Disease Modifying Therapies – Risk Management Poster Presentation

P0413 - Tumefactive demyelinating lesions under fingolimod. A Tunisian case report (ID 579)

Speakers
  • C. Mhiri
Authors
  • A. Ghariani
  • S. Sakka
  • K. Moalla
  • N. Farhat
  • M. Damak
  • C. Mhiri
Presentation Number
P0413
Presentation Topic
Disease Modifying Therapies – Risk Management

Abstract

Background

Fingolimod (FTY) is a second-line treatment which changed the course of remittent recurrent multiple sclerosis (RRMS) in the real world by ensuring an increase in the proportion of NEDA 3 (No Evidence of Disease Activity 3). However, some studies have suggested a worsening MS under FTY with tumefactive demyelinating lesions (TDLs).

Objectives

ours objectives are to show TDLs under FTY and the different possibility of treatments that can be used to avoid the morbidity / mortality then to show long term clinical and radiological evolution of the patient after management of TDLs

Methods

Our patient was admitted at Habib Bourguiba hospital, Sfax, Tunisia. The diagnosis of MS was defined according to McDonald 2017 crietria. The patient was treated initially by interferonB and then by FTY. The TDLs was appeared under FTY with clinically worsening and radiological extensive pseudotumoral lesions in cerebral MRI

Results

Our patient is a 47-year-old who in 2016 had symptomatology evoking a Lhermite syndrome. Neurological examination was normal. Cervical MRI revealed C3/C4 spinal cord hyperintensity without contrast enhancement (CE). A complement by brain MRI showed three white matter hyperintensities (WMH) lesions on T2/FLAIR without CE. Analysis of the cerebrospinal fluid (CSF) shows the presence of oligoclonal bands (OCBs). The diagnosis of RRMS was made. The patient was then put on Interferon Béta-1a. Brain and spinal MRI were done every 6 months for 3 years which was all stable. In 03/2019, he developed a dizziness and left hemiplegia with decrease in bilateral visual acuity. A cerebral and medullary MRI were made objectifying the appearance of active lesions in the brain and brainstem (BS). In front of aggravation under interferon, the the patient was put under FTY in 05/2019 (natalizumab was contraindicated in the face of a high index JCV. Two months later, his wife noticed the appearance of sudden confusion with visual hallucinations, right hemiplegia, language disorder and vigilance disorders. A brain MRI showed multiple WMH with CE. Some of these lesions are confluent, others appear to be infiltrating with a large swelling of the BS. A progressive multifocal leukoencephalopathy under FTY was evoked and the patient was transferred to intensive care. A CSF JCV serology was negative. Infectious serology in the blood and CSF were negative (HIV, HSV, CMV, EBV, VZV). The diagnosis of TDLs under FTY was made. The patient was treated with 4 sessions of plasmapheresis with clinical and radiological improvement. Then, he was treated with mitoxantrone with spectacular clinical and radiological improvement.

Conclusions

The occurrence of TDLs with FTY in our patient was an evolutionary turning point of poor prognosis with a significant risk of neurological sequelae. Its put on mitoxantrone allowed a clinical and radiological recovery suggesting the immunological mechanism of the TDLs. The etiopathogenic association between FTY and TDLs is not clear.

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