Warning: Undefined variable $zfal in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Deprecated: str_replace(): Passing null to parameter #3 ($subject) of type array|string is deprecated in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 530
 free
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 531
 free
 free
 
English Wikipedia
Nephropedia Template TP (
Twit Text
DeepDyve
Pubget Overpricing |  
lüll
Association of anthracycline-related cardiac histological lesions with NADPH oxidase functional polymorphisms Cascales A; Pastor-Quirante F; Sanchez-Vega B; Luengo-Gil G; Corral J; Ortuno-Pacheco G; Vicente V; de la Pena FAOncologist 2013[]; 18 (4): 446-53OBJECTIVE: Treatment with anthracyclines may cause cardiac dysfunction, but the sequence of anthracycline-induced heart lesions has been incompletely characterized. NADPH oxidase, a key mediator of oxidative cardiac damage and remodeling, modulates anthracycline clinical cardiotoxicity. Our aim was to determine which cardiac histological lesions are specifically induced by anthracycline treatment and to investigate the role of NADPH functional genetic polymorphisms in their development. PATIENTS AND METHODS: Using a retrospective case-control design, we evaluated cardiac histological lesions and NADPH genotype (polymorphisms rs1883112, rs4673, and rs13058338) in 97 consecutive decedents with a cancer diagnosis (48 treated with anthracyclines). RESULTS: Myocytolysis (60%), patched myocardial necrosis (19%), and myocardial fibrosis (diffuse and patched; 62% and 23%, respectively) were associated with anthracycline treatment. In patients receiving anthracyclines, NADPH oxidase polymorphism rs4673 protected against focal myocardial necrosis (odds ratio [OR], 0.11; 95% confidence interval [CI], 0.20-0.63) whereas rs1883112 was strongly associated with cardiac fibrosis (OR, 5.11; 95% CI, 1.59-16.43), which was present in all homozygotes. CONCLUSION: Anthracyclines induce a cardiac remodeling pattern characterized by interstitial or patched fibrosis. The contribution of the functionally relevant NADPH polymorphisms rs1883112 and rs4673 to anthracycline-related heart lesions provides a plausible explanation for their modulation of cardiotoxicity. If confirmed, these findings may lead to better individualized strategies for early detection and prevention of anthracycline cardiotoxicity.|Adult[MESH]|Anthracyclines/*administration & dosage/adverse effects[MESH]|Autopsy[MESH]|Case-Control Studies[MESH]|Drug-Related Side Effects and Adverse Reactions/genetics/pathology[MESH]|Female[MESH]|Genetic Association Studies[MESH]|Heart Failure/chemically induced/*genetics/pathology[MESH]|Heart/*drug effects[MESH]|Humans[MESH]|Male[MESH]|Middle Aged[MESH]|Myocardium/*pathology[MESH]|NADPH Oxidases/*genetics[MESH]|Neoplasms/drug therapy/pathology[MESH]|Oxidative Stress[MESH]|Polymorphism, Genetic[MESH]|Retrospective Studies[MESH] |
