This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.This is a pilot study to evaluate whether there is an interaction between the drugs aspirin and salsalate in adults with Type 2 diabetes. Both aspirin and salsalate are in the non-steroidal anti-inflammatory class of medications known as salicylates. Aspirin is currently used to treat fever, aches, and pains, and is recommended by the American Diabetes Association and the American Heart Association to reduce risk of heart attack and stroke, an effect it achieves through inhibition of the COX enzyme in platelets. Salsalate is commonly used to treat pain associated with arthritis and has much less associated stomach irritation and bleeding. Previous studies have demonstrated that salicylates may be useful to treat type 2 diabetes by reducing markers of inflammation. We would like to confirm that treating patients with salsalate for this purpose will not interfere with the benefits of aspirin therapy. In this study we will be looking at 10 subjects ages 18-65 randomized into two groups. One group will receive a standard low dose of aspirin (81 mg) and two hours later TXB2 and PGE2 concentrations will be measured and platelet aggregation evaluated with the Verfiy Now Aspirin Assay. They will then receive a standard treatment dose of salsalate (1500 mg). Two hours later again coagulation will be assessed with the same methods. Twenty-four hours later blood will be drawn from subjects for coagulation parameters. Group two will follow the same protocol as above but will receive salsalate fist followed two hours later by aspirin. Two weeks later subjects will return and undergo the same protocol in the reverse order. Our hypothesis is that salsalate will have no effect to disrupt the anti-platelet effect of aspirin as measured by TXB2, PGE2 concentrations and platelet aggregation.
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