Ticlopidine Lowers Plasma Fibrinogen in Patients with Polycythaemia Rubra Vera and Additional Thrombotic Risk Factors

Abstract

Thirty-seven patients affected by polycythaemia rubra vera (PRV) and with at least one additional thrombotic risk factor (overt vascular disease, diabetes mellitus, treated hypertension, smoking habit, plasma hyperviscosity, hyperfibrinogenemia) were enrolled in a double-blind randomized placebo-controlled study, and 18 were given ticlopidine 250 mg, b.i.d., for 60 days. All the patients had previously been submitted to cytoreduction, and PRV was under control in all cases at the start of the study. During the study, the haematological parameters were controlled every 15 days, and venesection was performed if haematocrit was > 46%. Whole blood viscosity, at low and high shear rates, plasma viscosity, and fibrinogen were measured on days 0 and 60. In the ticlopidine group, we recorded a significant 13.14% reduction of the mean fibrinogen level after treatment (390 ± 63 vs. 449 ± 97 mg/dl, p < 0.01). All the other haemorheological parameters were not significantly modified by ticlopidine treatment, nor were there significant modifications recorded in the placebo group. Our study shows that ticlopidine may reduce a probable thrombotic risk factor (hyperfibrinogenemia) in PRV patients.

Antithrombotic therapy in hypertension: a Cochrane Systematic review

“…24 Five studies investigating ticlopidine and glycoprotein IIb/IIIa inhibitors and their impact on cardiovascular and haemorrhagic events lacked sufficient follow-up data. [25][26][27][28][29] A further publication was excluded due to the inability to acquire the relevant data. 30 Most of the excluded trials were less than 1-month duration; in particular, the five GPIIb/IIIa inhibitor trials were only observing the effects over a few days.…”

Polycythemia Vera: Perspectives for Future Clinical Trials

“…Inefficacy but not increased risk of bleeding was confirmed in another study [11]. However, many clinicians claim to have had better experi ences and trials with much smaller doses of ASA or newer anti-aggregating or platelet-lowering agents [46,47] may be justified.…”

Enhanced generation of monocyte tissue factor and increased plasma prothrombin fragment1+2 levels in patients with polycythemia vera: Mechanism of activation of blood coagulation

“…Therefore, we have to assume that the activation of the coagulation system is more complex and involves other mechanisms that act synergistically with the monocyte TF. Other mechanisms that have been described include thrombocytosis [3], activated platelets [8], decreased tissue plasminagen activator [33], increased fibrinogen level [34], activated protein C resistance and reduced levels of protein C, protein S, and antithrombin III [21].…”