Improved metabolic control decreases platelet activation markers in patients with type‐2 diabetes

Abstract

We conclude therefore that improvement of metabolic control has a beneficial effect on platelet activation. This may have an implication in the pathogenesis of vascular disease in patients with type-2 diabetes.

A study to find correlation of platelet indices with HbA1c in diabetic patients with absence/presence of vascular complications

“…16 CD62 and CD 63 with increasing availability of blood cell analyzers related to platelets are being estimated most important parameters among them are platelet count, platelet distribution width / and mean platelet volume, the most commonly used measure of platelet size is a potential markers of platelet reactivity. [17][18][19] It's a new emerging risk factor for atherosclerosis. 20 Patient with larger platelets can be easily identified during routine hematological analysis and could possibly benefit from the treatment for predicting the possibility of impending acute events.…”

Dyslipidemia and Type 2 Diabetes Mellitus: Implications and Role of Antiplatelet Agents in Primary Prevention of Cardiovascular Disease

“…Platelets from patients with type 2 diabetes mellitus found to have increased expression of adhesion molecules CD31, CD36, CD49b, CD62P and CD63 (Eibl et al, 2004). Glycemic control www.intechopen.com improvement led to a significant decline in their expression (Eibl et al, 2004). In type 2 diabetes patients, platelets increased surface expressionof GP Ib and GP IIb/IIIa (Vinik et al, 2001).…”

“…TXA 2 is a potent activator and its synthesis is suppressed by aspirin (Natarajan et al, 2008). Platelets from patients with type 2 diabetes mellitus found to have increased expression of adhesion molecules CD31, CD36, CD49b, CD62P and CD63 (Eibl et al, 2004). Glycemic control www.intechopen.com improvement led to a significant decline in their expression (Eibl et al, 2004).…”

Digami too?

“…We know from data on use of fibrinolytics that early intervention in the thrombotic process saves lives, and door-to-needle time for streptokinase is an important concept. We also know that control of blood glucose normalises the thrombotic pathways [5][6][7][8]10]. Is there not some urgency in achieving near-normoglycaemia after acute myocardial infarction?…”

“…The effect of high glucose levels on thrombosis and endothelial function in vivo and in vitro has been well described. High glucose promotes platelet activation, which can be reversed by glucose lowering [5,6]. Vascular endothelial dysfunction and inhibition of the fibrinolytic system are brought about by persistent high glucose levels, and circulating levels of the adhesion molecules intracellular adhesion molecule 1 (ICAM-I) and E-selectin are downregulated by normalisation of blood glucose [7,8].…”