PREVENTION OF THROMBOSIS IN PATIENTS ON HEMODIALYSIS BY LOW-DOSE ASPIRIN

Since platelet cyclo-oxygenase is much more sensitive to inactivation by aspirin than is the enzyme in the arterial wall and low doses of aspirin may prevent thrombosis by blocking thromboxane synthesis, we conducted a randomized, double-blind trial of aspirin (160 mg per day) vs. placebo in 44 patients on chronic hemodialysis. The study was continued until there were 24 patients with thrombi and both groups had been under observation for a mean of nearly five months. Thrombi occurred in 18 of 25 (72 per cent) of patients given placebo and 16 of 19 (32 per cent) of those given aspirin (P<0.01). The incidence of thrombosis was reduced from 0.46 thrombi per patient month in the placebo group to 0.16 thrombi per patient month in the aspirin group (P<0.005). A dose of 160 mg of aspirin per day is an effective, nontoxic antithrombotic regimen in patients on hemodialysis. (N Engl J Med 301:577–579, 1979) RECENT clinical trials of aspirin and sulfinpyrazone have suggested that drugs that inhibit prostaglandin and thromboxane synthesis in platelets decrease the death rate in men who have had a myocardial infarction.1 2 3 These studies have not been conclusive, and the wisdom of this therapeutic approach has been challenged; the major product of prostaglandin synthesis in vascular tissue, prostacyclin, is postulated to be a naturally occurring antithrombotic agent,4 and inhibition of vascular prostaglandin synthesis may therefore promote thrombosis. Aspirin acetylates cyclo-oxygenase,5 the first enzyme in prostaglandin synthesis. This effect is permanent in platelets, which do not synthesize protein, and thus the effects. © 1979, Massachusetts Medical Society. All rights reserved.