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Case Reports
. 2022 Dec 23;13(1):33.
doi: 10.3390/brainsci13010033.

Posterior Reversible Encephalopathy Syndrome after Lenvatinib Therapy in a Patient with Olfactory Neuroblastoma

Yu-Ju Tseng  1 , Chun-Nan Chen  2 , Ruey-Long Hong  3 , Woon-Man Kung  4   5 , Abel Po-Hao Huang  6
Affiliations
Case Reports

Posterior Reversible Encephalopathy Syndrome after Lenvatinib Therapy in a Patient with Olfactory Neuroblastoma

Yu-Ju Tseng et al. Brain Sci. .

Abstract

Posterior reversible encephalopathy syndrome (PRES) is a rare but severe neurological syndrome that may stem from the use of some medications. Although its mechanism is not well-known, hypertension and endothelial dysfunction have been mentioned in previous literature as being related. Lenvatinib serves as a neoplastic agent that inhibits the tyrosine kinase of vascular endothelial growth factor receptors (VEGFR). VEGFR inhibitors result in endothelial dysfunction and consequent hypertension by nitric oxide pathway suppression and endothelin (ET)-1 stimulation. We hypothesized that VEGFR inhibitors would cause PRES. Herein, we report the case of a 40-year-old man with olfactory neuroblastoma who developed PRES while undergoing treatment with lenvatinib, 7 months after initiation. The symptoms included loss of consciousness and seizures. Fortunately, the symptoms and presence of PRES in imaging resolved, 7 days and 1 month, respectively, after cessation of lenvatinib.

Keywords: lenvatinib; olfactory neuroblastoma; posterior reversible encephalopathy syndrome.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Timeline of the lenvatininb and anti-hypertensive agents use.
Figure 2
Figure 2
MRI was conducted on 5 March 2021. The yellow arrow indicates a bilateral occipital cortico-subcortical lesion with low T1-weighted SI, high T2-weighted SI, and faint scattered foci of enhancement.
Figure 3
Figure 3
MRI was conducted on 10 April 2021. Subcortical lesions were resolved at bilateral occipital lobes.
Figure 4
Figure 4
The hypothesis of anti-VEGF signaling induces PRES. Anti-VEGF signaling causes increasing peripheral resistance and, consequently, leads to hypertension. In addition, the anti-VEGF pathway results in endothelial dysfunction. Both hypertension and endothelial dysfunction damage the blood–brain barrier and increase vasogenic edema, and further cause cytotoxic edema by hypoxia. Endothelial cell damage itself contributes to cytotoxic edema. The sum of vasogenic edema and cytotoxic edema leads to PRES. VEGF = vascular endothelial growth factors; PRES = posterior reversible encephalopathy syndrome.
See this image and copyright information in PMC

References

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