Increased Thrombopoietin and Mean Platelet Volume in Patients With Ischemic Stroke

Abstract

I read the article published by Balcik et al with great interest. They examined both the mean platelet volume (MPV) and the thrombopoietin (TPO) values in patients with ischemic stroke and compared this with healthy controls. Both TPO and MPV values were significantly higher in patients with stroke. Although previous studies have reported higher MPV values in ischemic stroke, the mechanism of this is still not clear. This is the first study demonstrating both increased TPO and MPV in the same patient group with ischemic stroke. Since TPO is considered the primary physiological regulator of megakaryopoiesis, increased TPO levels may increase both platelet counts and platelet size, resulting in hemostatically more active platelets. Senaran have reported that MPV and TPO values were found to be elevated in patients with acute myocardial infarction and unstable angina pectoris when compared with control participants. They have reported similar results in ischemic stroke. This is an interesting study from this aspect. On the other hand, we want to mention minor criticism about this study from methodological aspect. First, they used ethylenediaminetetraacetic acid (EDTA) anticoagulated tubes for sample collection. However, 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 minutes and an overall increase of 13.4% over 24 hours having been reported, although the majority of this increase occurs within the first 6 hours. The recommended optimal measuring time of MPV is 120 minutes maximum, after venipuncture. For reliable MPV measurement, the potential influence of anticoagulant on the MPV must be carefully controlled by standardizing the time delay between sampling and analysis (less than 2 hours). This situation is not clear in this study. Second, there are significant associations of MPV with type 2 diabetes mellitus, prediabetes, smoking, hypertension, hypercholesterolemia, obesity, coronary artery disease, metabolic syndrome, statin use, and atrial fibrillation. In patients group, there were more patients with hypertension and diabetes mellitus. In patients group 22 patients had coronary artery disease and none in control group. Higher MPV values were reported in patients with hypertension, diabetes mellitus, and coronary artery disease. As a result, increased MPV values might be due to these factors. The factors must have been adjusted in 2 groups to say that the increase in MPV is solely dependent on the stroke. Third, they did not mention the rhythm of the patients. Atrial fibrillation is major risk factor for stroke. The MPV values were reported to be higher in patients with paroxysmal atrial fibrillation. Moreover, Ha et al reported that MPV was a predictive marker for stroke; its predictive power for stroke was independent of age, gender, and other CHADS(2) score components in patients with AF. They had to mention the presence or absence of atrial fibrillation or how many people were in atrial fibrillation. Moreover, laboratory findings in Table 2 do not seem to be consistent with the findings stated in results and discussion section (platelet count, MPV, and age). They also did not mention the physical examination and echocardiographic findings of patients to search the cardioembolic source of stroke. In all patients with stroke echocardiographic examination was performed to determine the cardiac source of emboli. For example, rheumatic mitral stenosis is an important source of ischemic stroke. The MPV has been shown to be significantly elevated in patients with mitral stenosis who were in sinus rhythm compared to control participants. As a result, presence of mitral stenosis or other cardiac sources of emboli may have a role in higher MPV values in patients with stroke.