Cangemi Roberto, Calvieri Camilla, Bucci Tommaso, Carnevale Roberto, Casciaro Marco, Rossi Elisabetta, Calabrese Cinzia Myriam, Taliani Gloria, Grieco Stefania, Falcone Marco, Palange Paolo, Bertazzoni Giuliano, Celestini Andrea, Pignatelli Pasquale, Violi Francesco
1 I Clinica Medica, Department of Internal Medicine and Medical Specialties, Sapienza University of Rome , Rome, Italy .
Antioxid Redox Signal. 2014 Jun 20;20(18):2949-54. doi: 10.1089/ars.2013.5766. Epub 2014 Mar 14.
In the present study, we tested the hypothesis that oxidative stress could be implicated in myocardial damage during the acute phase of pneumonia. NOX2 activation, the catalytic subunit of NADPH oxidase, and high-sensitivity cardiac troponin T (hs-cTnT) elevation have been analyzed in two hundred forty-eight consecutive patients hospitalized for community-acquired pneumonia. Serum NOX2-derived peptide (sNOX2-dp), a marker of NOX2 activation, and 8-isoprostaglandin F2α (8-iso-PGF2α), a marker of oxidative stress, were measured upon admission; serum hs-cTnT and ECG were measured every 12 and 24 h, respectively. One hundred thirty-five patients (54%) showed elevated serum levels of hs-cTnT (>0.014 μg/L). A logistic regression analysis showed sNOX2-dp (p<0.001), Pneumonia Severity Index score (p<0.001), renal failure (p=0.024), and ejection fraction (p<0.001) as independent predictors of elevated serum levels of hs-cTnT. Serum sNOX2-dp was linearly correlated with hs-cTnT (Rs=0.538; p<0.001) and 8-iso-PGF2α (Rs=0.354; p<0.001). The study provides the first evidence of a significant association between serum cardiac Troponin T elevation and NOX2 upregulation in patients with pneumonia. This finding raises the hypothesis that NOX2-derived oxidative stress may be implicated in myocardial injury and that its inhibition could be a novel therapeutic strategy to limit it.
在本研究中，我们检验了氧化应激可能与肺炎急性期心肌损伤有关的假设。我们分析了248例因社区获得性肺炎住院的连续患者的NOX2激活情况（NADPH氧化酶的催化亚基）以及高敏心肌肌钙蛋白T（hs-cTnT）升高情况。入院时检测了血清中NOX2衍生肽（sNOX2-dp，一种NOX2激活的标志物）和氧化应激标志物8-异前列腺素F2α（8-iso-PGF2α）；分别每12小时和24小时检测血清hs-cTnT和心电图。135例患者（54%）血清hs-cTnT水平升高（>0.014μg/L）。逻辑回归分析显示，sNOX2-dp（p<0.001）、肺炎严重程度指数评分（p<0.001）、肾衰竭（p=0.024）和射血分数（p<0.001）是血清hs-cTnT水平升高的独立预测因素。血清sNOX2-dp与hs-cTnT呈线性相关（Rs=0.538；p<0.001），与8-iso-PGF2α也呈线性相关（Rs=0.354；p<0.001）。该研究首次提供了肺炎患者血清心肌肌钙蛋白T升高与NOX2上调之间存在显著关联的证据。这一发现提出了一个假设，即NOX2衍生的氧化应激可能与心肌损伤有关，抑制该氧化应激可能是限制心肌损伤的一种新的治疗策略。
