Fulminant MS Reactivation Following Combined Fingolimod Cessation and Yellow Fever Vaccination.
Leoni RolfesMarc PawlitzkiSteffen PfeufferChristian ThomasJonas Schmidt-ChanasitCatharina C GrossAndreas Schulte-MecklenbeckHeinz WiendlSven G MeuthOliver M GrauerTobias RuckPublished in: International journal of molecular sciences (2019)
A major concern caused by the discontinuation of disease modifying treatment for multiple sclerosis (MS) is a rebound of disease activity. Hypotheses about the underlying mechanism of fingolimod (FTY) induced exaggerated inflammatory responses are diverse. So far, vaccinations as a trigger for rebound activity following FTY suspension have not been described. However, several reports have highlighted the occurrence of neurological and autoimmune side effects after single or combined multi-vaccination procedures. Here, we describe the case of a highly active female MS patient demonstrating recurrent, severe MS relapses accompanied by extensive MRI activity, subsequent to yellow fever vaccination two months following FTY withdrawal. Blood and cerebrospinal fluid immunophenotyping indicated a B cell/plasma cell autoreactivity. Following a therapy with natalizumab the clinical, laboratory, MRI, and disease course improved significantly. This case hints towards a combined immunological mechanism characterized by molecular mimicry, bystander activation, and lymphocyte re-egress, resulting in extensive neurological impairment and shows that natalizumab represents a therapeutic option to counteract B cell mediated autoreactivity. Especially, the diagnostic and therapeutic management of this complex scenario might be instructive for clinical practice.
Keyphrases
- multiple sclerosis
- disease activity
- white matter
- rheumatoid arthritis
- systemic lupus erythematosus
- magnetic resonance imaging
- clinical practice
- contrast enhanced
- rheumatoid arthritis patients
- ankylosing spondylitis
- risk assessment
- emergency department
- juvenile idiopathic arthritis
- cell therapy
- ms ms
- stem cells
- early onset
- high glucose
- mesenchymal stem cells
- endothelial cells
- subarachnoid hemorrhage
- blood brain barrier
- smoking cessation
- hepatitis b virus
- adverse drug
- oxidative stress
- single molecule
- stress induced