Thromb Haemost 2010; 104(04): 724-733
DOI: 10.1160/TH10-01-0048
Blood Coagulation, Fibrinolysis and Cellular Haemostasis
Schattauer GmbH

The effect of ethanol and its metabolism on fibrinolysis

Authors

  • Marlien Pieters

    1   TReNDS Centre of Excellence – Nutrition, North-West University, Potchefstroom, South Africa
  • Hester H. Vorster

    1   TReNDS Centre of Excellence – Nutrition, North-West University, Potchefstroom, South Africa
  • Johann C. Jerling

    1   TReNDS Centre of Excellence – Nutrition, North-West University, Potchefstroom, South Africa
  • Christine S. Venter

    1   TReNDS Centre of Excellence – Nutrition, North-West University, Potchefstroom, South Africa
  • Retha C. M. Kotze

    1   TReNDS Centre of Excellence – Nutrition, North-West University, Potchefstroom, South Africa
  • Elsabe Bornman

    2   School of Nursing Science, North-West University, Potchefstroom, South Africa
  • Joyce J. M. C. Malfliet

    3   Department of Hematology, Erasmus University Medical Center, Rotterdam, The Netherlands
  • Dingeman C. Rijken

    3   Department of Hematology, Erasmus University Medical Center, Rotterdam, The Netherlands

Financial support:This study was supported by the National Research Foundation of South Africa.
Weitere Informationen

Publikationsverlauf

Received: 18. Januar 2010

Accepted after major revision: 24. Mai 2010

Publikationsdatum:
24. November 2017 (online)

Preview

Summary

The role of ethanol metabolism in possible haemostatic cardioprotective effects has not yet been determined. To this end, we investigated the effect of a moderate dose of ethanol (35 g) and its metabolism, on haemostatic variables over 14 hours (h). Eighteen Caucasian males participated in a placebo-controlled, randomised, cross-over study. Blood was collected prior to alcohol consumption, and at 10 time points for 14 h. Blood ethanol peaked at 1 h and was cleared after 8 h following ethanol consumption, significantly increasing plasma acetate (p=0.0028). Ethanol did not influence the coagulation factors significantly. PAI-1act increased (p<0.0001) and tPAact (p=0.047) decreased following alcohol consumption, reaching maximum (0.69 to 22.2 IU/ml) and minimum (0.88 to 0.33 IU/ml) levels at 5 h, respectively. Significantly increased plasma clot lysis times (46.8 to 67.6 minutes) and reduced global fibrinolytic capacity of whole blood, measured as D-dimer production during incubation of blood clots (2.26 to 0.29 μg/ml), were found at 5 h. Except for PAI-1act (borderline significance; p=0.05), there was no significant difference in the fibrinolytic markers between the two groups the following morning. Moderate ethanol consumption resulted in a significant temporary fibrinolysis inhibition. Any protective effects of moderate ethanol consumption on cardiovascular disease do not appear to be due to improvement in fibrinolytic potential within the first 14 h following consumption. The use of global fibrinolytic assays is recommended for determining the true effect of ethanol on fibrinolysis.