Linked Life Data

17466923

Source:http://linkedlifedata.com/resource/pubmed/id/17466923

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2007-4-30
pubmed:abstractText
Cytokines play a role in the immunopathological and molecular mechanisms of sulfonamide-induced hypersensitivity reactions (HSRs). The objective of this study was to analyze the reliability and correlation between the clinical symptoms observed in affected patients (n = 86) because of a sulfonamide-induced HSR and their lymphocyte toxicity assay (LTA) values. Another goal was to determine the cytokine secretion in the patient's sera and their expression in the peripheral blood mononuclear cells (PBMCs) and to explore whether a correlation exists among positive LTA score, cytokine levels, and HSR occurrence. The final goal is to determine whether these measures could be used to predict the likelihood of a patient to experience an HSR during sulfonamide treatment. Such a predictive ability would be valuable to the clinician to know whether the patient would tolerate sulfonamides or whether an alternative antibiotic should be prescribed. The LTA showed a good correlation with the clinical involvement of patients with hypersensitivity syndromes. In addition, the pro-inflammatory cytokines presented significant differences in patients that had rash, fever, and organ involvement than in control patients or any of the other patient groups. Expression of tumor necrosis factor alpha (TNF-alpha) is significantly higher in patients presenting rash, fever, and organ involvement versus all other groups. It is concluded that a positive LTA is a predictor for sulfonamide-induced true HSR. In addition, T-helper cell 1 cytokines [TNF-alpha, interleukins (ILs) 1 and 2] as well as the chemokine regulated upon activation, normal T-cell expressed and secreted (RANTES) control the pathogenesis of sulfonamide-induced HSR and may be used in early diagnosis of the syndrome.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1931-5244
pubmed:author
pubmed:issnType
Print
pubmed:volume
149
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
243-53
pubmed:dateRevised
2008-6-2
pubmed:meshHeading
pubmed-meshheading:17466923-Adult, pubmed-meshheading:17466923-Aged, pubmed-meshheading:17466923-Chemokine CCL5, pubmed-meshheading:17466923-Cytokines, pubmed-meshheading:17466923-Cytotoxicity Tests, Immunologic, pubmed-meshheading:17466923-Drug Hypersensitivity, pubmed-meshheading:17466923-Early Diagnosis, pubmed-meshheading:17466923-Female, pubmed-meshheading:17466923-Humans, pubmed-meshheading:17466923-Inflammation Mediators, pubmed-meshheading:17466923-Interleukin-1, pubmed-meshheading:17466923-Interleukin-2, pubmed-meshheading:17466923-Likelihood Functions, pubmed-meshheading:17466923-Male, pubmed-meshheading:17466923-Middle Aged, pubmed-meshheading:17466923-Predictive Value of Tests, pubmed-meshheading:17466923-Sulfonamides, pubmed-meshheading:17466923-Syndrome, pubmed-meshheading:17466923-Tumor Necrosis Factor-alpha
pubmed:year
2007
pubmed:articleTitle
Immunopathogenesis of hypersensitivity syndrome reactions to sulfonamides.
pubmed:affiliation
In Vitro Drug Safety and Biotechnology Laboratory, University of Toronto, Toronto, Ontario, Canada. manuela.neuman@utoronto.ca
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural