Coagulation and fibrinolysis abnormalities in familial amyloid polyneuropathy.
Amyloid
; 19(3): 129-32, 2012 Sep.
Article
in En
| MEDLINE
| ID: mdl-22624582
ABSTRACT
OBJECTIVE:
Familial amyloid polyneuropathy (FAP) is an autosomal dominant form of hereditary amyloidosis. Several studies reported coagulation factor X deficiency and excessive fibrinolysis in immunoglobulin light chain amyloidosis. However, few have investigated coagulation and fibrinolysis in FAP. The objective of this study was to determine abnormalities in plasma biomarkers of coagulation and fibrinolysis in FAP.METHODS:
We prospectively recruited eight FAP patients with transthyretin mutations and ten age-matched control patients with other neuropathies in our university. We examined plasma biomarkers of coagulation and fibrinolysis including prothrombin time, activated partial thromboplastin time, fibrinogen, fibrin/fibrinogen degradation products, D-dimer, α2-antiplasmin, antithrombin, plasminogen, thrombin-antithrombin complex, plasmin-α2-antiplasmin complex, prothrombin fragment 1+2, and coagulation factor X. The Mann-Whitney U test was performed for statistical comparisons between FAP and control groups.RESULTS:
FAP patients exhibited significantly decreased levels of coagulation factor X, plasminogen and α2-antiplasmin, and significantly increased levels of prothrombin fragment 1+2 compared to control patients.CONCLUSION:
Our results indicate abnormalities of coagulation and fibrinolysis in FAP patients.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Blood Coagulation Disorders
/
Amyloid Neuropathies, Familial
/
Fibrinolysis
Type of study:
Observational_studies
Limits:
Adult
/
Aged
/
Female
/
Humans
/
Male
/
Middle aged
Language:
En
Journal:
Amyloid
Journal subject:
BIOQUIMICA
Year:
2012
Document type:
Article
Affiliation country:
Japan