The influence of time of storage, temperature of storage, platelet number in platelet-rich plasma, packed cell, mean platelet volume, hemoglobin concentration, age, and sex on platelet aggregation test

1995 ◽  
Vol 71 (3) ◽  
pp. 129-133 ◽  
Author(s):  
C. -H. Ho ◽  
I. -H. Chan
1987 ◽  
Author(s):  
R Abbate ◽  
M Boddi ◽  
S Favilla ◽  
G Costanzo ◽  
R Paniccia ◽  
...  

The aim of this study has been to investigate the reliability of platelet aggregation in whole blood in some clinical conditions associated to thromboembolic complications.18 healthy subjects, 15 patients affected by ischemic heart disease (IHD) and 15 patients affected by insulin independent diabetes, free of vascular complications, were studied. Collagen induced (2.5 mg/L f.c.) platelet aggregation was evaluated both in whole blood (WB) by using impedance whole blood aggregometer (Chrono-Log) and in platelet rich plasma (PRP) by Born aggregometer. Aggregation was significantly higher in whole blood than in PRP in all the groups investigated (p < 0.01). No significant difference was found in PRP aggregation among the three groups, whereas WB aggregation was significantly higher in the two patient groups (IHD 79.5 + 14.2%, Diabetes 81.3 + 17.6%) than in controls (64.8 ± 14.1%) (p < 0.01 for both comparisons). No relationship was found between WB aggregation and Hct or platelet number in any of the groups studied. A slight relationship was found between megathrombocyte count and WE aggregation values (r=0.31, p < 0.05).Collagen platelet aggregation in WB seems to be provided with higher sensibility than PRP aggregation in detecting hyper-aggregability, probably because it does not imply the selection of platelet populations with loss of larger platelets and of other blood cells.


1981 ◽  
Author(s):  
E Tremoli ◽  
P Maderna ◽  
S Colli ◽  
M Sirtori ◽  
C R Sirtori

The platelet sensitivity to aggregating agents and the production of arachidonic acid (AA) metabolites were studied in 97 hypercholesterolemic patients (WHO types IIA and IIB;serum cholesterol levels >250 mg/dl, LDL>170 mg/dl,triglycerides >180 mg/dl). The findings were compared with those of 55 age and sex matched normocholesterolemic subjects.Platelet aggregation was studied in platelet rich plasma (PRP) with ADP, collagen, epinephrine and thrombofax* as aggregating agents. Malondialdehyde (MDA) production was determined according to Smith et al.. Thromboxane B2 (TXB2) was measured in washed platelets stimulated with AA by a specific RIA. The platelet sensitivity to the inhibitory effect of synthetic prostacyclin (PGI2) was also assessed in 40 of the patients and in 20 age and sex matched control subjects, using fixed concentrations of aggregating agents.Platelets from patients required to aggregate significantly lower concentrations of collagen, epinephrine and thrombofax* (p< 0.001) and of ADP ( p<O.05); MDA production by thrombin and collagen and TXB formation were significantly raised (p<0.001) in the patient group. Higher concentrations of PGI2 were required to inhibit the aggregation of platelets in the type II patients.The reported findings confirm in a large clinical series the potential role of platelet hyperreactivity in the thrombotic risk of type II hypercholesterolemia.


2014 ◽  
Vol 112 (07) ◽  
pp. 137-141 ◽  
Author(s):  
Elad Asher ◽  
Paul Fefer ◽  
Michael Shechter ◽  
Roy Beigel ◽  
David Varon ◽  
...  

SummaryPrior studies have demonstrated significant individual variability of platelet response to clopidogrel, which affects clinical outcome. In patients with stable coronary artery disease (CAD) smoking, diabetes mellitus, elevated body mass index and renal insufficiency, significantly impact response to clopidogrel. The determinants of platelet response to clopidogrel in patients with acute coronary syndrome are unknown. Adenosine diphosphate (ADP)-induced platelet aggregation (PA), hs C-reactive protein, platelet count and mean platelet volume (MPV) were determined 72 hours post clopidogrel loading in 276 consecutive acute myocardial infarction (AMI) patients. Patients with ADP-platelet aggregation ≥ 70% were considered to be clopidogrel non-responders. Eighty-four patients (30%) were clopidogrel non-responders and 192 (70%) were responders (ADP-induced PA: 81 ± 17% vs 49 ± 17%, respectively, p<0.001). Both study groups were comparable with respect to age, gender, prior cardiovascular history, prior aspirin use and risk factors for CAD, including smoking (42% for both groups) and diabetes mellitus (26% vs 22%, respectively, p=0.4). Responders and non-responders had similar angiographic characteristics, indices of infarct size, and similar hs-CRP (29 ± 34 vs 28 ± 34 mg/l, p=0.7) and creatinine (1.08 ± 0.4 mg% vs 1.07 ± 0.4, p=0.9) levels. On the contrary non-responders had significantly larger mean MPV (9 ± 1.2 fl vs 8 ± 1 fl, respectively, p=0.0018), and when patients were stratified into quartiles based on MPV, ADP-induced PA increased gradually and significantly across the quartiles of MPV (p<0.001). In conclusion, increased MPV associated with platelet activation, predicts non-responsiveness to clopidogrel among patients with acute coronary syndrome.


