corneal transplantation, and immunosuppressive therapy. ( info)

2/231. Increased risk of erythema multiforme major with combination anticonvulsant and radiation therapies.

    erythema multiforme major (EMM; stevens-johnson syndrome) is a cutaneous disorder associated with a wide variety of factors including ingestion of drugs such as phenytoin and exposure to intracranial radiation therapy. Based on observations of a 47-year-old black man with brain metastases who developed EMM after combined phenytoin and radiation therapy, we conducted a medline literature search for articles on similar cases from 1966 to the present. Twenty cases were identified that support the hypothesis that EMM is associated with combined phenytoin and radiation therapy. The reaction, or its severity, has no relationship to the phenytoin or radiation therapy dosage, or to the histologic type of brain tumor. Also, EMM has no apparent age or gender predisposition in association with phenytoin-radiation therapy. Thus this is a clinical phenomenon that occurs with unusual frequency in patients with brain tumor who undergo radiation therapy while taking phenytoin. phenytoin and other anticonvulsants such as phenobarbital and carbamazepine induce cytochrome P450 3A and produce oxidative reactive intermediates that may be implicated in hypersensitivity reactions such as EMM. Both carbamazepine and barbiturates have shown cross-sensitivity with phenytoin; furthermore, a case of EMM in a patient receiving carbamazepine and whole brain radiation therapy has been reported. As carbamazepine, valproate, and barbiturates have been associated with EMM, gabapentin may be considered as alternative anticonvulsant therapy when appropriate. ( info)

3/231. 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. ( info)

4/231. stevens-johnson syndrome limited to multiple sites of radiation therapy in a patient receiving phenobarbital.

    stevens-johnson syndrome (SJS) is a severe cutaneous eruption that most often appears as an adverse reaction to a medication. There have been 21 reported cases of atypical erythema multiforme, toxic epidermal necrolysis, and SJS arising in patients receiving radiation therapy in addition to phenytoin, phenobarbital, or carbamazepine. We report the second case of SJS resulting from concomitant phenobarbital and radiation therapy, in which the eruption was limited to the sites of radiation, which were multiple. ( info)

5/231. stevens-johnson syndrome in patients on phenytoin and cranial radiotherapy.

    The use of phenytoin as a prophylactic anticonvulsant after brain surgery, particularly for brain tumors, is a common practice, regardless of whether the patient has a previous history of convulsions. This treatment policy assumes that the benefits exceed the risks. Four cases are described of adverse reactions to phenytoin during the concomitant use of cranial radiotherapy. In one patient this proved fatal. There is increasing anecdotal support in the literature for a synergistic effect between phenytoin therapy and cranial radiotherapy that can result in the life-threatening stevens-johnson syndrome. While the association is uncommon, four cases within 24 months in one department suggest that the routine use of postoperative phenytoin as a prophylactic anticonvulsant in the absence of a history of seizures may not be warranted, particularly if the patient is to receive cranial radiotherapy. ( info)

6/231. stevens-johnson syndrome caused by indinavir.

    A case is presented of an HIV-infected man who developed stevens-johnson syndrome shortly after the initiation of treatment with indinavir. This is the first case ever reported of this adverse drug reaction occurring with an hiv protease inhibitor. ( info)

7/231. The efficacy of therapeutic plasmapheresis for the treatment of fatal hemophagocytic syndrome: two case reports.

    A potentially fatal hemophagocytic syndrome (HPS) has been noted in patients with reactive HPS. We describe 2 patients with reactive HPS treated with a regimen of therapeutic plasmapheresis and evaluate the efficacy of plasmapheresis for fatal HPS. Case 1 was a 31 year-old woman who had been treated for systemic lupus erythematosus (SLE) with corticosteroid hormones and immunosuppressants. She presented with persistent leukopenia and thrombocytopenia with spiking fever. She had an elevated level of serum ferritin, liver dysfunction, coagulopathy, and plasma inflammatory cytokines. Her bone marrow smear disclosed numerous hemophagocytosis of histiocytes. She was administered therapeutic plasmapheresis with total plasma exchange by fresh frozen plasma. There was an immediate and prominent decrease of cytokines, and she completely recovered. Case 2 was a 34 year-old woman who had been receiving high doses of corticosteroids and plasmapheresis for severe Stevens-Johnson's syndrome. After 18 months, she presented with physical and laboratory findings resembling lupus-like conditions and was administered high doses of corticosteroids and immunosuppressants. Human parvovirus B19 infection was detected by IgM and IgG antibodies and viral dna from a bone marrow sample; moreover, a bone marrow smear disclosed findings of HPS. Repeated therapeutic plasmapheresis was effective for improving her symptoms and laboratory abnormalities; however, she suffered from septic methicilline resistant staphylococcus aureus infection and finally died of a brain hemorrhage resulting from disseminated intravascular coagulation (DIC). ( info)

8/231. amoxicillin/clavulanate-associated hepatic failure with progression to stevens-johnson syndrome.

