Abstract and Introduction
Background: Pulmonary embolism (PE) is a common and potentially life-threatening disorder. Our study was aimed to investigate whether oxidative stress markers can be used as clinical markers in the evaluation of acute PE (APE) severity.
Methods: 47 patients with objectively documented diagnosis of APE were recorded. Of these patients, 14 had low-risk PE, 16 had moderate-risk PE, and 17 had high-risk PE. 21 healthy subjects were also enrolled in this study. Ischemia-modified albumin (IMA), prooxidants-antioxidants balance (PAB), advanced protein oxidation products (AOPPs), and ferric reducing antioxidant power (FRAP) were measured as oxidative stress parameters to evaluate the role of oxidative stress.
Results: In the low-risk and moderate-risk APE groups, AOPPs and PAB levels were significantly higher and FRAP levels were significantly lower than those in the control group. AOPPs and IMA levels in the patients with high-risk PE were significantly higher than those in both the low-risk and moderate-risk APE patients. There was a significant correlation between levels of AOPPs and the levels of both IMA (r: 0.462, p < 0.001) and PAB (r:0.378, p < 0.005). Serum FRAP levels were negatively correlated with PAB (r:− 0.683, p < 0.001) and AOPPs levels (r:− 0,384, p < 0.001). There was also a significant positive correlation between the serum IMA and PAB levels.
Conclusions: We clearly demonstrated that reactive oxygen species formation is significantly enhanced in APE. IMA and AOPPs may be used as clinical markers in the evaluation of APE severity in clinical practice. However, further studies with larger patient populations and longer follow-up periods are required to confirm the mechanisms underlying these findings.
Pulmonary embolism (PE) is a relatively common cardiovascular emergency. By occluding the pulmonary arterial bed, it may lead to acute life-threatening situations. PE is a difficult diagnosis that may be missed because of its non-specific clinical presentation.
On the other hand, acute PE (APE) is a life-threatening disease leading to reperfusion of previously ischemia of the lung parenchyma. Pulmonary infarction occurs with the development of hemorrhagic necrosis in the lung parenchyma distal to the pulmonary artery occluded in PE. Oxidative stress accompanies this phenomenon. Previous studies have proven that hypoxia-reoxygenation and ischemia-reperfusion cause oxidative stress accompanied by the production of oxygen free radicals exceeding the endogenous antioxidant capacity.[3,4] In addition, in the case of ischemia, an albumin molecule called ischemia-modified albumin (IMA) is formed as a result of structural changes in the last amino terminal that binds metal in the serum albumin structure. The increase in IMA concentration is currently used in the evaluation of patients with coronary syndrome as a marker of myocardial ischemia. There are also studies evaluating IMA measurements in the diagnosis of PE.[7,8]
In our clinical research, it was aimed to investigate the changes in oxidative and antioxidant markers such as IMA, advanced oxidation protein products (AOPPs), prooxidants-antioxidants balance (PAB) and ferric reducing antioxidant power (FRAP) levels in patients diagnosed with APE were classified as high-risk, moderate-risk, low-risk before the initiation of anticoagulant/thrombolytic therapy.
BMC Pulm Med. 2022;22(382) © 2022 BioMed Central, Ltd.