Nitric oxide in immune thrombocytopenic purpura.

Nitric oxide (NO), initially described as the endothelial derived relaxation factor, is an important messenger molecule involved in many physiological and pathological processes. Endothelium-derived NO causes vasorelaxation and also inhibits platelet adhesion and aggregation, thus maintaining blood fluidity and preventing thrombosis. As such, this molecule has been extensively studied in cardiology for its role in atherosclerosis and ischemic heart disease. An important alternate function of NO is in the modulation of platelet production from the megakaryocytes. Immune thrombocytopenic purpura (ITP) can be associated with a decrease in NO bioavailability which contributes to the thrombocytopenia and other clinical characteristics associated with this condition. At the same time, some of the treatment modalities for ITP may be exerting their beneficial effects by increasing the levels of NO and thus improving platelet production.