Mean Platelet Factor 4 Research Articles

Standardize plasma sample collection method for biomarker searching study in oncology

22163 Background: Sample quality is critical for biomarker searching in oncology. Platelet degradation and contamination in plasma has a remarkable impact on many blood markers. Platelet factor 4 (PF4) can be used as a surrogate of this condition and a monitor for the sample quality. This multicenter study aimed to validate the impact of blood sample handling process on platelet degradation/contamination and to establish an optimal method for platelet poor plasma. Methods: Six centers participated. Blood were drawn from 12–13 healthy volunteers from each center. Blood samples were prepared to serum or plasma by 9 methods (table). These samples were sent to the University of Michigan (American samples) or Peking Union Medical College Cancer Hospital (Chinese samples) for measurement of PF4 with ELISA. Paired-T test was used for statistic analysis. Results: A total of 74 subjects enrolled. The methods generated the lowest level of PF4 was the ones prepared by 3000×g for 30 min, and with blood samples set on ice <30 min. Comparing to results of this, PF4 was significantly higher in serum samples (P5 min (P<0.001), inadequate spinning gravity (P<0.001), and 3–4 hours blood setting on ice. There was no significant difference among PF levels of each method between centers. The mean PF4 levels of all centers of each method are shown in table. There was no significant difference in PF4 levels between Chinese and American subjects. Conclusion: This multicenter study demonstrates 7 conditions to cause platelet degradation and optimal methods of plasma preparation. Future blood maker study should take this into consideration. Platelet factor 4 (PF4) levels in different handling methods Sample Setting Temperature Setting Time (Min) RCF and Duration PF4 (ng/ml) Plasma 1 On ice 5 3,000×g 30 min 27.9 ± 29.6 Plasma 2 On ice 30 3,000×g 30 min 23.0 ± 23.2 Plasma 3 On ice 240 1,200×g 10 min 50.1 ± 36.3 Plasma 4 On ice 240 3,000×g 30 min 26.8 ± 26.4 Plasma 5 RT 5 3,000×g 30 min 55.9 ± 45.1 Plasma 6 RT 30 3,000×g 30 min 83.2 ± 59.1 Plasma 7 RT 60 3,000×g 30 min 82.6 ± 38.5 Serum 1 On ice 240 3,000×g 30 min 67.3 ± 54.9 Serum 2 RT 60 3,000×g 30 min 124.7 ± 79.2 RT: Room temperature; RCF: relative centrifugation force No significant financial relationships to disclose.

Elevated platelet factor 4 and β-thromboglobulin plasma levels in depressed patients with ischemic heart disease

Clinical depression has recently been recognized as an independent risk factor for cardiac mortality in patients after myocardial infarction. The underlying mechanisms of this increased mortality remain unclear. This study investigated the hypothesis that patients suffering from ischemic heart disease (IHD) and depression concurrently may have abnormal platelet activation resulting in an increased risk of thrombosis. Platelet factor 4 (PF4) and beta-thromboglobulin (beta-TG) were measured in young healthy control subjects, in nondepressed patients with IHD, and in depressed patients with IHD. Mean PF4 and beta-TG plasma levels in the IHD group with depression were found to be significantly higher than those of the control and IHD groups. This increase was not related to age, gender, racial difference, aspirin use, or severity of cardiac disease. This finding suggests that in depressed patients with IHD there is greater platelet activation, and may indicate an increased risk of thrombotic complications.

Platelet factor 4 (PF4) and heparin-released platelet factor 4 (HR-PF4) in patients with cardiovascular disorders

The recent introduction of the determinations of platelet factor 4 (PF4) and β-thromboglobulin (βTG) by radioimmunoassay provided a new tool to obtain knowledge of in vivo platelet activation. We evaluated the plasma level of PF4 and βTG in 14 normal subjects (mean PF4 7.7 ng/ml; βTG 28.8 ng/ml), in 29 patients with chronic stable cardiovascular disorders (mean PF4 9.8 ng/ml; βTG 32.6 ng/ml) and in 15 diabetics with vascular disease (mean PF4 14.5 ng/ml; βTG 41.8 ng/ml). The great majority had normal values and no statistical differences were noted among the three groups (p > 0.05). Fifteen days of treatment with 150 mg daily of dipyridamole produced a significant reduction in the levels of both proteins (p < 0.01), in contrast of the daily administration of 650 mg of aspirin, which failed to produce any significant change (p > 0.5). The patients and the normal subjects were also administered 3,000 USP units intravenously of porcine heparin. The values of the heparin released-platelet factor 4 (HR-PF4), evaluated 5 minutes after the injection, showed a good correlation between platelet concentration and HR-PF4 levels (z = 2.37, p < 0.02) in the patients. The determination of standard residual following linear regression analysis of HR-PF4 indicated the presence of two distinct patient populations. One group, including the vast majority of patients, did not differ from the control (patients mean HR-PF4 111.1 ng/ml; controls: mean HF-PF4 136 ng/ml). The other group, with severe cardiovascular disease, but with normal levels of PF4 and βTG in almost all patients and similar platelet concentrations, showed a significantly higher HR-PF4 (219 ng/ml). Neither aspirin nor dipyridamole had any effect on the level of HR-PF4. This HR-PF4 could represent a possible marker of the interaction of platelets with a seriously damaged atherosclerotic vessel wall.