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Acute psychosis with Coricidin cold medicine.
Sharma A, Dewan V, Petty F.
Publication Types:
PMID: 16076908 [PubMed - indexed for MEDLINE]
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Hypersensitivity syndrome and pure red cell aplasia following allopurinol therapy in a patient with chronic kidney disease.
Chao SC, Yang CC, Lee JY.
Department of Dermatology, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
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.
Publication Types:
PMID: 16076905 [PubMed - indexed for MEDLINE]
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Amoxicillin/telithromycin-induced rash in infectious mononucleosis.
Wargo KA, McConnell V, Jennings M.
Publication Types:
PMID: 16046485 [PubMed - indexed for MEDLINE]
Vulval adenosis associated with toxic epidermal necrolysis.
Noel JC, Buxant F, Fayt I, Bebusschere G, Parent D.
Publication Types:
PMID: 16086774 [PubMed - indexed for MEDLINE]
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Docetaxel-induced recall dermatitis on previous laser treatment sites.
Chu CY, Yang CH.
Publication Types:
PMID: 16086765 [PubMed - indexed for MEDLINE]
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Adverse cutaneous reactions to anakinra in patients with rheumatoid arthritis: clinicopathological study of five patients.
Vila AT, Puig L, Fernandez-Figueras MT, Laiz AM, Vidal D, Alomar A.
Department of Dermatology, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain. avila@hsll.es
BACKGROUND: Anakinra, a recombinant human form of interleukin-1 receptor antagonist, is used to treat patients with active rheumatoid arthritis (RA). OBJECTIVES: To report five patients with cutaneous adverse drug reactions due to anakinra and to evaluate the histopathological and immunohistochemical findings with the aim of understanding the possible mechanisms involved. METHODS: Five patients of a series of 10 patients with RA undergoing treatment with anakinra in a clinical trial presented inflammatory lesions at the anakinra injection sites. In each case, clinical features were recorded and skin biopsy specimens were obtained. In one patient sequential biopsy specimens were obtained from skin lesions at different stages of development. Tissue sections of the biopsy specimens were stained with haematoxylin and eosin and May-Grunwald-Giemsa, and were immunoreacted with antibodies to leucocyte common antigen, CD68, CD3, CD45RO, CD20 and CD45RA. RESULTS: The onset of reaction was within the first month of treatment and appeared as well-defined erythema and oedema involving the injection sites. In two patients the treatment had to be discontinued because of the skin reaction, and in one patient it was associated with systemic involvement. All biopsy specimens exhibited marked dermal oedema and a lichenoid dermal infiltrate composed mainly of lymphomononuclear cells with prominent populations of eosinophils and large CD68+ dermal macrophages and an increase in the number of mast cells, which were spindle shaped in a significant proportion. CONCLUSIONS: Cutaneous toxicity is a frequent, usually well-tolerated complication of treatment with anakinra in patients with RA, although in some cases it can be associated with systemic involvement. The most relevant histopathological findings include dermal oedema and a lichenoid, perivascular and periadnexal predominantly lymphomononuclear infiltrate, with many eosinophils and the presence of enlarged CD68+ macrophages. These findings resemble those seen in skin reactions in patients receiving chemotherapy and colony-stimulating factors. We also found an increase in mast cell numbers that could be a specific effect of anakinra.
PMID: 16086759 [PubMed - indexed for MEDLINE]
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Toxic epidermal necrolysis: current evidence, practical management and future directions.
Chave TA, Mortimer NJ, Sladden MJ, Hall AP, Hutchinson PE.
Department of Dermatology, Leicester Royal Infirmary, University Hospitals of Leicester NHS Trust, Leicester LE1 5WW, UK. toby.chave@rcht.cornwall.nhs.uk
Toxic epidermal necrolysis (TEN) is a rare disorder characterized by extensive epidermal death. Almost all cases appear to be caused by an idiosyncratic drug reaction. Proposed pathogenic mechanisms are conflicting, and the evidence for the benefits of individual treatments is inadequate, and in some cases contradictory. The mortality rate remains high. We review the literature pertaining to the pathogenesis of TEN and drug reactions in general. The rationale for therapeutic interventions, together with reported evidence of efficacy, are considered. We present a composite model of TEN, based on previous work and suggested pathogeneses of TEN, mechanisms of drug reactions and reported cytotoxic lymphocyte (CTL) cytolytic pathways. In this system, TEN, like some other cutaneous drug eruptions, is an HLA class I-restricted, specific drug sensitivity, resulting in clonal expansion of CD8+ CTLs. Cytotoxicity is mediated by CTL granzyme and possibly death receptor (DR) ligand (DR-L), probably Fas ligand (FasL). Particular to TEN, there is then an amplification sequence involving further DR-L expression. FasL is likely to be particularly important but tumour necrosis factor (TNF) may well contribute, via the TNF receptor 1 (TNF-R1) death pathway. Alternatively, we suggest the possibility of upregulation of an antiapoptotic TNF-R1-nuclear factor kappaB pathway, which would proscribe treatments which downregulate this pathway. None of the published data on individual treatment efficacies is sufficiently strong to suggest a definitive single treatment. Currently a multifaceted regimen appears indicated, targeting various likely intermediary mechanisms, including elimination of residual drug, immunosuppression, inhibition of DR pathways, general antiapoptotic strategies, and aggressive supportive care. Particular attention has been directed at avoiding potential conflicts between different treatments and avoiding agents that theoretically might have a net proapoptotic rather than antiapoptotic effect. Nursing on a specialized unit is of paramount importance.
