Ultra-low-dose aspirin may reduce bleeding in portal hypertension patients

November 14th, 2007 - 1:58 am ICT by admin  
The study led by Professor C. Doutremepuich, has shown a normalizing effect of platelet-endothelial cell alterations and bleeding time.

Further, this effect is mediated by Cyclooxygenase 2 inhibition.

Ultra-low-dose aspirin has a prothrombotic effect that is the opposite of that observed with usual doses for the prevention of stroke or heart attack. The antithrombotic properties of low-dose aspirin are achieved by the inhibition of COX 1 in platelets.

Aspirin is the most widely used antithrombotic agent. Prior studies in rats have shown that the prothrombotic properties of ultra-low-dose aspirin are not mediated by platelets but by endothelial cells, and as such they have the potential of reversing the platelet-endothelial cell interaction alterations observed in portal hypertension.

According to researchers, till date no clear explanation has existed to explain the effect of such a small dose of aspirin, and no mechanism has been found to explain this contradictory action.

The prothrombotic effects of COX 2 inhibitors became evident in 2004 when one of the most widely accepted non-steroidal anti-inflammatory drugs was withdrawn from the market because of concerns about increased risk of heart attack and stroke associated with long-term, high-dosage use. Only aspirin has been demonstrated to have a prothrombotic effect at a very low dose.

Portal hypertension is a major complication of chronic liver disease, and bleeding is one of its most severe problems, leading often to death. Currently no treatment is used to modify the altered platelet activity observed in this pathology.

The new research, is published in the October 14 issue of the World Journal of Gastroenterology. (ANI)

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