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Journal of Clinical Oncology, Vol 25, No 33 (November 20), 2007: pp. 5320-5321 © 2007 American Society of Clinical Oncology. DOI: 10.1200/JCO.2007.13.5954
Reversible Posterior Leukoencephalopathy Syndrome Associated With OxaliplatinSouthern Illinois University School of Medicine, Department of Internal Medicine, Springfield, IL A 62-year-old woman started having seizures while she was having dinner and was brought to the emergency room. Eight days prior, she had received chemotherapy for a nonresectable metastatic adenocarcinoma of the rectum. She received antineoplastic chemotherapy consisting of oxaliplatin 130 mg intravenously, bevacizumab 5 mg/kg subcutaneously, and capecitabine 1,000 mg/m2 orally for 8 days. She had a history of essential hypertension, which was well controlled with oral hydrochlorothiazide 25 mg daily. On arrival at the emergency room, her vital signs were: temperature 36.8° Celsius, blood pressure of 190/88 mmHg, pulse rate 112 beats per minute, and respiratory rate of 16 breaths per minute. Seizures were controlled after administration of diazepam and fosphenytoin. Neurological exam showed altered mental status, cranial nerves II-XII were intact, bilateral lower extremity weakness (right side 0/5, left side 3/5) with right side hyperreflexia and positive Babinski's sign was noted. Rest of the physical examination was unremarkable. Computed tomography (CT) scan of her head was unremarkable. Lumbar puncture showed WBC 1/mm3 (normal, 0 to 5), RBC 7/mm3 (normal, 0), protein 38 mg/dL (normal, 15 to 45), albumin 17.2 mg/dL (normal, 10 to 30), and glucose 72 mg/dL (normal, 45 to 75). Cultures did not reveal an infectious etiology. A subsequent magnetic resonance imaging (MRI) scan with gadolinium done a day after admission showed areas of subcortical white matter edema (Fig 1; white arrow) seen as hyperintense signals predominantly in the posterior hemispheres on T2-weighted images, best seen on fluid attenuated inverse recovery sequences. These radiographic and clinical findings were consistent with reversible posterior leukoencephalopathy (RPLS). After 48 hours, she was alert and following commands. Her motor strength now was 3/5 in the right lower extremity and 5/5 in the left lower extremity. Follow-up MRI done 10 days later showed complete resolution from the previously described changes. The antineoplastic therapy was switched to bevacizumab and irinotecan. She tolerated this combination without any complications. On repeat exposure to bevacizumab there was no recurrence of RPLS.
RPLS was first described in 19961 as a clinicoradiological entity characterized by neurological disturbances associated with predominant posterior cerebral circulation involvement. We report a unique case of a patient with classic clinical and radiological findings of RPLS after receiving a dose of antineoplastic agent oxaliplatin. Hypertension is the most common feature described with RPLS.1 A wide spectrum of inflammatory disorders and medications, such as immunosuppressive and chemotherapeutic agents, has been linked to RPLS in the medical literature.1,2 RPLS is thought to be secondary to breakdown of the blood-brain barrier with transudation of fluid and protein in the extra vascular space, resulting in cerebral edema.3 Cerebrovascular spasm with resulting ischemia within the involved territories followed by edema is another postulated mechanism.4 In our case, RPLS was attributed to oxaliplatin despite the use of multiple antineoplastic agents including, bevacizumab and capecitabine, a fluorouracil prodrug. As further continuation of therapy with bevacizumab was tolerated uneventfully we did not attribute this RPLS to bevacizumab. Capecitabine was also part of our patient's antineoplastic therapy though no association between capecitabine and RPLS is found in the medical literature. Platinum compounds especially cisplatin and oxaliplatin are described with various neurotoxicities and therefore we attributed this development of RPLS to oxaliplatin in our case. Two other cases with multiple chemotherapeutic agent regimens including oxaliplatin have been reported to be associated with RPLS.5,6 Similarly in the most recent case the patient received fluorouracil and oxaliplatin before becoming symptomatic, raising the question of whether this two-drug association may also predispose patients to a higher risk of developing CNS adverse events including RPLS. The etiology of RPLS can be multifactorial. High clinical suspicion is required in patients receiving antineoplastic therapies presenting with signs and symptoms of RPLS, as quick recognition will allow immediate alteration in chemotherapy and supportive measures to reverse this condition, as seen in our patient. AUTHORS' DISCLOSURES OF POTENTIAL CONFLICTS OF INTEREST The author(s) indicated no potential conflicts of interest.
REFERENCES
1. Hinchey J, Chaves C, Appignani B, et al: A reversible posterior leukoencephalopathy syndrome. N Engl J Med 334:494-500, 1996 2. Cooney MJ, Bradley WG, Symko SC, et al: Hypertensive encephalopathy: Complication in children treated for myeloproliferative disorders–report of three cases. Radiology 214:711-716, 2000 3. Robertson DM, Dinsdale HB, Ayashi T, et al: Cerebral lesions in adrenal regeneration hypertension. Am J Pathol 59:115-132,1970[Medline] 4. Dinsdale HB, Robertson DM, Chiang TY, et al: Hypertensive cerebral microinfarction and cerebrovascular reactivity. Eur Neurol 6:29-33, 1971-72[CrossRef][Medline] 5. Moris G, Ribacoba R, Gonzalez C: Delayed posterior encephalopathy syndrome following chemotherapy with oxaliplatin and gemcitabine. J Neurol 254:534-535, 2007[CrossRef][Medline] 6. Skelton MR, Goldberg RM, O'Neil BH: A case of oxaliplatin-related posterior reversible encephalopathy syndrome. Clin Colorectal Cancer 6:386-388, 2007[Medline]
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Copyright © 2007 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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