196 Letters to the Editor
Letters to the Editor Blood Coagulation and Fibrinolysis 2014, 25:196–197
Whether chicken or egg hatch? Sinan Is¸cen Diyarbakır Military Hospital, Diyarbakir, Turkey Correspondence to Sinan Is¸cen, MD, Diyarbakir Military Hospital, Diyarbakir, Turkey
We read the article, ‘Mean platelet volume in patients with nonvalvular atrial fibrillation’ written by Tekin et al. [1]. The authors concluded that to improve the clinical utility of mean platelet volume in the pathogenesis of atrial fibrillation, further studies need to be carried out. We know that atrial fibrillation (AF) is associated with a hypercoagulable state, which is related to the presence of dense spontaneous echo contrast (SEC) and thrombi in the left atrium or left atrial appendage on transesophageal echocardiography. SEC is a well recognized independent predictor for stroke and thromboembolism in AF. Spontaneous echo contrast is believed to represent erythrocyte aggregation in low shear rate conditions [2]. There is a very strong association between left atrial spontaneous echo contrast and left atrial thrombi. We know also that the thrombotic process is associated with platelet destruction. Thrombopoietin levels are elevated for increased platelet count and volume. When thrombopoietin binds to its platelet receptor, it induces phosphorylation of the c-Mpl receptor and a number of other molecules in several different signal transduction pathways [3,4], therefore it affects the function and volume of platelets. Platelet count and volume increase. The main point is whether AF increases platelet volume or whether increased platelet volume causes AF, which leads to a thrombotic process?
Acknowledgements Conflicts of interest
There are no conflicts of interest.
References 1 2
3
4
Tekin G, Tekin YK, Sivri N, Yetkin E. Mean platelet volume in patients with nonvalvular atrial fibrillation. Blood Coagul Fibrinolysis 2013. Black IW, Hopkins AP, Lee LC, Walsh WF. Left atrial spontaneous echo contrast: a clinical and echocardiographic analysis. J Am Coll Cardiol 1991; 18:398. Kubota Y, Arai T, Tanaka T, Yamaoka G, Kiuchi H, Kajikawa T, et al. Thrombopoietin modulates platelet activation in vitro through protein-tyrosine phosphorylation. Stem Cells 1996; 14:439. Montrucchio G, Brizzi MF, Calosso G, Marengo S, Pegoraro L, Camussi G. Effects of recombinant human megakaryocyte growth and development factor on platelet activation. Blood 1996; 87:2762. DOI:10.1097/MBC.0000000000000011
Mean platelet volume in patients with acute pancreatitis: insight from methodological aspect Ercan Varol and Mehmet Ozaydin Department of Cardiology, Suleyman Demirel University, Faculty of Medicine, Isparta, Turkey Correspondence to Ercan Varol, MD, Suleyman Demirel University, Faculty of Medicine, Isparta, Turkey Tel: +90 5323468258; fax: +90 2462324510; e-mail: [email protected]
We read the article by Akbal et al. with great interest [1]. They compared the platelet indices and coagulation parameters in patients with acute pancreatitis and in controls. They also compared the platelet indices and coagulation parameters in active and remission phase in acute pancreatitis. They found that mean platelet volume (MPV) was significantly higher in patients with acute pancreatitis at admission than controls. They also found no correlation between MPV and inflammatory markers. This is an interesting and important study. However, we want to make a minor criticism about this study from the methodological aspect. In the ‘Methods’ section of the article, the authors did not mention about the time between blood sampling and laboratory analysis. MPV increases over time in EDTA-anticoagulated samples, and this increase was shown to be proportional with the delay in time between sample collection and laboratory analysis. With impedance counting, the MPV increases over time as platelets swell in EDTA, with increases of 7.9% within 30 min. Although an overall increase of 13.4% occurs over 24 h, the majority of this increase occurs within the first 6 h [2]. The recommended optimal measuring time of MPV is 2 h after venipuncture [3]. For reliable MPV measurement, the potential influence of anticoagulant on the MPV must be carefully controlled, either using an alternative anticoagulant (such as citrate) or standardizing the time delay between sampling and analysis (
