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Immunopathogenesis of hypersensitivity syndrome reactions to sulfonamides.
Transl Res. 2007 May; 149(5):243-53.TR

Abstract

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.

Authors+Show Affiliations

In Vitro Drug Safety and Biotechnology Laboratory, University of Toronto, Toronto, Ontario, Canada. manuela.neuman@utoronto.caNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17466923

Citation

Neuman, Manuela G., et al. "Immunopathogenesis of Hypersensitivity Syndrome Reactions to Sulfonamides." Translational Research : the Journal of Laboratory and Clinical Medicine, vol. 149, no. 5, 2007, pp. 243-53.
Neuman MG, Shear NH, Malkiewicz IM, et al. Immunopathogenesis of hypersensitivity syndrome reactions to sulfonamides. Transl Res. 2007;149(5):243-53.
Neuman, M. G., Shear, N. H., Malkiewicz, I. M., Taeri, M., Shapiro, L. E., Krivoy, N., Haber, J., Gomez, M., Fish, J., Cartotto, R., & Cohen, L. (2007). Immunopathogenesis of hypersensitivity syndrome reactions to sulfonamides. Translational Research : the Journal of Laboratory and Clinical Medicine, 149(5), 243-53.
Neuman MG, et al. Immunopathogenesis of Hypersensitivity Syndrome Reactions to Sulfonamides. Transl Res. 2007;149(5):243-53. PubMed PMID: 17466923.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Immunopathogenesis of hypersensitivity syndrome reactions to sulfonamides. AU - Neuman,Manuela G, AU - Shear,Neil H, AU - Malkiewicz,Izabella M, AU - Taeri,Masud, AU - Shapiro,Lori E, AU - Krivoy,Norberto, AU - Haber,Julia, AU - Gomez,Manuel, AU - Fish,Joel, AU - Cartotto,Robert, AU - Cohen,Lawrence, PY - 2006/07/23/received PY - 2006/12/22/revised PY - 2006/12/22/accepted PY - 2007/5/1/pubmed PY - 2007/6/7/medline PY - 2007/5/1/entrez SP - 243 EP - 53 JF - Translational research : the journal of laboratory and clinical medicine JO - Transl Res VL - 149 IS - 5 N2 - 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. SN - 1931-5244 UR - https://www.unboundmedicine.com/medline/citation/17466923/Immunopathogenesis_of_hypersensitivity_syndrome_reactions_to_sulfonamides_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1931-5244(07)00011-4 DB - PRIME DP - Unbound Medicine ER -