Publication Types:
PMID: 16086734 [PubMed - indexed for MEDLINE]
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Thiodiglycolic acid as a possible causative agent of fixed drug eruption provoked only after continuous administration of S-carboxymethyl-L-cysteine: case report and review of reported cases.
Adachi A, Sarayama Y, Shimizu H, Yamada Y, Horikawa T.
Publication Types:
PMID: 16029368 [PubMed - indexed for MEDLINE]
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Cutaneous reaction induced by vincristine.
Nakashima H, Fujimoto M, Tamaki K.
Publication Types:
PMID: 16029367 [PubMed - indexed for MEDLINE]
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Methysergide-induced scleroderma-like changes of the legs.
Kluger N, Girard C, Bessis D, Guillot B.
Publication Types:
PMID: 16029366 [PubMed - indexed for MEDLINE]
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Nodal marginal zone lymphoma in association with hydroa vacciniforme-like papulovesicular eruption, hypersensitivity to mosquito bites and insect bite-like reaction.
Yoon TY, Kim YG, Kim JW, Kim MK.
Publication Types:
PMID: 16029356 [PubMed - indexed for MEDLINE]
Comment on:
Lepromatous leprosy and reversal reaction in a Micronesian immigrant.
Grandhe NP, Dogra S, Kumar B.
Publication Types:
PMID: 16101878 [PubMed - indexed for MEDLINE]
Differences between organophosphorus insecticides in human self-poisoning: a prospective cohort study.
Eddleston M, Eyer P, Worek F, Mohamed F, Senarathna L, von Meyer L, Juszczak E, Hittarage A, Azhar S, Dissanayake W, Sheriff MH, Szinicz L, Dawson AH, Buckley NA.
South Asian Clinical Toxicology Research Collaboration, Centre for Tropical Medicine, University of Oxford, Churchill Hospital, Oxford, UK. eddlestonm@eureka.lk
BACKGROUND: Although more than 100 organophosphorus insecticides exist, organophosphorus poisoning is usually regarded as a single entity, distinguished only by the compound's lethal dose in animals. We aimed to determine whether the three most common organophosphorus insecticides used for self-poisoning in Sri Lanka differ in the clinical features and severity of poisoning they cause. METHODS: We prospectively studied 802 patients with chlorpyrifos, dimethoate, or fenthion self-poisoning admitted to three hospitals. Blood cholinesterase activity and insecticide concentration were measured to determine the compound and the patients' response to insecticide and therapy. We recorded clinical outcomes for each patient. FINDINGS: Compared with chlorpyrifos (35 of 439, 8.0%), the proportion dying was significantly higher with dimethoate (61 of 264, 23.1%, odds ratio [OR] 3.5, 95% CI 2.2-5.4) or fenthion (16 of 99, 16.2%, OR 2.2, 1.2-4.2), as was the proportion requiring endotracheal intubation (66 of 439 for chlorpyrifos, 15.0%; 93 of 264 for dimethoate, 35.2%, OR 3.1, 2.1-4.4; 31 of 99 for fenthion, 31.3%, 2.6, 1.6-4.2). Dimethoate-poisoned patients died sooner than those ingesting other pesticides and often from hypotensive shock. Fenthion poisoning initially caused few symptoms but many patients subsequently required intubation. Acetylcholinesterase inhibited by fenthion or dimethoate responded poorly to pralidoxime treatment compared with chlorpyrifos-inhibited acetylcholinesterase. INTERPRETATION: Organophosphorus insecticide poisoning is not a single entity, with substantial variability in clinical course, response to oximes, and outcome. Animal toxicity does not predict human toxicity since, although chlorpyrifos is generally the most toxic in rats, it is least toxic in people. Each organophosphorus insecticide should be considered as an individual poison and, consequently, patients might benefit from management protocols developed for particular organophosphorus insecticides.
Publication Types:
PMID: 16243090 [PubMed - indexed for MEDLINE]
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