Thromb Haemost 2003; 89(01): 91-96
DOI: 10.1055/s-0037-1613547
Blood Coagulation, Fibrinolysis and Cellular Haemostasis
Schattauer GmbH

Peripheral artery disease in type 2 diabetes: the role of fibrinolysis

Annunziata Lapolla
1   University of Padova, Department of Medical and Surgical Sciences, Padova, Italy
,
Francesco Piarulli
1   University of Padova, Department of Medical and Surgical Sciences, Padova, Italy
,
Giovanni Sartore
1   University of Padova, Department of Medical and Surgical Sciences, Padova, Italy
,
Ciro Rossetti
1   University of Padova, Department of Medical and Surgical Sciences, Padova, Italy
,
Luigi Martano
1   University of Padova, Department of Medical and Surgical Sciences, Padova, Italy
,
Paolo Carraro
2   Azienda ospedaliera, Department of Laboratory Medicine, Padova, Italy
,
Massimo De Paoli
2   Azienda ospedaliera, Department of Laboratory Medicine, Padova, Italy
,
Domenico Fedele
1   University of Padova, Department of Medical and Surgical Sciences, Padova, Italy
› Author Affiliations
Further Information

Publication History

Received 13 September 2002

Accepted after revision 01 November 2002

Publication Date:
09 December 2017 (online)

Summary

The aim of the present study is to verify the relationship between peripheral artery disease (PAD) and some coagulation/fibrinolysis parameters in type 2 diabetic patients.

Sixty-three type 2 diabetic patients, without PAD, were studied at baseline and after 4 years. Assessments included tissue-Plasminogen Activator (t-PA), Plasminogen Activator Inhibitor-1 antigen (PAI-1 Ag), Plasminogen Activator Inhibitor-1 activity (PAI-1 Act), Plasminogen (Pl), Fibrin peptide A (FPA), Fibrinogen (Fr), and the ankle/brachial pressure index (ABI).

We observed a significant difference between diabetic patients and controls as regards tPA (11.8 ± 5.4 vs. 6.6 ± 3.0 ng/ml; p <0.05 ) and PAI-1 Act (17.8 ± 9.2 vs. 11.7 ± 6.6 ng/dl; p <0.005). After 4 years 13 diabetic patients became vasculo-pathic and, at baseline, had significantly lower tPA (8.9 ± 4.8 vs. 12.5 ± 5.3; p <0.011), and higher PAI-1 Ag (50.8 ± 22.2 vs. 32 ± 22.2; p <0.006), and PAI-1 Act values (24.1 ± 9.5 vs. 16.1 ± 8.4; p <0.014), compared with 50 diabetic patients who did not develop PAD after 4 years.

These data show that the physiological equilibrium which exists between t-PA and PAI-1 moves towards higher levels in our diabetic patients compared with controls, at baseline, whereas diabetic patients who developed PAD showed a shift towards an antifibrinolytic pathway with diminished t-PA, increased PAI-1 Ag and PAI-1 Act and consequently procoagulant activity. Our study suggests that hypofibrinolysis may be involved in the future onset of PAD in type 2 diabetic patients.

 
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