2016
DOI: 10.1155/2016/6852951
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Reversible Posterior Leukoencephalopathy Syndrome Developing After Restart of Sunitinib Therapy for Metastatic Renal Cell Carcinoma

Abstract: A 64-year-old Japanese man had started molecular-targeted therapy with sunitinib for lymph node metastasis 5 years after nephrectomy for left renal cell carcinoma (clear cell carcinoma, G2, pT2N0M0). He was transported to our emergency department because of generalized tonic-clonic seizure, vision loss, and impaired consciousness with acute hypertension after 8 cycles of treatment (2 years after the initiation of sunitinib therapy, including a drug withdrawal period for one year). MRI of the brain (FLAIR image… Show more

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Cited by 9 publications
(6 citation statements)
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“…All of these VEGF receptor antagonists can potentially cause RPLS. While cases of RPLS due to renal carcinoma targeted therapies are rare, reports involving sunitinib have been most frequent [5][6][7][8][9][10][11][12][13]. We report herein the second case, to our knowledge with RPLS induced by axitinib [13].…”
Section: Discussionmentioning
confidence: 80%
“…All of these VEGF receptor antagonists can potentially cause RPLS. While cases of RPLS due to renal carcinoma targeted therapies are rare, reports involving sunitinib have been most frequent [5][6][7][8][9][10][11][12][13]. We report herein the second case, to our knowledge with RPLS induced by axitinib [13].…”
Section: Discussionmentioning
confidence: 80%
“…parieto-occipital and cerebellar lobes, dorsal brain stem, and left thalamus) [16,17]. The diffusion-weighted imaging on MRI shows also the elevation of apparent diffusion coefficient mapping [14]. 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].…”
Section: Discussionmentioning
confidence: 96%
“…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%
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