Very Low Dose Aspirin May Lessen Bleeding in Portal Hypertension

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Very Low Dose Aspirin May Lessen Bleeding in Portal Hypertension

NEW YORK (Reuters Health) Nov 06 - Findings in a murine model of

portal hypertension suggest that the normalizing effect on platelet

and endothelial cell activity seen following ultra low-dose aspirin

(ULDA) administration may be mediated primarily through the COX 2

pathway.

In the October 14th issue of the World Journal of Gastroenterology,

Dr. Christian Doutremepuich and colleagues note that this is in

contrast to the antithrombotic effect of higher doses of aspirin,

which predominantly involves inhibition of the COX 1 pathway.

Dr. Doutremepuich of Universite Victor Segalen, Bordeaux, France and

his team add that ULDA has demonstrated a potentially beneficial

effect in animals with portal hypertension by normalizing altered

platelet activity and induced hemorrhagic time.

To investigate underlying mechanisms, the researchers studied the

effect of ULDA in rats with induced portal hypertension and animals

that had undergone a sham procedure, after they were pretreated with

a COX 1 inhibitor or a COX 2 inhibitor.

Although the investigators observe that the complex interactions such

as vascular responsiveness could not be evaluated, the prothrombotic

effect of ULDA was confirmed in animals with and without portal

hypertension.

This, the researchers note, was underscored by findings that use of

the COX 2 inhibitor induced a mild prothrombotic effect in the rats

with portal hypertension, similar to that seen following ULDA alone.

Moreover, addition of ULDA to animals already dosed with the COX 2

inhibitor produced no further effect.

This study, Dr. Doutremepuich told Reuters Health, shows the

possibility of using the ULDA effect therapeutically.