Microparticles in deep venous thrombosis, antiphospholipid syndrome and Factor V Leiden.
Microparticles (MPs) are blebs released from cellular surfaces during activation/apoptosis. They are procoagulant, pro-inflammatory and could contribute to pathogenesis of deep venous thrombosis (DVT). This study compared the number, cellular origin and procoagulant activity of MPs on DVT patients in different clinical situations: at diagnosis (n = 9, 5F/4M; mean age = 41.11), 1-3 years after warfarin withdrawal (n = 10, 7F/3M; mean age = 32.90), associated to antiphospholipid syndrome (APS; n = 11, 9F/2M; mean age = 33.82), or asymptomatic carriers of Factor V Leiden (FVL; n = 7, 7F/0M; mean age = 34.00) vs healthy controls (CTR). The quantification and characterization were performed by flow cytometry using CD235, CD61, CD45, CD31, CD14, CD45, anti-TF and Annexin V. The plasmatic procoagulant activity was investigated by prothrombin fragment 1 + 2 (F1 + 2) determination. The MPs procoagulant activity was analyzed by D-dimer (DD2) and Thrombin Generation Test (TGT) on a healthy pool of plasmas adjusted or not by their number (10,000 MPs). The MPs percentages were not different between the groups, but absolute number was increased in patients 1-3 years after warfarin withdrawal vs CTR (P = 0.02). There was no difference of the MPs cellular origin comparing patients to controls. TGT using 10,000 MPs was lower on these patients (P = 0.01). APS patients showed a reduction of plasmatic procoagulant activity (P = 0.004), but they were under warfarin therapy. DD2 in the presence of MPs, independently of its number, was higher in patients with DVT at diagnosis (P < 0.0001). MPs of patients with spontaneous DVT at diagnosis can promote coagulation activation demonstrated by increased DD2. Even the increased MPs from patients 1-3 years after thrombotic episode generated lower amount of thrombin, they can have a protective effect by activation of Protein C anticoagulant pathway.
Flores-Nascimento
M C
MC
Hematology-Hemotherapy Center, State University of Campinas, Campinas, SP, Brazil. flores_mariane@yahoo.com.br
Beltrame
M P
MP
De Paula
E V
EV
Montalvão
S L
SL
Pereira
F G
FG
Orsi
F L A
FL
Lorand-Metze
I
I
Annichino-Bizzacchi
J M
JM
D000328:Adult; D016736:Antiphospholipid Syndrome / Q000097:blood / Q000235:genetics / Q000473:pathology*; D001780:Blood Coagulation Tests; D016022:Case-Control Studies; D005165:Factor V / Q000235:genetics / Q000378:metabolism*; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005434:Flow Cytometry; D006801:Humans; D008074:Lipoproteins / Q000378:metabolism; D008297:Male; D010316:Particle Size; D013375:Substance Withdrawal Syndrome / Q000097:blood / Q000473:pathology; D013917:Thrombin / Q000235:genetics / Q000378:metabolism; D013927:Thrombosis / Q000097:blood / Q000235:genetics / Q000473:pathology; D020246:Venous Thrombosis / Q000097:blood / Q000235:genetics / Q000473:pathology*; D014859:Warfarin / Q000008:administration & dosage
D005338:Fibrin Fibrinogen Degradation Products; D008074:Lipoproteins; C095381:factor V Leiden; C036309:fibrin fragment D; D014859:Warfarin; D005165:Factor V; D013917:Thrombin