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Pulmonary thromboembolism (PE) is the third most common medical emergency with mortality due to ischemia and reperfusion lung injury. Lung ischaemia-reperfusion injury. Lung reperfusion damage is believed to cause cellular damage and apoptosis. The aim of the present study was to evaluate the levels of fetuin-A, albumin, and apoptosis biomarkers (Apaf-1, sFas, and sFasL) among pulmonary thromboembolic patients. MATERIAL AND METHODS: Blood samples were collected from 45 volunteer patients and 40 healthy control volunteers. Human apoptosis biomarkers (Apaf-1, sFas, sFasL, and caspase-9) and fetuin-A values were measured by ELISA device. Student’s t-test or Mann-Whitney U test were used for continuous variables, and categorical variables were compared with the chi-square test to assess the significance of intergroup differences. The mean values of apoptosis biomarkers and acute phase reactants between dead and survival patients were also compared. RESULTS: While the apoptosis mean values of Apaf-1, sFas, sFasL, and caspase-9 for the control group were 0.12 ± 0.01, 332.1 ± 28.0, 130.4 ± 34.6, and 74.3 ± 2.6, for the patient group they were 0.14 ± 0.02, 509.1 ± 67.6, 139.9 ± 23.7, and 79.4 ± 2.8, respectively. The group differences were significant for all the biomarkers (p = 0.01, p = 0.001, p = 0.19, and p = 0.01, respectively). The negative acute phase fetuin- A and albumin levels decreased significantly in the patient groups (p = 0.01 and p = 0.01, respectively). CONCLUSIONS: Intrinsic and extrinsic apoptosis pathways are stimulated during pulmonary embolism, and negative acute phase reactants are decreased. There was a correlation with the mortality and Apaf-1, sFas, caspase-9, fetuin, and albumin levels.

Apoptosis biomarkers (Apaf-1, sFa s, sFa s-L, and caspase-9), albumin, and fetuin-A levels in pulmonary thromboembolic patients