Platelets are small anucleate cell fragments that circulate in blood playing crucial role in managing vascular integrity and regulating hemostasis. Platelets are also involved in the fundamental biological process of chronic inflammation associated with disease pathology. Platelet indices like mean platelets volume (MPV), platelets distributed width (PDW), and platelet crit (PCT) are useful as cheap noninvasive biomarkers for assessing the diseased states. Dynamic platelets bear distinct morphology, where α and dense granule are actively involved in secretion of molecules like GPIIb , IIIa, fibrinogen, vWf, catecholamines, serotonin, calcium, ATP, ADP, and so forth, which are involved in aggregation. Differential expressions of surface receptors like CD36, CD41, CD61 and so forth have also been quantitated in several diseases. Platelet clinical research faces challenges due to the vulnerable nature of platelet structure functions and lack of accurate assay techniques. But recent advancement in flow cytometry inputs huge progress in the field of platelets study. Platelets activation and dysfunction have been implicated in diabetes, renal diseases, tumorigenesis, Alzheimer's, and CVD. In conclusion, this paper elucidates that platelets are not that innocent as they keep showing and thus numerous novel platelet biomarkers are upcoming very soon in the field of clinical research which can be important for predicting and diagnosing disease state.

/pdf/overview-of-platelet-physiology-its-hemostatic-and-uc12b5532z.pdf

Overview of Platelet Physiology: Its Hemostatic and Nonhemostatic Role in Disease Pathogenesis

Atherosclerotic cardiovascular disease and its thrombotic complications are the principal causes of morbidity and mortality in patients with type-2 diabetes.Aspirin reduces the risk of thrombotic events in a broad range of patients with vascular disease and, in selected individuals, is beneficial for primary prevention. Although recommended by existing guidelines,in secondary and in primary prevention trials the clinical efficacy of low-dose aspirin in patients with diabetes appears to be substantially lower than in individuals without diabetes. In this review, we discuss possible mechanisms that may contribute to reduce the antithrombotic activity of aspirin in diabetes.We also discuss adjuvant therapies used in diabetic patients that may potentially improve the antithrombotic efficacy of aspirin.

/pdf/prevention-of-cardiovascular-disease-in-type-2-diabetes-how-35ipqduenv.pdf

Prevention of cardiovascular disease in type-2 diabetes: how to improve the clinical efficacy of aspirin.

Platelet function in diabetes mellitus.

Diabetes mellitus is associated with micro and macrovascular complications. Cardiovascular complications are the major cause of mortality in diabetics. Platelets of patients with diabetes show a large number of structural, functional and metabolic changes. Aim of this review is to discuss all these changes and provides a better understanding of the diseae process.

Platelets structural, functional and metabolic alterations in diabetes mellitus

Diabetic patients are at higher risk of development of cardiovascular complications than the general population. The role of platelets in the pathogenesis of these complications is still controversial, it being difficult to ascertain whether altered platelet function is a cause or consequence of vascular complications of diabetes. Measurement of urinary 11-dehydro-thromboxane has been proposed as a reliable index of in vivo platelet activation and has been reported to be significantly higher in non insulin-dependent diabetic patients with micro- or macrovascular complications. We therefore studied the effect of ticlopidine, an antiplatelet drug acting through mechanisms different from cyclo-oxygenase inhibition, on urinary 11-dehydro-TXB2 excretion in diabetic patients with macrovascular complications. The results indicate that urinary excretion of 11-dehydro-TXB2 after ticlopidine treatment is not different from pre-treatment values, suggesting that the chosen parameter might not be reliable for monitori...

Ticlopidine does not reduce in vivo platelet thromboxane biosynthesis and metabolism in diabetic patients.

Increased platelet function and thromboxane (Tx) A2 generation in diabetes mellitus have been suggested by some investigators (1), but not by others (2, 3). Such discrepancies may be due to limitations of the test systems used to investigate platelet function ex vivo. More recently urinary excretion of products of arachidonic acid metabolism was measured in' diabetic patients as an index of platelet activation in vivo. In patients with diabetes without evidence of macrovascular complications, platelet function ex vivo and urinary excretion of 2,3 dinor-TxB2 did not differ from non-diabetic controls (4), while urinary excretion of 11dehydro-TxB2 was significantly higher in diabetic patients with clinical evidence of macrovascular disease than in controls (5). Increased excretion of TxA2 metabolites in urine from diabetic patients with severe atherosclerosis involving large blood vessels had also been reported (6). On the basis of these findings, we measured both platelet response to arachidonic acid and capacity to synthesize TxA2 ex vivo and TxA2 biosynthesis in vivo in seven insulin-treated patients (3 non-insulin dependent and 4 insulin-dependent) and in 5 healthy volunteers. Mean duration of diabetes was 19.8 years (range 10-33) and mean HbA1 value was 10.7 ± 1.0%. All patients had retinopathy (3 proliferative, 4 non proliferative), but no signs of clinical nephropathy. Two of them had clinical signs of macrovascular complications. Serum TxB2 measurements and aggregation studies were performed as described (7). A 6-h urine collection was performed in the morning for the analysis of 11-dehydro-TxB2 excretion, according to a method previously validated (8). Platelet capacity to generate TxA2 during spontaneous blood clotting in vitro as well as platelet aggregation response to sodium arachidonate were similar in diabetic patients and healthy controls. In contrast, the urinary excretion of 11-dehydro-TxB2 was significantly higher in patients than in controls (Table 1). Administration of indobufen (200 mg x 2), a cyclooxygenase inhibitor, to patients resulted in an almost complete suppression of serum TxB2 generation (>95% inhibition) and of platelet aggregation and in a very marked reduction of 11-dehydro-TxB2 urinary excretion (19.6 ± 12.4 vs 113.9 ± 31.2 ng/h). The discrepancy between in vitro and in vivo platelet function in diabetes could be the consequence of platelets essentially normal in a test tube being exposed in vivo to atherosclerotic or otherwise damaged vascular walls. The abnormal platelet-vessel

Normal platelet function, but increased platelet activation in vivo in diabetic patients.

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Normal platelet function, but increased platelet activation in vivo in diabetic patients.