*5.4.2 Anti-platelet treatments*

Aspirin suppressed platelet functions TXA secretion, LTA, and PFA although there are no observable differences between healthy and DM individuals [35]. In case of stable (>1 month) dual 100 mg aspirin and 75 mg clopidogrel, insulin-treated DM has elevated platelet reactivity as assessed by LTA and PFA compared with NIDM and non-diabetic controls [29]. The refractory effect of antiplatelets in the presence of insulin has been reported [123]. Aspirin has been shown to attenuate maximum aggregation in newly diagnosed T1DM via its effects on ADP, epinephrine, and thrombin. The effects are most marked in reducing the secondary [26] indicating propensity for secretory phase. The refractory state to anti-platelets responses of platelets to agonists in the presence of high glucose is dependent on the signaling pathways tested. For example, hyperglycemia blocks the NO-cGMP-protein kinase pathway but spares the thromboxane secretion [124].
