Normalisation of tissue factor pathway inhibitor activity after glycaemic control optimisation in type 1 diabetic patients

Citation
M. Rigla et al., Normalisation of tissue factor pathway inhibitor activity after glycaemic control optimisation in type 1 diabetic patients, THROMB HAEM, 84(2), 2000, pp. 223-227
Citations number
33
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
THROMBOSIS AND HAEMOSTASIS
ISSN journal
03406245 → ACNP
Volume
84
Issue
2
Year of publication
2000
Pages
223 - 227
Database
ISI
SICI code
0340-6245(200008)84:2<223:NOTFPI>2.0.ZU;2-X
Abstract
Increased plasma concentrations of various markers of endothelial damage ha ve been observed in type I diabetic patients, particularly in those with mi croangiopathy. Objective. To evaluate the effect of near-normalisation of g lycaemic control on different markers of endothelial injury involved in hae mostasis in poorly-controlled type 1 diabetic patients. Material and Method s. TFPI, thrombomodulin (TM), plasminogen activator inhibitor, tissue-type plasminogen activator and von Willebrand factor were measured in 14 poorly- controlled type 1 diabetic patients free of diabetes-related complications (8 men, 6 women; mean age 29.8 +/-: 9.9 years) before (baseline) and after 3 months of intensive therapy and in 14 sex-, age- and BMI-matched control subjects. Results. After a mean follow-up of 107 +/- 49 days (56-210), Hb A (1c) decreased from 11.2 +/- 2.3 to 6.7 +/- 0.7% (p <0.0001). TFPI activity at baseline was higher than in the control group (126.9 +/- 34 vs 92.0 +/- : 13%, p <0.005) and decreased after good glycaemic control was achieved (p <0.005), becoming similar to that in the control group (91.0 +/- 16.5%). T he TFPI descent correlated with the variations observed in HbA(1c) (p <0.05 ; r = 0.54). TM levels at baseline were significantly hi her than in the co ntrol group (42.3 +/- 9.1 vs 29.00 +/- 10.9; P <0.005) and did not change. The remaining parameters studied were similar between patients and controls and did not change after glycaemic optimisation. Conclusions. Optimisation of glycaemic control normalises the increased activity of TFPI but not the higher TM levels observed in poorly-controlled type 1 diabetic patients wi thout chronic complications.