Author(s):  
Agus Sunardi ◽  
Nadjwa Zamalek Dalimoenthe ◽  
Coriejati Rita ◽  
Adhi Kristianto Sugianli

     Diabetic nephropathy is the most important cause of end-stage renal failure. Chronic hyperglycemia will cause glomerular endothelial damage, and this damage will stimulate hemostasis activation including platelets so that platelet aggregation will increase. The increase of platelet aggregation will increase platelet consumption, which further stimulates thrombopoiesis which will lead to immature platelets of large size to be released into the circulation. This research aimed to determine the positive correlation between MPV with platelet aggregation in patients with diabetic nephropathy. This study was an analytic observational study with a cross-sectional study design. The research was conducted in the Dr. Hasan Sadikin Hospital Bandung from July 2016 to October 2017. A total of 52 subjects who met the inclusion criteria were included in the study. Mean platelet volume and platelet aggregation were performed with venous examination with EDTA and sodium citrate 3.2% anticoagulants. The result of platelet aggregation examination showing platelet hyper-aggregation was found in 44.2% of subjects, 50% normal-aggregation, 5.8% hypo-aggregation. While the median value of MPV in this study was 9.2 fL with the range of 8.00 – 11.80 fL. A positive correlation was found  between MPV value with platelet aggregation with r= 0.067, p= 0.634. The conclusion was that there was no correlation between MPV values with platelet aggregation in diabetic nephropathy patients. This small and insignificant r-value might be due to several factors that also affect platelet aggregation in diabetic nephropathy patients, requiring further investigation.


Author(s):  
Nindia Sugih Arto ◽  
Adi Koesoema Aman ◽  
Dharma Lindarto

The hyperactivity of platelet had been seen in patients with metabolic syndrome which can be caused by several factors, such as:insulin resistance, obesity, dyslipidemia and hypertension. The hyperactivity of platelet leads to its aggregation that can be increased therisk of cardiovascular disease. This study is aimed to know the platelet aggregation and mean platelet volume in patients with metabolicsyndrome and obesity by determination 30 patients were choosen for this cross sectional study, those whom attended to the laboratoryand policlinic at H. Adam Malik Medan Hospital, between May 2013 until August 2013. The diagnosis used of metabolic syndromecriteria established by the International Diabetic Federation 2005. From the 30 patients with 15 metabolic syndrome and 15 obesity,four patients were excluded because of their tryglyceride were more than 200 mg/dL. There is no significant differences between theplatelet aggregation with the agonist adenosin difosfat (ADP) in patient with metabolic syndrome and obesity. And there is no significantdifferences of the mean platelet volume values between the metabolic syndrome (9.6±0.93) and the obesity group (9.73±0.74), with pvalue 0.846. Based on this study there is no significant differences between the platelet aggregation and the Mean Platelet Volume values(MPV) in the metabolic syndrome and the obese group


2014 ◽  
Vol 8 (2) ◽  
pp. 134-142
Author(s):  
S. G. Khaspekova ◽  
I. T. Zyuryaev ◽  
V. V. Yakushkin ◽  
Ya. A. Naimushin ◽  
O. V. Sirotkina ◽  
...  

Author(s):  
L R Ranganath ◽  
J Christofides ◽  
M J Semple

The effect of hormone replacement therapy (HRT) on platelet size was examined in 38 post-menopausal women before and at end of a 6 week period of HRT. Subjects were treated with cyclical L-norgestrel 75 mg daily from days 17 to 28 of a 28-day cycle combined with continuous conjugated equine oestrogens 0.625 mg daily. Platelet-rich plasma was obtained to measure platelet indices by Coulter analysis. Plasma measurements of luteinizing hormone, follicle stimulating hormone and 17β-oestradiol were measured by immunoassays. Platelet membrane fatty acids were measured by gas-liquid chromatography. A significant reduction in platelet membrane linoleic acid, di-homo-γ-linoleic acid and arachidonic acid of 8.1%, 14.3% and 17.8%, respectively was noted after 6 weeks of HRT ( P < 0.01). There was an increase in the platelet count (not significant) and platelet volume (MPV) ( P < 0.05) after 6 weeks of hormone therapy. HRT appears to increase mean platelet volume which may indicate an increase in platelet reactivity. There was no correlation between the changes in mean platelet volume and membrane fatty acid changes in platelets after such therapy.


2017 ◽  
Vol 25 (2) ◽  
pp. 91-94
Author(s):  
İbrahim Çevik ◽  
Hüseyin Narcı ◽  
Güllü Akbaydoğan Dündar ◽  
Cüneyt Ayrık ◽  
Seyran B Babuş

Background: Pulmonary embolism is a common disease with a high mortality risk. It has recently been reported that platelet indices may be diagnostic in pulmonary embolism. Objective: In this study, we aimed to determine the diagnostic value of platelet indices in acute pulmonary embolism. Methods: The study group was composed of 61 patients diagnosed with pulmonary embolism and a control group of 67 subjects without pulmonary embolism. Patient age, sex, leukocyte and platelet number, hemoglobin concentration (Hb), mean platelet volume, platelet distribution width, red blood cell distribution width, C-reactive protein, D-Dimer, and troponin I levels were retrospectively analyzed and compared between the two groups. Results: There was no significant difference between age and platelet number of pulmonary embolism and control group. In pulmonary embolism group, platelet distribution width level was significantly high (p = 0.002), whereas mean platelet volume level was significantly lower (p = 0.038). Receiver operating characteristic curve analysis revealed that a mean platelet volume cut-off of 9 fL had a sensitivity of 35%, a specificity of 89.55%, and area under the curve of 0.589 for pulmonary embolism, while a platelet distribution width cut-off of 12.8 fL had a sensitivity of 61%, a specificity of 71.64%, and area under the curve of 0.661. Platelet distribution width and D-dimer levels had a significant positive correlation with each other, whereas there was no significant correlation between mean platelet volume and D-dimer. Conclusion: Platelet distribution width values of the pulmonary embolism group were higher than those of control group. Although the area under the curve of platelet distribution width is slightly better than for platelet number or mean platelet volume, it does not seem that this parameter has better diagnostic accuracy than the other two.


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