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PubMed1985

Aspirin and other platelet-aggregation inhibiting drugs.

The biochemistry of platelets is surprisingly complex, and offers the opportunity for numerous platelet-aggregation inhibiting ("antiplatelet") drugs to interfere with different aspects of their metabolism and function. Thus, aspirin inhibits platelet aggregation by irreversibly inactivating cyclo-oxygenase, a key enzyme in platelet prostaglandin metabolism, while the other nonsteroidal anti-inflammatory drugs and sulphinpyrazone cause reversible and dose-dependent inhibition of the same enzyme. Dipyridamole can inhibit both platelet adhesion and aggregation by raising the platelet cyclic AMP level through phosphodiesterase inhibition. The use of aspirin, sulphinpyrazone, and dipyridamole as antithrombotic agents has now been extensively evaluated. In general, treatment with these drugs has been more likely to prevent arterial than venous thromboembolism, and aspirin or the combination of aspirin and dipyridamole has been more effective in this respect than has sulphinpyrazone. Recent evidence strongly suggests that aspirin reduces the risk of non-fatal myocardial infarction in patients with unstable angina, and that the administration of aspirin in combination with dipyridamole significantly improves graft patency after aortocoronary bypass. Aspirin also appears to reduce the likelihood of stroke or death in men with transient cerebral ischaemic attacks.

Aspirin↗
PubMed1985

Fulminant gangrene in transient cold agglutinemia associated with Escherichia coli infection.

Fulminant gangrene of the fingers, toes and nose developed in a 57-year-old woman with Escherichia coli pneumonia. Cryoglobulinemia was noted, and the cryoglobulin was identified as IgM-IgG with anti-I cold agglutinin activity. The cold agglutinins possessed potent lymphocytotoxic and monocytotoxic activity and weaker granulocytotoxic activity. Treatment with plasmapheresis, steroids and antibiotics led to complete clinical recovery, although amputation of several toes was necessary. The patient died 1 1/2 years later; the main findings at autopsy were chronic and acute pyelonephritis and acute bacterial endocarditis. This seems to be the first case of IgM-IgG cold agglutinemia occurring during the course of E. coli infection and the third case of fulminant gangrene complicating transient cold agglutinemia.

Anemia, Hemolytic, Autoimmune↗
PubMed1985

Interaction of non-steroidal anti-inflammatory drugs on platelet cyclo-oxygenase and lipoxygenase activity.

Non-steroidal anti-inflammatory drugs inhibit platelet cyclo-oxygenase activity. This study shows that salicylate, diflunisal, sulphinpyrazone and indomethacin prevent the in vivo inhibitory effect of aspirin on cyclo-oxygenase activity as measured by the formation of malondialdehyde and thromboxane B2, two products of platelet arachidonic acid metabolism. Salicylate also prevents the inhibitory effect of indomethacin. All these drugs therefore appear to interact with the same site on platelet cyclo-oxygenase. Since salicylate is inactive by itself on this platelet enzyme and diflunisal and sulphinpyrazone were used at ineffective doses, it is suggested that they interact with aspirin (or indomethacin) at a supplementary binding site, rather than directly on the substrate active site. Interaction with this putative supplementary site is necessary but not sufficient for the efficacy of these drugs as cyclo-oxygenase inhibitors. Acetylation by aspirin of the active site appears to be secondary to binding of the salicylate moiety to the supplementary site. Sodium salicylate is also inactive on platelet lipoxygenase. It prevents the inhibition of cyclo-oxygenase induced by aspirin, but does not counteract the inhibitory effect of 5, 8, 11, 14-eicosatetraynoic acid on both enzymes. It also fails to interfere with the inhibitory activity of nordihydroguaiaretic acid on lipoxygenase. These data confirm that, unlike eicosatetraynoic acid, nonsteroidal anti-inflammatory drugs interact with a site on cyclo-oxygenase distinct from the catalytic site, although related to it. Such a supplementary binding site is lacking on lipoxygenase.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1985

[Eicosanoids, myocardial ischemia and sudden death].

An activation of the arachidonic acid cascade has long been reported in coronary artery diseases. However, no clear-cut connection has been demonstrated between this activation and the clinical manifestations of myocardial ischemia. Controlled trials with the available cyclooxygenase inhibitory drugs support the view that these agents might be useful in subgroups of patients. However, these are not known. The peculiar pharmacologic properties of prostacyclin and PGE1 have been documented to improve experimental and clinical acute myocardial ischemia. Further efforts are needed to elucidate the usefulness of some PGs in the management of patients with ischemic heart disease and their contributory role to the disease.

Animals↗