    OBJECTIVE: To describe a patient who developed hepatic failure, stevens-johnson syndrome (SJS), and died after receiving amoxicillin/clavulanate therapy. CASE SUMMARY: A 37-year-old white man without significant past medical history received a 10-day course of amoxicillin/clavulanate for treatment of pneumonia. Thirty-two days after starting amoxicillin/clavulanate, he developed jaundice, rash, pruritus, and increasing fatigue. On further evaluation, with the exclusion of toxicity from other drugs or diseases, the time course to development of cholestatic jaundice correlated with the use of amoxicillin/clavulanate. The patient consequently died with progressive hepatic failure, renal failure, and SJS. DISCUSSION: Hepatic injury has been reported with amoxicillin/clavulanate. signs and symptoms of jaundice and pruritus may appear up to to six weeks after stopping therapy. Most cases of liver injury have been benign and reversible on discontinuation of the amoxicillin/clavulanate. Reported hepatic reactions have been mainly cholestatic, with some mixed cholestatic/hepatocellular liver function test abnormalities. CONCLUSIONS: Clinicians should be aware of amoxicillin/clavulanate as a drug capable of causing hepatitis with eventual systemic dysfunction. While recovery is usually complete following withdrawal of the drug, in patients with rash associated with hepatic dysfunction, renal insufficiency, or other unusual symptoms, earlier consideration of initiating systemic steroids or liver transplantation referral, in hopes of avoiding progressive systemic response, might be worthwhile. ( info)

9/231. Dermatological adverse effects with the antimalarial drug mefloquine: a review of 74 published case reports.

    mefloquine is a relatively new antimalarial drug which has been associated with a wide variety of adverse effects, including skin reactions. In order to evaluate the range and frequency of mefloquine's dermatological effects, we searched the scientific literature for published case reports of such effects. We found 74 case reports, published between the years 1983 and 1997. pruritus and maculopapular rash are the dermatological effects most commonly associated with mefloquine: their approximate frequency is 4-10% for pruritus, and up to 30% for nonspecific maculopapular rash. Adverse effects associated less commonly with mefloquine include urticaria, facial lesions and cutaneous vasculitis. One case of stevens-johnson syndrome and one fatal case of toxic epidermal necrolysis occurred. Appropriate primary studies of mefloquine use should be carried out to elucidate the epidemiology and aetiology of dermatological and other adverse effects of the drug. ( info)

10/231. Paraneoplastic pemphigus associated with Castleman tumor, myasthenia gravis and bronchiolitis obliterans.

    BACKGROUND: Cases of paraneoplastic pemphigus (PNP) have been reported associated with various lymphoproliferative malignancies and benign Castleman tumors, with the most severe course and fatal outcome seen in patients with bronchiolitis obliterans. OBJECTIVE: The aim was to establish immunologic associations by coexistence of Castleman tumor, myasthenia gravis, and bronchiolitis obliterans and to evaluate the treatment modalities. methods: Clinical studies included computed tomography of the mediastinum, computed tomography and magnetic resonance imaging of the abdominal cavity, and quantitative electromyography. Direct and indirect immunofluorescence on various substrates, immunoblot analysis, immunoprecipitation, and specific enzyme-linked immunosorbent assay using recombinant desmogleins (Dsg) were performed as immunologic assays. RESULTS: Direct and indirect immunofluorescence including rat bladder showed intercellular antibodies. immunoblotting disclosed antibodies to envoplakin (210 kd protein) and periplakin (190 kd protein); in addition, immunoprecipitation detected antibodies to desmoplakin I (250 kd protein). antibodies to Dsg3 (pemphigus vulgaris antigen) were detected by specific enzyme-linked immunosorbent assay. myasthenia gravis was controlled by drugs; however, mucocutaneous changes were not fully responsive to corticosteroids and cyclophosphamide pulses, cyclosporine, and intravenous immunoglobulins. The surgical removal of Castleman tumor did not change the course of the disease. The fatal outcome was the result of bronchiolitis obliterans that occurred after the surgery and was only transitionally controlled by plasmapheresis. CONCLUSION: This is the first case of paraneoplastic pemphigus associated with Castleman tumor, myasthenia gravis, and bronchiolitis obliterans. Despite a benign character of the tumor the patient died, as do all patients with bronchiolitis obliterans. Massive plasmapheresis has only a transient effect. We confirmed the presence of antibodies to Dsg 3, in addition to the set of specific paraneoplastic pemphigus antibodies against various proteins of plakin family. ( info)
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