Aspirin and numerous NSAIDs, including acetaminophen and those inhibiting selectively COX-2, are amongst the most commonly consumed drugs on the planet. Aspirin at doses less than 100 mg per day or greater than 1 gm per day have equivalent effects on platelet COX-1 derived TxA2. They both suppress it completely. However, increasing daily doses of aspirin increasingly inhibit PGI2 coincidentally with this effect, which suggest that the cardioprotective efficacy of aspirin may be progressively attenuated as the dose is increased. Similarly, locally formed, COX-1 derived PGE2 and PGI2 are protective of gastroduodenal epithelial integrity and platelet COX-1 derived TxA2 contributes to hemostatic competence. Disruption of these pathways by NSAIDs (even those which selective for inhibition of COX-2) resulted in serious gastrointestinal events. That may reflect their impact on gastroduodenal epithelial COX-2 dependent prostanoids that accelerate ulcer healing. As we still poorly understand inter-individual differences in anti-inflammatory efficacy amongst the reversibly acting NSAIDs, the hard evidence how to address the above question is in short supply.
By WHO's recommendations the only safesr dosage for permanent daily use is 80 mg of Aspirin. In my own practice I recommend 75mg of Cardiomagnil, which is combination of Aspirin and additional substance preventing negative gastro impact.
An enteric coating prevents gastric ulcer and ASA is then absorbed in small intestine maintaining the cardioprotective effects. You only neeed to control the thickness of the enteric coating (do not use exccesive amount of coating).
Because aspirin is a medicine with a high platelet turnover rate (approximately 77% inhibition of platelet aggregation was achieved within 2 hours after aspirin treatment), it was recommended to administer NSAIDs over 2 hours after aspirin. In fact, none of the tested NSAIDs altered the aspirin effect if administration followed that of aspirin.
Enteric coated aspirin only avoids local irriatation caused by the drug. It does not prevent the GI effects resulting from inhibition of protective PGs in stomach. Use of Misoprostol alongwith aspiirn may be helpful in patients intolerant of low doses of the drug.
The co-administration of Aspirin and Misoprostol maintain ample mucous lining in the intestine. Misoprostol mitigates the negative effect of Asprin on COX-1 with respect to mucous production.This may be the way to go
Even low dose aspirin is known to cause gastropathy, erosions and continued low grade GI blood loss particularly in elderly.. Identifying patients at risk is important. In addition use of PPIs. Misoprostol can be useful althought not fully effective. Using enteric coated or bufferred aspirin ma reduce gastric symptoms. Use of concurrent lactoferrin is under investigations. It is prudent to avoid concomitant use of other NSAIDs with low dose aspiriin. NO-aspirin has been tried. We need to have a highly selective COX inhibitor(Not COX-2 inhibitor) which spares stomach and acts on platelets only!
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