Thromb Haemost 2006; 95(05): 802-806
DOI: 10.1160/TH05-12-0816
Blood Coagulation, Fibrinolysis and Cellular Haemostasis
Schattauer GmbH

Interleukin-6 and interleukin-6 promoter polymorphism (−174) G>C in patients with spontaneous venous thromboembolism

Rainer Vormittag
1   Division of Haematology and Haemostaseology, Department of Internal Medicine I Vienna, Austria
,
Kety Hsieh
2   Department of Radiology, Vienna, Austria
,
Alexandra Kaider
3   Section of Clinical Biometrics, Department of Medical Computer Sciences Vienna, Austria
,
Erich Minar
4   Division of Angiology, Department of Internal Medicine II, Vienna, Austria
,
Christine Bialonczyk
6   Department of Dermatology, Wilhelminenspital Vienna, Vienna, Austria
,
Mirko Hirschl
7   7Department of Angiology, Hanusch-Krankenhaus Vienna, Vienna, Austria
,
Christine Mannhalter
5   Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University Vienna, Vienna, Austria
,
Ingrid Pabinger
1   Division of Haematology and Haemostaseology, Department of Internal Medicine I Vienna, Austria
› Institutsangaben

Financial support: This work was supported by a grant from the Hochschuljubiläumsfonds of the University Vienna.
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Publikationsverlauf

Received 22. Dezember 2005

Accepted after resubmission 10. März 2006

Publikationsdatum:
01. Dezember 2017 (online)

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Summary

Increased levels of interleukin-6 (IL-6) have been reported in patients with a history of venous thromboembolism (VTE); however, prospective studies did not confirm an association between inflammatory markers that are highly correlated with IL-6 and the risk of VTE. It was the aim of our study to investigate the association of IL-6 and its promoter polymorphism (−174) G>C with the risk of spontaneous VTE. IL-6 was measured in 128 patients with deep venous thrombosis (DVT, 70 w / 58 m),105 with pulmonary embolism (PE, 58w/ 47 m) and 122 healthy controls (60 w / 62 m) with a highly sensitive ELISA (Quantikine HS Human IL-6 Immunoassay, RnDSystems®). The promoter polymorphism was determined by genotyping, allele specific PCR was followed by high resolution gel-electrophoresis. Median concentrations [interquartile ranges] were 2.37 [1.51–3.89] (pg/ ml) in patients with DVT, 2.83 [1.83–4.87] in those with PE and 2.51 [1.71–4.78] in controls (p = 0.6, p = 0.4). Hetero- or homozygous carriers of the C allele (71% in DVT, 67% in PE and 59% among controls) did not have higher IL-6 levels than homozygous carriers of the G allele (median 2.60 vs. 2.59 pg/ml, p = 0.7). In conclusion, we found no association of IL-6 and its promoter polymorphism (−174) G>C with the risk of spontaneous VTE.