Plasminogen activators (t-PA and u-PA) and plasminogen activators inhibitors (PAI-1 and PAI-2) in some myeloproliferative syndromes.
BACKGROUND
Clinical observations and laboratory data indicate that patients with myeloproliferative syndrome (MPS) have hemostasis disorders that manifest with haemorrhagic diathesis or thrombotic disease. The role of fibrinolytic system is not clear in the pathomechanism of the disorders. In the study we aimed to evaluate fibrinolysis system in blood plasma of the patients with selected myeloproliferative syndromes on the basis of examinations of plasminogen activators (tissue--t-PA and urokinase-type--u-PA) and type 1 and type 2 plasminogen activator inhibitors (PAI-1 and PAI-2).


METHODS
Forty-two patients (F/M 28/14) aged 36-78 years (average age--54 years) were enrolled into the study. Among the patients were 20 individuals with chronic myeloid leukaemia (CML), 17 with essential thrombocytemia (ET) and 5 with myelofibrosis (MF) treated in Provincial Haematological Outpatient Clinic in Bydgoszcz. Forty healthy volunteers (F/M 30/10) aged 24-65 (average 53) were included in control group. In citrate venous blood, the following parameters were determined: concentrations of antigen t-PA, u-PA, PAI-1, PAI-2, concentration of plasmin-alpha-2-antiplasmin complexes (PAP) determined with the use of ELISA technique, PAI-1 activity with amidolytic method, euglobulin lysis time (ELT) according to Kowarzyk-Buluk and fibrinogen/fibrin degradation products (FDP) concentration with the use of Merskey's method.


RESULTS
Performed evaluations show that besides normal ELT elevated concentrations of FDP and PAP complexes occur in the blood of patients with myeloproliferative syndromes (MPS.). In studied myeloproliferative syndromes, high concentration of PAI-1 Ag and very low activity of PAI-1 were observed. In the patients with MPS intensified plasminogenesis and increased fibrin degradation were demonstrated. The role of granulocyte elastase is considered in activation of fibrinolysis system.
Rość
D
D
Department of Pathophysiology, Medical University, ul. M. Skłodowskiej-Curie 9, 85-094 Bydgoszcz, Poland.
Kremplewska-Nalezyta
E
E
Gadomska
G
G
Zastawna
E
E
Michalski
A
A
Drewniak
W
W
D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D005260:Female; D005342:Fibrinolysis; D006801:Humans; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000097:blood; D008297:Male; D008875:Middle Aged; D009196:Myeloproliferative Disorders / Q000097:blood*; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*; D017396:Plasminogen Activator Inhibitor 2 / Q000097:blood*; D055728:Primary Myelofibrosis / Q000097:blood; D013920:Thrombocythemia, Essential / Q000097:blood; D010959:Tissue Plasminogen Activator / Q000097:blood*; D014568:Urokinase-Type Plasminogen Activator / Q000097:blood*
D017395:Plasminogen Activator Inhibitor 1; D017396:Plasminogen Activator Inhibitor 2; D010959:Tissue Plasminogen Activator; D014568:Urokinase-Type Plasminogen Activator