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Anti-factor V auto-antibody in the plasma and platelets of a patient with repeated gastrointestinal bleeding

Ajzner, E; Balogh, I; Haramura, G; Boda, Z; Kalmar, K; Pfliegler, G; Dahlbäck, Björn LU and Muszbek, L (2003) In Journal of Thrombosis and Haemostasis 1(5). p.943-949
Abstract
Development of autoantibody against coagulation factor V (FV) is a rare clinical condition with hemorrhagic complications of varying severity. The aim of this study was to establish the pathomechanism of an acquired FV deficiency and characterize the FV inhibitor responsible for the clinical symptoms. A 78-year-old female was admitted to hospital with severe gastrointestinal bleeding. General clotting tests and determination of clotting factors were performed by standard methods. FV antigen and FV containing immune complexes were measured by ELISA. The FV molecule was investigated by Western blotting and by sequencing the f5 gene. The binding of patient's IgG to FV and activated FV (FVa) was demonstrated in an ELISA system and its effect... (More)
Development of autoantibody against coagulation factor V (FV) is a rare clinical condition with hemorrhagic complications of varying severity. The aim of this study was to establish the pathomechanism of an acquired FV deficiency and characterize the FV inhibitor responsible for the clinical symptoms. A 78-year-old female was admitted to hospital with severe gastrointestinal bleeding. General clotting tests and determination of clotting factors were performed by standard methods. FV antigen and FV containing immune complexes were measured by ELISA. The FV molecule was investigated by Western blotting and by sequencing the f5 gene. The binding of patient's IgG to FV and activated FV (FVa) was demonstrated in an ELISA system and its effect on the procoagulant activity of FVa was tested in clotting tests and in a chromogenic prothrombinase assay. Localization of the epitope for the antibody was performed by blocking ELISA. FV activity was severely suppressed both in plasma and platelets. FV antigen levels were normal by ELISA using polyclonal anti-FV antibody or monoclonal antibody against the connecting region of FV, but depressed when HV1 monoclonal antibody against the C2 domain in the FV light-chain was used as capture antibody. The FV molecule was found intact. An IgG reacting with both FV and FVa was present in the patient's plasma and its binding to FV was inhibited by HV1 antibody. FV-containing immune complexes were detected in the patient's plasma and platelet lysate. The patient's IgG inhibited the procoagulant function of FVa. An anti-FV IgG was present in the patient's plasma and platelets. The autoantibody reacted with an epitope in the C2 domain of FV light chain and neutralized the procoagulant function of FVa. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
hemorrhagic diathesis, factor V, factor V inhibitor, platelets
in
Journal of Thrombosis and Haemostasis
volume
1
issue
5
pages
943 - 949
publisher
Federation of European Neuroscience Societies and Blackwell Publishing Ltd
external identifiers
  • wos:000183062300012
  • pmid:12871359
  • scopus:3042618865
ISSN
1538-7933
DOI
10.1046/j.1538-7836.2003.00143.x
language
English
LU publication?
yes
id
aeb7684d-17ea-4641-8cbb-5a288042933d (old id 310406)
date added to LUP
2007-08-02 09:55:15
date last changed
2017-01-01 04:48:37
@article{aeb7684d-17ea-4641-8cbb-5a288042933d,
  abstract     = {Development of autoantibody against coagulation factor V (FV) is a rare clinical condition with hemorrhagic complications of varying severity. The aim of this study was to establish the pathomechanism of an acquired FV deficiency and characterize the FV inhibitor responsible for the clinical symptoms. A 78-year-old female was admitted to hospital with severe gastrointestinal bleeding. General clotting tests and determination of clotting factors were performed by standard methods. FV antigen and FV containing immune complexes were measured by ELISA. The FV molecule was investigated by Western blotting and by sequencing the f5 gene. The binding of patient's IgG to FV and activated FV (FVa) was demonstrated in an ELISA system and its effect on the procoagulant activity of FVa was tested in clotting tests and in a chromogenic prothrombinase assay. Localization of the epitope for the antibody was performed by blocking ELISA. FV activity was severely suppressed both in plasma and platelets. FV antigen levels were normal by ELISA using polyclonal anti-FV antibody or monoclonal antibody against the connecting region of FV, but depressed when HV1 monoclonal antibody against the C2 domain in the FV light-chain was used as capture antibody. The FV molecule was found intact. An IgG reacting with both FV and FVa was present in the patient's plasma and its binding to FV was inhibited by HV1 antibody. FV-containing immune complexes were detected in the patient's plasma and platelet lysate. The patient's IgG inhibited the procoagulant function of FVa. An anti-FV IgG was present in the patient's plasma and platelets. The autoantibody reacted with an epitope in the C2 domain of FV light chain and neutralized the procoagulant function of FVa.},
  author       = {Ajzner, E and Balogh, I and Haramura, G and Boda, Z and Kalmar, K and Pfliegler, G and Dahlbäck, Björn and Muszbek, L},
  issn         = {1538-7933},
  keyword      = {hemorrhagic diathesis,factor V,factor V inhibitor,platelets},
  language     = {eng},
  number       = {5},
  pages        = {943--949},
  publisher    = {Federation of European Neuroscience Societies and Blackwell Publishing Ltd},
  series       = {Journal of Thrombosis and Haemostasis},
  title        = {Anti-factor V auto-antibody in the plasma and platelets of a patient with repeated gastrointestinal bleeding},
  url          = {http://dx.doi.org/10.1046/j.1538-7836.2003.00143.x},
  volume       = {1},
  year         = {2003},
}