TY - JOUR
T1 - Blood glutathione as a marker of cardiac allograft vasculopathy in heart transplant recipients
AU - De Chiara, Benedetta
AU - Bigi, Riccardo
AU - Campolo, Jonica
AU - Parolini, Marina
AU - Turazza, Fabio
AU - Masciocco, Gabriella
AU - Frigerio, Maria
AU - Fiorentini, Cesare
AU - Parodi, Oberdan
PY - 2005/6
Y1 - 2005/6
N2 - Background: Cardiac allograft vasculopathy (CAV) limits survival after heart transplantation (HTx). Between immunologic and non-immunologic factors, reactive oxygen species generation has been proposed as pathogenetic mechanism. This study was aimed at evaluating redox status in HTx recipients and verifying whether it could be independently associated with CAV. Methods: Fifty-five consecutive male HTx recipients, median [interquartile range] age 60 yr [50, 64], underwent angiography 67 months [21, 97] after HTx to assess CAV, defined as significant stenosis in ≥1 epicardial vessel or any distal vessel attenuation. All patients underwent blood sampling 89 months [67, 119] after HTx for biochemical (glucose, creatinine, total and LDL cholesterol, and cyclosporin levels) and redox evaluation [plasma reduced and total homocysteine, cysteine, cysteinylglycine, glutathione, blood reduced glutathione (GSHbl) and vitamin E]. Univariate Odds Ratios (OR) with 95% confidence interval (95% CI, highest vs. lowest quartile) were estimated on the basis of a logistic regression analysis between clinical, conventional biochemical and redox data. Only the significant variables at univariate entered into multivariate analysis. Results: CAV was documented in 15 (27%) patients. Univariate analysis showed that time from HTx to angiography (OR 3.97, 95% CI 1.15-14, p = 0.03) and GSHbl (OR 0.31, 95% CI: 0.14-0.70, p = 0.005) were significantly associated with CAV. However, multivariate analysis revealed GSHbl as the only independent predictor of CAV (OR 0.31, 95% CI: 0.13-0.74, p = 0.008). Conclusions: In HTx recipients reduced levels of GSHbl are independently associated with CAV. Given its potent intracellular scavenger properties, GSHbl may serve as a marker of antioxidant defence consumption, favouring CAV development.
AB - Background: Cardiac allograft vasculopathy (CAV) limits survival after heart transplantation (HTx). Between immunologic and non-immunologic factors, reactive oxygen species generation has been proposed as pathogenetic mechanism. This study was aimed at evaluating redox status in HTx recipients and verifying whether it could be independently associated with CAV. Methods: Fifty-five consecutive male HTx recipients, median [interquartile range] age 60 yr [50, 64], underwent angiography 67 months [21, 97] after HTx to assess CAV, defined as significant stenosis in ≥1 epicardial vessel or any distal vessel attenuation. All patients underwent blood sampling 89 months [67, 119] after HTx for biochemical (glucose, creatinine, total and LDL cholesterol, and cyclosporin levels) and redox evaluation [plasma reduced and total homocysteine, cysteine, cysteinylglycine, glutathione, blood reduced glutathione (GSHbl) and vitamin E]. Univariate Odds Ratios (OR) with 95% confidence interval (95% CI, highest vs. lowest quartile) were estimated on the basis of a logistic regression analysis between clinical, conventional biochemical and redox data. Only the significant variables at univariate entered into multivariate analysis. Results: CAV was documented in 15 (27%) patients. Univariate analysis showed that time from HTx to angiography (OR 3.97, 95% CI 1.15-14, p = 0.03) and GSHbl (OR 0.31, 95% CI: 0.14-0.70, p = 0.005) were significantly associated with CAV. However, multivariate analysis revealed GSHbl as the only independent predictor of CAV (OR 0.31, 95% CI: 0.13-0.74, p = 0.008). Conclusions: In HTx recipients reduced levels of GSHbl are independently associated with CAV. Given its potent intracellular scavenger properties, GSHbl may serve as a marker of antioxidant defence consumption, favouring CAV development.
KW - Antioxidants
KW - Cardiac allograft vasculopathy
KW - Free radicals
KW - Glutathione
KW - Heart transplantation
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U2 - 10.1111/j.1399-0012.2005.00352.x
DO - 10.1111/j.1399-0012.2005.00352.x
M3 - Article
C2 - 15877800
AN - SCOPUS:19044381132
VL - 19
SP - 367
EP - 371
JO - Clinical Transplantation
JF - Clinical Transplantation
SN - 0902-0063
IS - 3
ER -