Elevation of serum lactate dehydrogenase at posterior reversible encephalopathy syndrome onset in chemotherapy-treated cancer patients |
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| Affiliation: | 1. Department of Neurological Surgery, University of California at San Francisco, 505 Parnassus Avenue, San Francisco, CA 94143-0112, USA;2. Department of Pathology, University of California at San Francisco, San Francisco, CA, USA;3. Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA;1. NEUROFARBA Department, Neuroscience Section, University of Florence, Italy;2. Interventional Neuroradiology Unit, Azienda Ospedaliero Universitaria Careggi, Florence, Italy;3. Stroke Unit and Neurology, Azienda Ospedaliero Universitara Careggi, Largo Brambilla 3, 50134 Firenze, Italy;1. Department of Neurosurgery, Stephen E. and Catherine Pappas Center for Neuro-Oncology, Massachusetts General Hospital, 55 Fruit Street, Yawkey 9E-9026, Boston, MA 02114, USA;2. Department of Neurosurgery, University of California, San Francisco, San Francisco, CA, USA;3. Biostatistics Center, Massachusetts General Hospital, Boston, MA, USA;4. Department of Radiation Oncology, Massachusetts General Hospital, Boston, MA, USA;1. Department of Neurosurgery, University of California San Francisco, 505 Parnassus Avenue, M 779, San Francisco, CA 94143-0112, USA;2. Department of Radiation Oncology, University of California San Francisco, CA, USA;1. Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China;2. Clinical Medical Examination, The Sixth People Hospital of Jinan, Shandong, China;3. School of Public Health and Family Medicine, Capital Medical University, Beijing, China;4. Beijing Neurosurgical Institute, Capital Medical University, No. 6 Tiantan Xili, Dongcheng District, Beijing 100050, China |
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| Abstract: | The pathophysiology of posterior reversible encephalopathy syndrome (PRES) is incompletely understood; however, an underlying state of immune dysregulation and endothelial dysfunction has been proposed. We examined alterations of serum lactate dehydrogenase (LDH), a marker of endothelial dysfunction, relative to the development of PRES in patients receiving chemotherapy. A retrospective Institutional Review Board approved database of 88 PRES patients was examined. PRES diagnosis was confirmed by congruent clinical diagnosis and MRI. Clinical features at presentation were recorded. Serum LDH values were collected at three time points: prior to, at the time of, and following PRES diagnosis. Student’s t-test was employed. LDH values were available during the course of treatment in 12 patients (nine women; mean age 57.8 years [range 33–75 years]). Chemotherapy-associated PRES patients were more likely to be normotensive (25%) versus the non-chemotherapy group (9%). LDH levels at the time of PRES diagnosis were higher than those before and after (p = 0.0263), with a mean difference of 114.8 international units/L. Mean time intervals between LDH measurement prior to and following PRES diagnosis were 44.8 days and 51.4 days, respectively. Mean elapsed time between last chemotherapy administration and PRES onset was 11.1 days. In conclusion, serum LDH, a marker of endothelial dysfunction, shows statistically significant elevation at the onset of PRES toxicity in cancer patients receiving chemotherapy. Our findings support a systemic process characterized by endothelial injury/dysfunction as a factor, if not the prime event, in the pathophysiology of PRES. |
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| Keywords: | Chemotherapy Hypertensive encephalopathy LDH Posterior reversible encephalopathy syndrome PRES |
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