Thrombotic complications constitute an important risk in myeloproliferative disorders. The aim of this work was to investigate the PAI-1 behavior in 29 patients affected with primary thrombocythosis (PT) as compared with 9 patients with secondary thrombocytosis (TS) and 30 normal controls. On each subject, the following tests were carried out: platelet count and serotonin, plasma and intreplatelet levels of PAI-l, both antigen and activity, and plasma t-PA antigen and activity. t-PA values were similar in patients and in controls. On the contrary, plasma levels of PAI-1 activity and antigen were significantly higher in both PT and ST patients than in normals. In the two pathological groups intreplatelet PAI-1 levels were significantly lower than in normal controls. No difference in fibrinolytic tests was seen between patients with primary and secondary thrombocytosis. In patients with PT, a significant inverse correlation was found between platelet count and intreplatelet PAI-1 antigen; moreover, PAI-1 concentration in platelets was not correlated with mean platelet volume. In conclusion, in PT and ST patients the reduction of intraplatelet content of PAI-1 and the parallel increase of plasma PAI-1 values suggest a contribution of platelets to PAI-1 concentration in plasma. Subclinical platelet activation with consequent release of PAI-1 from α-granules could be assumed as the underlying pathogenetic mechanism. Hypofibrinolysis due to increased PAI-1 plasma levels can be considered a new factor which may explain the thrombotic tendency in myeloproliferative disorders.

Contribution of platelets to PAI-1 concentration in plasma of patients with primary and secondary thrombocytosis

RANDI, MARIA LUIGIA;GIROLAMI, ANTONIO
1997

Abstract

Thrombotic complications constitute an important risk in myeloproliferative disorders. The aim of this work was to investigate the PAI-1 behavior in 29 patients affected with primary thrombocythosis (PT) as compared with 9 patients with secondary thrombocytosis (TS) and 30 normal controls. On each subject, the following tests were carried out: platelet count and serotonin, plasma and intreplatelet levels of PAI-l, both antigen and activity, and plasma t-PA antigen and activity. t-PA values were similar in patients and in controls. On the contrary, plasma levels of PAI-1 activity and antigen were significantly higher in both PT and ST patients than in normals. In the two pathological groups intreplatelet PAI-1 levels were significantly lower than in normal controls. No difference in fibrinolytic tests was seen between patients with primary and secondary thrombocytosis. In patients with PT, a significant inverse correlation was found between platelet count and intreplatelet PAI-1 antigen; moreover, PAI-1 concentration in platelets was not correlated with mean platelet volume. In conclusion, in PT and ST patients the reduction of intraplatelet content of PAI-1 and the parallel increase of plasma PAI-1 values suggest a contribution of platelets to PAI-1 concentration in plasma. Subclinical platelet activation with consequent release of PAI-1 from α-granules could be assumed as the underlying pathogenetic mechanism. Hypofibrinolysis due to increased PAI-1 plasma levels can be considered a new factor which may explain the thrombotic tendency in myeloproliferative disorders.
1997
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11577/2503807
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