Commonly recommended aspirin is given to prevent irritation to the stomach.
It has been recommended for years for patients with diabetes, one baby aspirin EC 81mg. daily. A limitation of aspirin is that some patients, particularly those with diabetes, may not have an optimal antiplatelet effect. The goal of this study was to determine if oral bioavailability mediates non-responsiveness.
What’s not clear is whether aspirin lowers the risk of a cardiovascular event if the patient hasn’t experienced one before and is not experiencing symptoms of peripheral artery disease. More study is needed on the potential benefits and risks of aspirin therapy in these people. Aspirin therapy does have potential side effects, such as bleeding ulcers and stroke caused by a leaking or burst blood vessel (hemorrhagic stroke).
Studies suggest that taking a low-dose aspirin every day may lower the risk of heart attacks for some people with diabetes.
This is usually recommended for men over 50 and women over 60 years old with other risk factors such as high blood pressure or cholesterol problems. It may also help people with diabetes who have had a heart attack or a stroke, or who have heart disease.
Exactly why aspirin works is not completely understood, but it may be because it helps keep red blood cells from clumping together. These cells seem to clump together more readily in people with diabetes. When blood cells clump, a blood clot can form and narrow or block a blood vessel. This can lead to a heart attack or stroke.
Taking a daily low-dose aspirin may not be safe for everyone. Those patients with certain meds and indications may not be suitable for daily aspirin. Most people take a pill containing a dosage of 81 milligrams and is usually labeled as low-dose aspirin.
The rate and extent of serum thromboxane generation and aspirin pharmacokinetics were measured in 40 patients with diabetes in a randomized, single-blind, triple-crossover study. Patients were exposed to three 325-mg aspirin formulations: plain aspirin, PL2200 (a modified-release lipid-based aspirin), and a delayed-release enteric-coated (EC) aspirin. Onset of antiplatelet activity was determined by the rate and extent of inhibition of serum thromboxane B2 (TXB2) generation. Aspirin nonresponsiveness was defined as a level of residual serum TXB2 associated with elevated thrombotic risk (<99.0% inhibition or TXB2 >3.1 ng/ml) within 72 h after 3 daily aspirin doses.
The rate of aspirin non-responsiveness was 15.8%, 8.1%, and 52.8% for plain aspirin, PL2200, and EC aspirin, respectively (p < 0.001 for both comparisons vs. EC aspirin; p = 0.30 for comparison between plain aspirin and PL2200). Similarly, 56% of EC aspirin-treated subjects had serum TXB2 levels >3.1 ng/ml, compared with 18% and 11% of subjects after administration of plain aspirin and PL2200 (p < 0.0001). Compared with findings for plain aspirin and PL2200, this high rate of non-responsiveness with EC aspirin was associated with lower exposure to acetylsalicylic acid (63% and 70% lower geometric mean maximum plasma concentration and 77% and 82% lower AUC0-t [area under the curve from time 0 to the last time measured]) and 66% and 72% lower maximal decrease of TXB2, with marked inter-individual variability.
From the results it was concluded that a high proportion of patients treated with EC aspirin failed to achieve complete inhibition of TXB2 generation due to incomplete absorption. Reduced bioavailability may contribute to “aspirin resistance” in patients with diabetes.
- The authors sought to determine if oral bioavailability mediates non-responsiveness in 40 patients with diabetes taking plain aspirin, PL2200 (lipid-based aspirin), and enteric-coated (EC) aspirin.
- The rate of non-responsiveness was 15.8%, 8.1%, and 52.8% in the plain aspirin, PL2200, and EC groups respectively (P < .001 for both comparisons vs EC). The high rate of non-responsiveness in the EC group was associated with lower exposure to acetylsalicylic acid.
- In this group of diabetes patients, a high proportion treated with EC aspirin failed to achieve complete inhibition of thromboxane B2 due to incomplete absorption.
Journal of the American College of Cardiology, January 2017: DOI: 10.1016/j.jacc.2016.11.050