Letters to the Editor Blood Coagulation and Fibrinolysis 2014, 25:196–197
Whether chicken or egg hatch? Sinan Is¸cen Diyarbakır Military Hospital, Diyarbakir, Turkey Correspondence to Sinan Is¸cen, MD, Diyarbakir Military Hospital, Diyarbakir, Turkey
We read the article, ‘Mean platelet volume in patients with nonvalvular atrial fibrillation’ written by Tekin et al. [1]. The authors concluded that to improve the clinical utility of mean platelet volume in the pathogenesis of atrial fibrillation, further studies need to be carried out. We know that atrial fibrillation (AF) is associated with a hypercoagulable state, which is related to the presence of dense spontaneous echo contrast (SEC) and thrombi in the left atrium or left atrial appendage on transesophageal echocardiography. SEC is a well recognized independent predictor for stroke and thromboembolism in AF. Spontaneous echo contrast is believed to represent erythrocyte aggregation in low shear rate conditions [2]. There is a very strong association between left atrial spontaneous echo contrast and left atrial thrombi. We know also that the thrombotic process is associated with platelet destruction. Thrombopoietin levels are elevated for increased platelet count and volume. When thrombopoietin binds to its platelet receptor, it induces phosphorylation of the c-Mpl receptor and a number of other molecules in several different signal transduction pathways [3,4], therefore it affects the function and volume of platelets. Platelet count and volume increase. The main point is whether AF increases platelet volume or whether increased platelet volume causes AF, which leads to a thrombotic process?
Acknowledgements Conflicts of interest
There are no conflicts of interest.
References 1 2
3
4
Tekin G, Tekin YK, Sivri N, Yetkin E. Mean platelet volume in patients with nonvalvular atrial fibrillation. Blood Coagul Fibrinolysis 2013. Black IW, Hopkins AP, Lee LC, Walsh WF. Left atrial spontaneous echo contrast: a clinical and echocardiographic analysis. J Am Coll Cardiol 1991; 18:398. Kubota Y, Arai T, Tanaka T, Yamaoka G, Kiuchi H, Kajikawa T, et al. Thrombopoietin modulates platelet activation in vitro through protein-tyrosine phosphorylation. Stem Cells 1996; 14:439. Montrucchio G, Brizzi MF, Calosso G, Marengo S, Pegoraro L, Camussi G. Effects of recombinant human megakaryocyte growth and development factor on platelet activation. Blood 1996; 87:2762. DOI:10.1097/MBC.0000000000000011
Mean platelet volume in patients with acute pancreatitis: insight from methodological aspect Ercan Varol and Mehmet Ozaydin Department of Cardiology, Suleyman Demirel University, Faculty of Medicine, Isparta, Turkey Correspondence to Ercan Varol, MD, Suleyman Demirel University, Faculty of Medicine, Isparta, Turkey Tel: +90 5323468258; fax: +90 2462324510; e-mail: [email protected]
We read the article by Akbal et al. with great interest [1]. They compared the platelet indices and coagulation parameters in patients with acute pancreatitis and in controls. They also compared the platelet indices and coagulation parameters in active and remission phase in acute pancreatitis. They found that mean platelet volume (MPV) was significantly higher in patients with acute pancreatitis at admission than controls. They also found no correlation between MPV and inflammatory markers. This is an interesting and important study. However, we want to make a minor criticism about this study from the methodological aspect. In the ‘Methods’ section of the article, the authors did not mention about the time between blood sampling and laboratory analysis. MPV increases over time in EDTA-anticoagulated samples, and this increase was shown to be proportional with the delay in time between sample collection and laboratory analysis. With impedance counting, the MPV increases over time as platelets swell in EDTA, with increases of 7.9% within 30 min. Although an overall increase of 13.4% occurs over 24 h, the majority of this increase occurs within the first 6 h [2]. The recommended optimal measuring time of MPV is 2 h after venipuncture [3]. For reliable MPV measurement, the potential influence of anticoagulant on the MPV must be carefully controlled, either using an alternative anticoagulant (such as citrate) or standardizing the time delay between sampling and analysis (
