Serum Lactate Dehydrogenase as a Predictor of Outcome in Posterior Reversible Encephalopathy Syndrome: Imperative to Unify

摘要

We read with great interest the study of Junewar et al1 in the September issue of the American Journal of Neuroradiology, which justified the statements that higher serum lactate dehydrogenase (LDH) levels were possible predictors of poor outcome (P = .009) but were not correlated with the severity of posterior reversible encephalopathy syndrome (PRES). Prior small series investigating the relationship between LDH and PRES have shown elevation of serum LDH at the time of symptom onset in patients with a variety of underlying conditions.2 Elevation of LDH levels has also been reported to precede the development of brain edema in pre-eclampsia/eclampsia by several days. Variable degrees of edema expression in PRES may be related to the variance of arterial anatomy, pre-existing disease processes, or an underlying clinical toxic condition. Hypoxia could induce tissue morphologic change and LDH increase, which is likely to result in microcirculation disturbance, followed by either enhanced vascular permeability, vasoconstriction with altered intrinsic vascular tone from platelet aggregation, or inflammatory cytokine expression. In fact, elevated serum LDH levels should also be regarded as an early biochemical marker of PRES, which has potential practical value in predicting the degree of brain edema in patients with eclampsia or cancer chemotherapy or in those receiving immunosuppression therapy in clinical practice.3