Thromb Haemost 1998; 79(02): 286-290
DOI: 10.1055/s-0037-1614979
Letters to the Editor
Schattauer GmbH

Impaired Haemostasis by Intravenous Administration of a Gelatin-based Plasma Expander in Human Subjects

E. de Jonge
1   From the Academic Medical Center, University of Amsterdam, Departments of Intensive Care
,
M. Levi
3   Center for Haemostasis, Thrombosis, Atherosclerosis and Inflammation Research Amsterdam, The Netherlands
,
F. Berends
2   From the Academic Medical Center, University of Amsterdam, Clinical Chemistry
,
A. E. van der Ende
3   Center for Haemostasis, Thrombosis, Atherosclerosis and Inflammation Research Amsterdam, The Netherlands
,
J. W. ten Cate
3   Center for Haemostasis, Thrombosis, Atherosclerosis and Inflammation Research Amsterdam, The Netherlands
,
C. P. Stoutenbeek
1   From the Academic Medical Center, University of Amsterdam, Departments of Intensive Care
› Author Affiliations
Further Information

Publication History

Received 14 April 1997

Accepted after resubmission 22 September 1997

Publication Date:
08 December 2017 (online)

Summary

The aim of this study was to investigate the effects of a gelatin-based plasma expander on blood coagulation and haemostasis in human subjects.

Six healthy men were studied in a randomised, controlled cross-over study to investigate the effects of a 60 min intravenous infusion of either 1 l gelatin-based plasma substitute (Gelofusine) or 0.9% NaCl (control). The infusion of gelatin resulted in a 1.7 fold increase in bleeding time at 60 min and a 1.4 fold increase at 120 min, while saline had no effect (p <0.05). Aggregation studies revealed a significant impairment of ristocetin-induced platelet aggregation (p <0.05), associated with a substantial decrease of vWF:ag (–32% vs. –5%, p <0.05) and ristocetin co-factor (–29% vs. +1%, p <0.05) and without in vitro impairment of the platelet glycoprotein 1b receptor. Gelatin caused a decrease in thrombin-antithrombin complexes (–45% vs. –4%, p <0.05) and F1+2 (–40% vs. +1%, p <0.05). The decrease in circulating levels of vWF:ag, vWF R:Co, thrombin-antithrombin complexes and F1+ 2 was more than could be expected by the calculated plasma-dilution generated by Gelofusine.

Our results demonstrated that the administration of a gelatin-based plasma substitute results in a significant impairment of primary haemostasis and thrombin generation. The defect in primary haemostasis appears to be related to a gelatin-induced reduction in von Willebrand factor, whereas the decreased thrombin generation may be due to the dilution of coagulation factors induced by Gelofusine.

 
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