**6.2 Hyperglycemia**

Persistent hyperglycemia leads to formation of non-enzymatic glycation of proteins, so-called advanced glycation end products (AGEs). Accumulation of these products facilitates cytoskeletal reorganization causing externalization of membrane phosphatidyleserine (PS) [132], altered membrane fluidity [133], and increased expression of glycoproteins GPIb, IIbIIIa [134], P-selectin, and PLA [135].

Hyperglycemia induces secretion of TPO that potentiates agonist-induced activation of mature platelets. Levels positively correlate with blood glucose and level of control HbA1C [17].
