Evidence that Modifications of Lp(a) In Vivo Inhibit Plasmin Formation on Fibrin

Thierry Soulat; Stéphane Loyau; Veronique Baudouin; Vincent Durlach; Philippe Gillery; Roselyne Garnotel; Chantal Loirat; Eduardo Anglés-Cano

doi:10.1055/s-0037-1614640

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 1999; 82(01): 121-127
DOI: 10.1055/s-0037-1614640

Rapid Communication

Schattauer GmbH

Evidence that Modifications of Lp(a) In Vivo Inhibit Plasmin Formation on Fibrin

A Study with Individual Plasmas Presenting Natural Variations of Lp(a)

Authors

Thierry Soulat

¹From Inserm U.143, Hôpital de Bicêtre, Reims, France
Stéphane Loyau

¹From Inserm U.143, Hôpital de Bicêtre, Reims, France
Veronique Baudouin

²Pediatric Nephrologic Department, Hòpital Robert Debré, Paris, France
Vincent Durlach

³Medical Clinic and Biochemistry Department, Hôpital Robert Debré, Reims, France
Philippe Gillery

³Medical Clinic and Biochemistry Department, Hôpital Robert Debré, Reims, France
Roselyne Garnotel

³Medical Clinic and Biochemistry Department, Hôpital Robert Debré, Reims, France
Chantal Loirat

²Pediatric Nephrologic Department, Hòpital Robert Debré, Paris, France
Eduardo Anglés-Cano

¹From Inserm U.143, Hôpital de Bicêtre, Reims, France

Abstract

Summary

In the present study we have investigated the effect of individual variations in the concentration of Lp(a) on plasmin formation at the surface of fibrin. The plasma Lp(a) concentrations from 20 nephrotic children were high at flare-up of the disease (0.43 ± 0.45 g/l) and decreased progressively with remission at both 6 weeks (0.28 ± 0.24 g/l) and 6 months (0.24 ± 0.288 g/l). In contrast, the concentration of plasminogen showed an inverse variation, with low values at flareup (1.27 ± 0.34 μM) and normal values at remission (1.66 ± 0.17 μM at 6 weeks and 1.99 ± 0.21 μM at 6 months). An increase in plasmin formation (from 0.62 ± 0.49 to 0.73 ± 0.61, and 0.84 ± 0.75 pmol/well) and a decrease in apo(a) binding (from 5.45 ± 2.42 to 4.54 ± 2.12, and 3.93 ± 1.51 fmol/well) on the surface of fibrin, were concomitantly observed from flare-up to remission at 6 weeks and at 6 months, respectively. Values for plasmin formation parallel the amount of plasminogen bound. The low concentration of plasminogen found at flare-up may also have contributed to the increased binding of Lp(a) as indicated by a decrease in the maximal amount of Lp(a) bound (B_max) to fibrin as a function of plasma plasminogen concentrations. B_max was 1.51 fmol in the absence of plasminogen and decreased to 1.1 fmol and 0.93 fmol at respectively 1 and 2 μM of plasminogen. Altogether, these data constitute the first quantitative evidence indicating that plas-min formed at the surface of fibrin may vary with modifications of the concentration of Lp(a) in vivo.

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References

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