Ms Marie-Christine Alessi
Clinical guidelines have recommended that individuals with risk factors for coronary heart disease should take aspirin for primary and secondary prevention. However subgroups analyses did not demonstrate any significant effect on reducing vascular events in patients suffering diabetes. More recently, two large primary prospectively designed prevention trials confimed these findings (JPAD, JAMA 2008 and POPADAD , Brit Med J 2008). These data question the causes of the clinical and biological non responsivness to aspirin in diabetics. Several hypotheses were put forward by Professor Patrono (Roma, It) to explain aspirin resistance in diabetic patients : glycation of COX1, rendering COX1 more effective, increased COX2 expression bypassing COX 1 and lastly a faster recovery of COX 1 activity in diabetic patients, reducing aspirin efficiency. This last hypothesis was nicely documented. Some heterogeneity in COX1 recovery has been observed suggesting that enhanced platelet turnover in a fraction of type 2 diabetes may allow sufficient recovery of COX1 activity and may blunt the aspirin effect.
Similarly to aspirin resistance, clopidogrel non responsivness is more frequently observed in diabetics. To overcome this difficulty, DJ angiolillo (Jacksonville, US) nicely described recent data showing the advantages of increasing clopidogrel doses, the benefit of combining clopidogrel with cilostazol or picotamide and the promise of new antiplatelet drugs.
In association to strict metabolic control, it is probable that ongoing trials focusing on the use of antiplatelet agents in diabetics will help to explore alternative regimens of antiplatelet therapy and to identify patients that may benefit from tailored antiplatelet treatment.
The diabetic platelet - an unsolved problem
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