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2017
DOI: 10.1007/s13691-017-0306-x
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Axitinib-induced reversible posterior leukoencephalopathy syndrome in a patient with metastatic renal cell carcinoma

Abstract: A 61-year-old woman with metastatic renal carcinoma was treated with axitinib as a second-line tyrosine kinase inhibitor. Thirteen days after the treatment, the patient developed reversible posterior leukoencephalopathy syndrome (RPLS). Her symptoms and imaging findings resolved after withdrawal of axitinib, blood pressure control, and administration of glycerin and levetiracetam. RPLS should be kept in mind as a possible rare adverse event after axitinib administration.

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Cited by 6 publications
(2 citation statements)
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“…This syndrome has been described related to different clinical circumstances, such as uncontrolled hypertension, eclampsia, collagen vascular disorders and Guillan-Barré syndrome, and drugs, especially immunosuppressive agents and cytotoxic drugs such as cyclosporine, tacrolimus, cisplatin, cytarabine, antiangiogenic agents, and tyrosine kinase inhibitors [15,18]. In the literature, several case reports are reported on the onset of PRES in RCC patients treated with anti-VEGFR drugs sorafenib, sunitinib, pazopanib, and axitinib [13,15,16,19,20].…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…This syndrome has been described related to different clinical circumstances, such as uncontrolled hypertension, eclampsia, collagen vascular disorders and Guillan-Barré syndrome, and drugs, especially immunosuppressive agents and cytotoxic drugs such as cyclosporine, tacrolimus, cisplatin, cytarabine, antiangiogenic agents, and tyrosine kinase inhibitors [15,18]. In the literature, several case reports are reported on the onset of PRES in RCC patients treated with anti-VEGFR drugs sorafenib, sunitinib, pazopanib, and axitinib [13,15,16,19,20].…”
Section: Discussionmentioning
confidence: 99%
“…Nevertheless, the exact pathogenesis of PRES remains unclear but it is most likely due to the development of hypertension and endothelial dysfunction, which are the direct effect of anti-VEGFR agents, with subsequent damage of the blood-brain barrier, impaired cerebrovascular autoregulation, hyperperfusion, and vasogenic edema [14,17,[19][20][21][22].…”
Section: Discussionmentioning
confidence: 99%