Platelets play a central role in the pathogenesis of thrombo-embolic diseases. Platelet size reflects platelet activation. Large platelets are more metabolic and enzymatically active than small ones and produce greater amounts of thromboxane A2 and express more glycoprotein Ib and IIb / IIIa receptors. MPV and PDW are indicators of platelet activation. While MPV is a measure of mean platelets size, PDW measures platelets size variability and may be an indicator of active platelets release
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MPV is one of the platelet volume indicators and is a simple and reliable parameter showing platelets activation and function. There are studies showing increased MPV levels in patients with coronary artery disease 11,12. MPV has been defined as an independent risk factor for myocardial infarction and stroke 13,14. In a hospital-based cohort study (n: 206,554), the relationship between MPV quintiles and vascular mortality was assessed. In patients with MPV ≥11.01 fL (highest quintile), vascular mortality was shown to be at the highest level in patients with MPV below 8.7 fL. This increased risk is beginning to become evident in the values above the MPV of 9.61 fL. 15. Also in a study performed by Berger and colleagues in 6354 patients 16, a positive correlation was found between MPV and peripheral artery disease. The above data pertain purely to arterial thromboembolism. There are limited such data concerning venous thromboembolism.
In Tromsø study conducted by Braekkan et al. 17 on 25923 patients, it was shown that there was a correlation between acute unprovoked venous thromboembolism and increased MPV (≥9.5fL) values. In a study on platelets indices on 2013 patients with acute deep vein thrombosis; Cay et al. 18 found that MPV values were higher than the control group and they stated that the presence of DVT may be closely related to increased platelet activation. Similarly Gulcan et al. 19 found that MPV values in newly diagnosed acute DVT patients were significantly higher than in the control group. In a study, including 147 patients, examining the relationship between acute deep vein thrombosis and mean platelet volume in patients staying hospital, MPV values were found as high in these patients and it was suggested that this was an independent predictor 20. In another study examining the relationship between recurrent pulmonary embolism and platelet indices, the MPV and PDW values in recurrent cases were detected significantly higher than in non-recurrent cases. In addition, recurrent pulmonary embolism cases after treatment showed that MPV was still higher than those who did not recur. As a result, it has been determined that MPV may be an indicator for recurrent pulmonary embolism and may be useful for predicting recurrence 21.
As it can be seen in these studies, there is a positive relationship between acute deep vein thrombosis and MPV values. However, in our examination of the literature, no study was found related to the relationship between MPV and recurrent deep vein thrombosis. Mean platelet volume values in this study; the MPV value in the acute phase (MPV1) in the patient group was measured as 10.24±1.83 fL on average and it was found to be significantly higher than the control group (mean value: 9.03±1.02) (P= 0.002) The mean platelet values in the recurrent periods of the patients (MPV2) were measured as 10.93±1.44 fL, which was higher in the mean level than the control group (P<0.001). MPV2 values were found to be significantly higher than MPV1 values in patients with acute and recurrent DVT (P<0.001).
PDW; measures the size of platelets and is another indicator of platelet activation at the same time 22. Increased PDW levels have been reported in myeloproliferative diseases, diabetes mellitus, and coronary artery disease 23.
Some authors have indicated that high PDW is associated with platelet anisocytosis and have suggested that this anisocytosis may be related to the formation of pseudopodia. Khandekar et al. 23 have found that the PDW is higher in patients with acute ST-segment elevation than in those with stable coronary artery disease. Celik et al. 24 have suggested that the PDW is an independent correlate of in-hospital major adverse cardiovascular events. In addition, Rechkinski et al. 25 have reported that the PDW is an independent risk factor for cardiac mortality and either death, recurrent MI or the need for an additional revascularization procedure. Further, Jindal et al. 26 have reported that the PDW is significantly increased in diabetic patients, and these authors have stressed that it may be even higher in patients who have developed microvascular complications.
There are few studies showing the relationship between platelet distribution width and venous thromboembolism. In a study of Kamisli and et al. 27 it was demonstrated that elevated MPV and PDW values in patients with cerebral sinus venosus thrombosis at early phase and this was related with the severity of the disease and the extent of parenchymal lesions.
In a study completed by Sevuk and et al. 28, they found that MPV and PDW values in acute DVT patients were higher than the control group. They also showed that MPV and PDW values were significantly higher in patients with acute DVT and pulmonary embolism compared to patients with DVT alone, and the serial MPV and PDW measurements and percent changes in these parameters may be a useful marker for pulmonary embolism after acute DVT.
As it was mentioned before, in a study fulfilled by Araz et al. 21, MPV and PDW values in recurrent pulmonary embolism cases were found significantly higher than non-recurrent cases.
In this study platelets distribution volume values in the acute phase in the patient group (PDW1) was measured as 16.54±3.07fL on average and it was found to be significantly higher than the control group (average value: 10.34±1.02 fL) (P<0.001). However, the mean PDW values (PDW2) of the patients in the recurrent period were measured as 15.75±3.39 fL, which was found to be higher in the average level than the control group (P<0.001). There was no meaningful difference found in PDW data between acute and recurrent periods in the patient group (P= 0.079).
In the light of literature and our study findings; the increased mean platelet volume and platelet distribution width values during platelet activation play a role at the development of unprovoked acute and recurrent deep vein thrombosis. Beside the platelet distribution width is more specific parameter than mean platelet volume; the evaluation of MPV and PDW together may provide a more effective idea for venous thrombosis predisposition. We consider that the antiagregan treatment as continuous therapy after the end of anticoagulant treatment of deep vein thrombosis may be useful in the prevention of recurrence.