RESUMO
48 subjects were included in this study. They are classified into 3 groups: group 1-16 patients with venous stasis ulceration [VSU] of the leg due to chronic venous insufficiency [CVI] group II-16 patients with varicose veins of the leg without VSU and group III-16 normal healthy controls without evidence of venous diseases. Full detailed history and physical examination for all was done. The venous status for all patients was documented by means of duplex ultra-sonography and descending venography. Blood samples were drawn from the superficial veins of the leg just proximal to the ulcer from the patients with VSU, and from the superficial veins of the lower part of the leg from patients with V.V. without VSU [Local blood Samples]. Blood was also drawn from the antecubital vein from all [48] subjects [systemic blood Samples]. Whole-blood flowcytometry was used to analyse the samples before and after activation with a panel of agonists for evidence of platelet activation and the formation of leucocyte - platelet aggregation either monocyte - platelet aggregates or neutrophil - platelet aggregates patients with venous stasis ulceration [VSU] had a greater number of monocyte platelet aggregates in both the arm and leg samples than did the patients with V.V. without ulceration and than did the control subjects [P<0.01]. Furthermore, systemic blood samples from patients with venous stasis ulceration stimulated with either thrombin-receptor agonist peptide [TRAP], Adinosine diphosphate [ADP], or phorbol myristate acetate [PMA] formed more monocyte - platelet aggregates than did patients with varicose veins without ulceration and than did control sujbects samples [P<0.05]. No significant differences were found between the patients with V.V. without ulceration and control sujbects in platelet activation and leucocyte - platelet aggregation either before or after agonist stimulation. Also, there are no differences in platelet activation or neutrophil-platelet aggregate formation were noted among the three groups. Patients with VSU have an increase in the number of monocyte - platelet aggregates in systemic venous blood as well as in local venous blood [adjacent to venous stasis ulcer], implicating the monocyte as the leucocyte involved in the pathogenesis of VSU. No association was identified between the presence of a venous stasis ulcer and either neutrophil-platelet aggregation or the activation of individual platelets. Because platelet activation is necessary for the formation of monocyte-platelet aggregates, these data also suggest that monocyte-platelet aggregation is a more sensitive marker for in-vivo platelet activation than is the identification of individual activated platelets