Functional Fibrinolysis Assays Reveal Different Mechanisms underlying Plasminogen Dysfunction in Ligneous Conjunctivitis.


Journal

Thrombosis and haemostasis
ISSN: 2567-689X
Titre abrégé: Thromb Haemost
Pays: Germany
ID NLM: 7608063

Informations de publication

Date de publication:
May 2020
Historique:
entrez: 6 5 2020
pubmed: 6 5 2020
medline: 25 8 2020
Statut: ppublish

Résumé

 Ligneous conjunctivitis (LC) is a rare disorder associated with plasminogen deficiency characterized by chronic fibrin deposits in the eyelids. All patients with plasminogen deficiency do not develop LC, whose underlying mechanisms remain unknown.  We investigated whether fibrinolytic activity was correlated with phenotype and/or genotype in patients suffering from LC and their relatives.  Plasminogen activity/antigen levels and  Plasminogen activity varied from <10 to 40% in patients, 36 to 105% in relatives, and >80% in control healthy individuals. Homozygous K19E mutation was associated with normal antigenic plasminogen levels. In front-lysis experiments, all patients had a lower fibrinolysis rate as compared with their relatives and to control individuals. The cell-based ECLT and plasminogen activation assay demonstrated that urokinase-mediated fibrinolysis was not impaired in patients with homozygous K19E mutation compared with the other mutants.  We confirm that plasminogen levels fail to predict LC occurrence. In these conditions, t-PA clot lysis front is useful to predict clinical outcome in plasminogen deficiency. Moreover, we provide evidence that occurrence of LC overlaps quantitative and qualitative plasminogen deficiencies. The homozygous K19E mutation is associated with isolated impaired t-PA-mediated fibrinolysis compared with other mutants.

Sections du résumé

BACKGROUND BACKGROUND
 Ligneous conjunctivitis (LC) is a rare disorder associated with plasminogen deficiency characterized by chronic fibrin deposits in the eyelids. All patients with plasminogen deficiency do not develop LC, whose underlying mechanisms remain unknown.
OBJECTIVE OBJECTIVE
 We investigated whether fibrinolytic activity was correlated with phenotype and/or genotype in patients suffering from LC and their relatives.
METHODS METHODS
 Plasminogen activity/antigen levels and
RESULTS RESULTS
 Plasminogen activity varied from <10 to 40% in patients, 36 to 105% in relatives, and >80% in control healthy individuals. Homozygous K19E mutation was associated with normal antigenic plasminogen levels. In front-lysis experiments, all patients had a lower fibrinolysis rate as compared with their relatives and to control individuals. The cell-based ECLT and plasminogen activation assay demonstrated that urokinase-mediated fibrinolysis was not impaired in patients with homozygous K19E mutation compared with the other mutants.
CONCLUSION CONCLUSIONS
 We confirm that plasminogen levels fail to predict LC occurrence. In these conditions, t-PA clot lysis front is useful to predict clinical outcome in plasminogen deficiency. Moreover, we provide evidence that occurrence of LC overlaps quantitative and qualitative plasminogen deficiencies. The homozygous K19E mutation is associated with isolated impaired t-PA-mediated fibrinolysis compared with other mutants.

Identifiants

pubmed: 32369847
doi: 10.1055/s-0040-1709526
doi:

Substances chimiques

Membrane Proteins 0
PLAU protein, human 0
Fibrin 9001-31-4
Plasminogen 9001-91-6
Tissue Plasminogen Activator EC 3.4.21.68

Types de publication

Comparative Study Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

758-767

Informations de copyright

Georg Thieme Verlag KG Stuttgart · New York.

Déclaration de conflit d'intérêts

None declared.

Auteurs

Marie-Charlotte Bourrienne (MC)

Université de Paris, INSERM UMR_S1148, Paris Cedex, France.
Laboratoire d'Hématologie, AP-HP, Hôpital Bichat, Paris Cedex, France.

Stéphane Loyau (S)

Laboratoire d'Hématologie, AP-HP, Hôpital Bichat, Paris Cedex, France.

Dorothée Faille (D)

Université de Paris, INSERM UMR_S1148, Paris Cedex, France.
Laboratoire d'Hématologie, AP-HP, Hôpital Bichat, Paris Cedex, France.

Emmanuelle de Raucourt (E)

Laboratoire d'Hématologie, AP-HP, Hôpital Bichat, Paris Cedex, France.
Laboratoire d'Hématologie, AP-HP, Hôpital Beaujon, Clichy Cedex, France.

Philippe de Mazancourt (P)

Laboratoire de Biochimie Hormonologie et Génétique Moléculaire, AP-HP, Hôpital Ambroise Paré, Boulogne-Billancourt, France.

Benoît Ho-Tin-Noé (B)

Université de Paris, INSERM UMR_S1148, Paris Cedex, France.

Eric Gabison (E)

Département d'Ophtalmologie, Fondation Ophtalmologique A. de Rothschild, Paris, France.

Nadine Ajzenberg (N)

Université de Paris, INSERM UMR_S1148, Paris Cedex, France.
Laboratoire d'Hématologie, AP-HP, Hôpital Bichat, Paris Cedex, France.

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Classifications MeSH