Rebound of disease activity after fingolimod withdrawal: Immunological and gene expression profiling

Mult Scler Relat Disord. 2020 May:40:101927. doi: 10.1016/j.msard.2020.101927. Epub 2020 Jan 3.

Abstract

Discontinuation of disease-modifying therapy with fingolimod can lead to severe Multiple Sclerosis (MS) rebound activity; however, this phenomenon remains mechanistically incompletely understood, and the short-term impact of a therapy switch on inflammatory gene expression in T lymphocytes is unknown. We present the clinico-radiological and immunological description of a case of rebound activity after fingolimod discontinuation and switching to rituximab treatment in a relapsing-remitting MS patient. After severe rebound, a reduction in the expression of inflammatory cytokines and transcription factors was rapidly observed after administration of methylprednisolone and rituximab. Rituximab led to an effective suppression of inflammatory activity, and at least in this specific case it represented a valid switching approach after fingolimod discontinuation.

Keywords: Cytokines gene expression; Fingolimod; Multiple sclerosis; Rituximab; T lymphocytes.

Publication types

  • Case Reports

MeSH terms

  • Adult
  • Female
  • Fingolimod Hydrochloride / administration & dosage*
  • Humans
  • Immunosuppressive Agents / administration & dosage*
  • Inflammation / drug therapy*
  • Inflammation / immunology
  • Magnetic Resonance Imaging
  • Multiple Sclerosis, Relapsing-Remitting / diagnostic imaging
  • Multiple Sclerosis, Relapsing-Remitting / drug therapy*
  • Multiple Sclerosis, Relapsing-Remitting / immunology
  • Recurrence
  • Rituximab / administration & dosage*
  • T-Lymphocytes*
  • Transcriptome*

Substances

  • Immunosuppressive Agents
  • Rituximab
  • Fingolimod Hydrochloride