DENGUE FEVER ACTIVATES THE l-ARGININE–NITRIC OXIDE PATHWAY: AN EXPLANATION FOR REDUCED AGGREGATION OF HUMAN PLATELETS

SUMMARY 1 In patients with Dengue fever, a viral inflammatory syndrome, haemorrhage is a significant pathological feature, yet the underlying mechanisms remain unclear. Nitric oxide (NO) is an important regulator of platelet function, inhibiting aggregation, recruitment and adhesion to the vascular endothelium. 2 We have investigated whether changes in the activity of the l-arginine–NO pathway in human platelets may account for increased bleeding in patients with Dengue fever. A total of 16 patients with Dengue fever and 18 age-matched healthy volunteers participated in the study. 3 Collagen induced platelet aggregation in a dose-dependent manner in both Dengue patients and controls, but the degree of platelet aggregation was significantly reduced in the patient group. Elevated rates of l-arginine transport in Dengue fever patients were associated with enhanced NO synthase activity and elevated plasma fibrinogen levels. 4 The present study provides the first evidence that Dengue fever is associated with increased l-arginine transport and NO generation and reduced platelet aggregation.