Jae H Chung1, Hye J Yeo1, Dohyung Kim2, Sun M Lee3, Junhee Han4, Minseok Kim5, Woo H Cho1. 1. Department of Internal Medicine, The Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Yangsan-si - Republic of Korea. 2. Department of Thoracic and Cardiovascular Surgery, The Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Yangsan-si - Republic of Korea. 3. Department of Laboratory Medicine, The Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Yangsan-si - Republic of Korea. 4. Department of Statistics, Hallym University, Chucheon, Kangwon - Republic of Korea. 5. Division of Biostatistics, The Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Yangsan-si - Republic of Korea.
Abstract
BACKGROUND: Extracorporeal membrane oxygenation (ECMO) has been associated with platelet dysfunction, but no markers of platelet dysfunction during ECMO have been identified. METHODS: We investigated the potential uses of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) as markers of platelet activation induced by ECMO in vivo. RESULTS: 13 patients who received ECMO for acute respiratory failure were included. Generalized estimating equations were used to examine the associations between days on ECMO and the plasma levels of beta-TG and PF4 and of proinflammatory markers. Analyses were performed before ECMO (baseline) and 24, 48, 72 and 168 hours after the commencement of ECMO. The plasma levels of biomolecules were measured by ELISA and Luminex assay.Percentages of platelets varied widely without statistical significance (p = 0.17). Beta-TG levels significantly decreased over the first 72 hours (p<0.001), but PF4 levels decreased nonsignificantly (p = 0.17). Inflammatory markers, that is, plasma IL-6 (p = 0.03), IL-18 (p<0.001), and MMP-8 (p<0.01) levels stabilized during an early period of ECMO support. CONCLUSIONS: Our data suggest that ECMO use may not affect platelet activation during the first 3 days of ECMO. Plasma beta-TG levels may allow assessment of the time-dependent extent of ECMO-induced platelet dysfunction in patients with acute respiratory failure.
BACKGROUND: Extracorporeal membrane oxygenation (ECMO) has been associated with platelet dysfunction, but no markers of platelet dysfunction during ECMO have been identified. METHODS: We investigated the potential uses of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) as markers of platelet activation induced by ECMO in vivo. RESULTS: 13 patients who received ECMO for acute respiratory failure were included. Generalized estimating equations were used to examine the associations between days on ECMO and the plasma levels of beta-TG and PF4 and of proinflammatory markers. Analyses were performed before ECMO (baseline) and 24, 48, 72 and 168 hours after the commencement of ECMO. The plasma levels of biomolecules were measured by ELISA and Luminex assay.Percentages of platelets varied widely without statistical significance (p = 0.17). Beta-TG levels significantly decreased over the first 72 hours (p<0.001), but PF4 levels decreased nonsignificantly (p = 0.17). Inflammatory markers, that is, plasma IL-6 (p = 0.03), IL-18 (p<0.001), and MMP-8 (p<0.01) levels stabilized during an early period of ECMO support. CONCLUSIONS: Our data suggest that ECMO use may not affect platelet activation during the first 3 days of ECMO. Plasma beta-TG levels may allow assessment of the time-dependent extent of ECMO-induced platelet dysfunction in patients with acute respiratory failure.