TO THE EDITOR:

Osteonecrosis is a frequent complication of therapy in patients with acute lymphoblastic leukemia (ALL), particularly children aged 10 years and older at diagnosis and young adults.1,2,3,4,5,6-7  Prior clinical and nonclinical data have demonstrated that arteriopathy in arterioles supplying the bone and marrow, characterized by vascular smooth muscle and endothelial cell injury, is the initiating lesion in the development of glucocorticoid-induced osteonecrosis. In patients with ALL, osteonecrosis has been linked to receptors for the vascular toxin glutamate. We therefore hypothesized that patients may exhibit other evidence of endothelial dysfunction and vascular toxicity before the onset of osteonecrosis. Because hypertension is a known adverse effect of glucocorticoid therapy10,11  and has been linked to adverse vascular remodeling,12,13  we hypothesized...

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