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Thromb Haemost 1997; 77(03): 472-476
DOI: 10.1055/s-0038-1655991
Clinical Studies
Schattauer GmbH Stuttgart

Increased Tissue Factor Pathway Inhibitor (TFPI) and Coagulation in Patients with Insulin-dependent Diabetes mellitus

Paul B Leurs
The Department of Internal Medicine, Division of Endocrinology and Metabolism, and Division of Hematology, University Hospital, Maastricht, The Netherlands
,
Rene van Oerle
The Department of Internal Medicine, Division of Endocrinology and Metabolism, and Division of Hematology, University Hospital, Maastricht, The Netherlands
,
Bruce H R Wolffenbuttel
The Department of Internal Medicine, Division of Endocrinology and Metabolism, and Division of Hematology, University Hospital, Maastricht, The Netherlands
,
Karly Hamulyak
The Department of Internal Medicine, Division of Endocrinology and Metabolism, and Division of Hematology, University Hospital, Maastricht, The Netherlands
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Publikationsverlauf

Received 10. Juni 1996

Accepted after revision 30. Oktober 1996

Publikationsdatum:
11. Juli 2018 (online)

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Summary

Recently, we found an increase in tissue factor pathway inhibitor (TFPI) activity in patients with insulin-dependent diabetes mellitus (IDDM). This increase in TFPI activity could be the result of increased thrombin formation and/or altered binding of TFPI to glycosaminoglycans. We studied TFPI activity (chromogenic assay) in relation to prothrombin F1+2 fragments and endogenous thrombin potential (ETP), in 46 IDDM patients, and 18 age and sex-matched healthy controls. Prothrombin, antithrombin and thrombomodulin were also determined. In IDDM patients, TFPI activity and F1+2 levels were significantly higher, while ETP, prothrombin antigen levels, and antithrombin activity were lower as compared to the controls. In IDDM patients with microalbuminuria, a manifestation of generalized angiopathy, TFPI activity, F1+2 and thrombomodulin levels were higher than in patients with only retinopathy or patients without complications. No correlation between TFPI activity, F1+2 levels and thrombomodulin was found, while TFPI activity was negatively correlated with ETP (r = -0.27). Microalbuminuria was significantly correlated with TFPI activity (r = 0.46), F1+2 (r = 0.56), and thrombomodulin (r = 0.52). In TFPI-depleted plasma, ETP increased, indicating that ETP is affected by TFPI. In conclusion, the increase in TFPI activity in IDDM patients may not be considered to be a reaction on a procoagulant state. It is hypothesized that vascular damage, leading to alterations in glycosaminoglycans, is in part responsible for the changes in TFPI activity, F1+2 levels and ETP.

 

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