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We evaluated the efficacy of HU for prevention of cerebrovascular complications in Italians with HbS-�� thalassemia and found a high incidence of cerebrovascular events in our treated patients. Overt stroke occurred in 6.7% and new silent cerebral infarction was found in 30%, rates similar to those reported in untreated patients. Most patients (75%, 24/32) already had silent cerebral infarction on MRI performed before beginning treatment and during follow-up had progression of their MRI lesions. Stroke and silent cerebral infarction were unrelated to the clinical, hematologic, and HbF response to HU. In HU treated patients followed for 17.5 years, the incidence of stroke did not decrease [3, 25, 26]. HU did not prevent secondary stroke in children with SCD when transfusions therapy was http://www.selleck.cn/products/gsk126.html switched to HU. A prospective multicentre [27] suggested that new silent cerebral infarction can develop in transfused children with a history of overt stroke. This high incidence of silent cerebral infarction in transfused patients was similar to our observations in HbS-? thalassemia. Neurocognitive function was impaired in our patients. Other studies reported poorer global intellectual function that was below the average range for the general population, but better than that of children with overt strokes [23, 28, 29]. Children with SCI also had lower cognitive test scores compared with children with a normal MRI of the brain [28]. Vichinsky et al. [30] reported a http://www.selleckchem.com/products/Cyclopamine.html poorer cognitive performance in neurologically intact adults with SCD that was associated with anemia and age. High HbF does not appear to benefit equally all complications of SCD and among the disease complications least affected by HbF are those attributed to sickle vasculopathy, like http://www.selleckchem.com/products/BI-2536.html cerebrovascular disease. Sickle vasculopathy is strongly associated with intravascular hemolysis. Patients with high LDH, one estimate of intravascular hemolysis, have a greater risk of cerebrovascular disease [31]. Hemolysis reduces bioavailable nitric oxide and is associated with chronic inflammation and endothelial damage [31]. Intimal proliferation was considered the likely primary event causing thrombosis [32]. Hemolysis [33] and reduced nitric oxide bioavailability are strongly associated with the clinical complications of pulmonary hypertension [34], priapism, leg ulcers, stroke, and mortality [35]. Probably as a result of its very early development, the management of sickle cerebrovascular disease has been an extremely difficult clinical problem. It follows that although HU is safe and can increase HbF levels with a marked decrease in common but serious adverse events, especially pain and ACS, it might not be effective in preventing cerebrovascular complications when vasculopathy is already present.