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Correspondence |

A Clue to the Pathophysiology of Posterior Reversible Encephalopathy Syndrome

Jecko Thachil, MRCP, FRCPath
Arch Neurol. 2010;67(12):1536-1537. doi:10.1001/archneurol.2010.315.
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The interesting study by Burrus and colleagues1 explains the relationship between renal impairment and PRES in patients with TTP. The article provides an important clue to the common role of nitric oxide (NO) depletion in the pathogeneses of PRES and TTP, where it leads to uninhibited platelet aggregation and vasoconstriction.2 Current evidence suggests that acute severe hypertension exceeds the limits of autoregulation, leading to breakthrough brain edema as the likely causative factor for PRES.3 Sudden NO depletion causes severe hypertension, being the endothelial derived relaxation factor, and can also lead to vasogenic edema. The latter can be explained by the role of NO produced by endothelial NO synthase in protecting the brain from ischemic injury by enhancing cerebral blood flow and inhibiting platelet and leukocyte adhesion.4 In TTP, the NO reduced state develops secondary to the acute severe hemolysis (when the free hemoglobin outside the red cell mops up the NO in the vasculature), which is characteristic of this condition.2 A common cause of PRES is preeclampsia in which, once again, NO plays an important pathophysiological role.5 The new antineoplastic agents, vascular endothelial growth factor inhibitors, also have been implicated in the development of PRES.5 The major adverse effects of these agents are hypertension, proteinuria, and renal TTP, which has been linked to NO depletion, particularly because the major downstream signal for vascular endothelial growth factor is NO.6

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