Thromb Haemost 2007; 97(02): 181-185
DOI: 10.1160/TH06-07-0407
Blood Coagulation, Fibrinolysis and Cellular Haemostasis
Schattauer GmbH

Genetic variation in thrombin-activatable fibrinolysis inhibitor (TAFI) is associated with the risk of splanchnic vein thrombosis

Emile L. E. de Bruijne
1   Departments of Hematology, Erasmus University Medical Center, Rotterdam
,
Sarwa Darwish Murad
2   Departments of Gastroenterology and Hepatology, Erasmus University Medical Center, Rotterdam
,
Moniek P. M. de Maat
1   Departments of Hematology, Erasmus University Medical Center, Rotterdam
,
Michael W. T. Tanck
3   Department of Clinical Epidemiology and Biostatistics, Academic Medical Center, Amsterdam
,
Elizabeth B. Haagsma
4   Department of Hepatogastroenterology, University Hospital Groningen, Groningen
,
Bart van Hoek
5   Department of Gastroenterology and Hepatology, Leiden University Medical Center, Leiden
,
Frits R. Rosendaal
6   Department of Clinical Epidemiology and Hematology, Leiden University Medical Center, Leiden; The Netherlands
,
Harry L. A. Janssen
2   Departments of Gastroenterology and Hepatology, Erasmus University Medical Center, Rotterdam
,
Frank W. G. Leebeek
1   Departments of Hematology, Erasmus University Medical Center, Rotterdam
,
for the Liver and Thrombosis Study Group › Author Affiliations
Further Information

Publication History

Received 20 July 2006

Accepted after resubmission 18 January 2006

Publication Date:
25 November 2017 (online)

Summary

Splanchnic vein thrombosis (SVT) has been associated with a hypercoagulable state. Thrombin-activatable fibrinolysis inhibitor (TAFI) may contribute to a hypercoagulable state, and therefore we were interested in the role of TAFI in SVT. Since the disease is frequently associated with liver insufficiency, which affects plasma levels ofTAFI, we studied the role of variation in theTAFI gene in SVT. In a multicenter case-control study on 118 patients with SVT (39 Budd-Chiari syndrome and 85 portal vein thrombosis) and 118 population-based controls, the relationship of SVT with single nucleotide polymorphisms (SNPs) and haplotypes in the TAFI gene (- 438G/A, Ala147Thr, Thr325Ile and 1583A/T) was determined. The risk for SVT was decreased (OR 0.2,95% CI 0.1–0.7) in 147Thr/Thr homozygotes and slightly,but not significantly,increased in carriers of the 325Ile allele (OR 1.6, 95%CI 0.9–2.7). Haplotype analysis confirmed that the Ala147Thr SNP has the strongest association with risk of SVT. In conclusion, genetic variation in the TAFI gene is associated with risk of SVT, suggesting a role for TAFI in the pathogenetic mechanism of SVT.

 
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