Ethanol Potentiation of Aspirin-Induced Prolongation of the Bleeding Time

Deykin, Daniel; Janson, Paul A.; McMahon, Louise

doi:10.1056/nejm198204083061406

Cited by 160 publications

(46 citation statements)

References 9 publications

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“…Because moderate doses of ASA abnormally prolong BT in uremics but not in control subjects (7), we became interested in the mechanism by which ASA impairs platelet function in uremia and the relationship between prolongation of BT and platelet cyclooxygenase inhibition. Although ASA has been reported to determine a moderate prolongation of BT in normals (25,26), the present results confirm our data reported previously (7) and show that ASA does not prolong BT in normal subjects at the doses employed in the present investigation. However, in all the chronic renal failure patients we studied, on regular hemodialysis, selected on the basis of a baseline BT within the normal range or slightly prolonged, post-ASA BT was significantly prolonged.…”

Section: Discussionsupporting

confidence: 92%

Aspirin prolongs bleeding time in uremia by a mechanism distinct from platelet cyclooxygenase inhibition.

Gaspari¹,

Viganò²,

Orisio³

et al. 1987

J. Clin. Invest.

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We reported that aspirin (ASA) abnormally prolongs bleeding time (BT) in uremia. The present study was designed to investigate whether (a) the abnormally prolonged post-ASA BT in uremia is due to different ASA pharmacokinetics and bioavailability that might be a consequence of uremic condition, (b) platelet cyclooxygenase is peculiarly sensitive to ASA in uremia, and (c) ASA affects primary hemostasis in uremia by a mechanism independent of cyclooxygenase inhibition. Our results showed that in patients with uremia, but not in normal subjects, ASA markedly prolongs the BT. This effect is transient and depends on the presence of ASA in the blood. The observed differences in ASA kinetic parameters are not an explanation of the exaggerated effect of ASA on primary hemostasis in uremia. The sensitivity of platelet cyclooxygenase to ASA inhibition is comparable in uremics and in normal subjects. The temporal dissociation between ASA-induced prolongation of BT and the effect on platelet thromboxane A2 generation suggests that ASA inhibits platelet function in uremia by a mechanism distinct from cyclooxygenase blocking. This possibility is strengthened by the observation that ibuprofen at a dose that fully inhibits platelet cyclooxygenase activity does not significantly prolong BT.

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Section: Discussionsupporting

confidence: 92%

Aspirin prolongs bleeding time in uremia by a mechanism distinct from platelet cyclooxygenase inhibition.

Gaspari¹,

Viganò²,

Orisio³

et al. 1987

J. Clin. Invest.

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“…Acute ingestion of ethanol was even found to increase the risk of subarachnoid hemorrhage. 2 This latter finding cannot be explained by enhanced platelet reactivity but, interestingly, ethanol was recently shown to potentiate aspirin-induced prolongation of the bleeding time 19 and to precipitate spasms in cerebral and coronary arteries of experimental animals. 20 Therefore, other mechanisms should be taken into account when trying to explain the increased risk of subarachnoid hemorrhage during ethanol intoxication.…”

Section: Table 3 Effects Of Ethanol Ingestion On Adp-induced Plateletmentioning

confidence: 92%

Acute ethanol ingestion increases platelet reactivity: is there a relationship to stroke?

Hillbom¹,

Kangasaho²,

Kaste³

et al. 1985

Stroke

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SUMMARYThe effects of ethanol ingestion on ADP-induced platelet aggregation and associated thromboxane formation were studied in the platelet-rich plasma of 10 healthy male volunteers, each serving as his own control. Ethanol caused a transient decrease in threshold concentration of ADP to produce irreversible aggregation. Over a wide range of ADP total platelet aggregation was increased. In the presence of irreversible aggregation, formation of thromboxane B 2 rose from 303 ± 56 to 950 ± 212 fmol per 10 7 platelets (p < 0.01). The effects lasted as long as ethanol was present in blood, did not significantly correlate to blood ethanol levels and exhibited great individual variation. It remains to be proved, whether these observations could contribute to the increased risk of ischemic brain infarction associated with acute ethanol ingestion.

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“…On the basis of our findings, the use of ketorolac and ketoprofen as analgesics in the early postoperative period should be carefully considered, particularly in patients undergoing surgery with a high risk of bleeding or with possible minor coagulation defects or if treated with agents known to prolong bleeding time [26,27]. In these conditions, ketorolac and ketoprofen treatment should be considered as a cause of increased postoperative bleeding and nefopam might be regarded as a safer drug with regard to bleeding tendency.…”

Section: Discussionmentioning

confidence: 99%