RESUMO
To assess retrospectively three antithrombotic treatments in the secondary prevention of thrombosis in the antiphospholipid syndrome (APS), 23 patients (six systemic lupus erythematosus, seven lupus-like disease and 10 primary antiphospholipid syndrome) were included in this study. Treatments assessed were: (1) aspirin 75 mg daily, (2) warfarin (international normalised ratios (INRs) 2.0-2.9) +/- aspirin 75 mg daily, and (3) warfarin (INRs > 2.9) +/- aspirin 75 mg daily. Where patients had received two or three of these treatments successively, the periods of time on each treatment were added and the number of patients with recurrence(s) on each treatment were compared by Fisher's exact probability test. 'High' anticoagulation (INRs > 2.9) +/- aspirin 75 mg daily was more effective than aspirin 75 mg daily, there was a trend in favour of 'high' anticoagulation (P = 0.066). No statistically significant difference could be demonstrated when comparing 'low' anticoagulation +/- aspirin 75 mg daily with aspirin 75 mg daily (P = 0.092). These results suggest that aggressive anticoagulation with or without low-dose aspirin is effective in preventing further thromboembolic events in APS.
Assuntos
Síndrome Antifosfolipídica/complicações , Fibrinolíticos/uso terapêutico , Trombose/tratamento farmacológico , Trombose/etiologia , Adolescente , Adulto , Anticorpos Anticardiolipina/uso terapêutico , Anticoagulantes/uso terapêutico , Síndrome Antifosfolipídica/epidemiologia , Aspirina/uso terapêutico , Relação Dose-Resposta a Droga , Quimioterapia Combinada , Feminino , Humanos , Lúpus Eritematoso Sistêmico/imunologia , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Trombose/prevenção & controle , Varfarina/uso terapêuticoRESUMO
Platelet function was studied in 11 patients with Raynaud's syndrome and 11 healthy controls. Platelets obtained from patients with Raynaud's syndrome were significantly more responsive to adrenaline, produced more thromboxane A2, and were resistant to prostaglandin inhibitors (prostacyclin and prostaglandin E1) of platelet aggregation. Platelets from control subjects and patients with Raynaud's syndrome were more resistant to prostaglandin inhibitors when reactions were carried out at 27 degrees C rather than at 37 degrees C. Patients with Raynaud's syndrome also had significantly increased plasma concentrations of beta-thromboglobulin, fibrinogen, and circulating platelet aggregates. In an attempt to elicit local platelet responses, the forearms of control subjects and patients with Raynaud's syndrome were cooled in water tanks and platelet function tests performed before and after cooling. No significant difference in the results was observed. The potential role of platelets in the pathogenesis of Raynaud's syndrome is discussed.