Contributions
Abstract: EP1723
Type: ePoster
Abstract Category: Therapy - disease modifying - 29 Risk management for disease modifying treatments
Awareness of Progressive multifocal leucoencephalopathy (PML) has increased in recent years, with the description of cases related to disease modifying therapy in multiple sclerosis (MS).
We present a case of PML affecting a patient with MS treated with fingolimod.
A 60 year-old female patient affected by MS since 1993, presented in June 2016 subacute onset of apraxia. She took fingolimod uneventfully since march 2012. She had previously received treatment with interferon Beta 1a for 3 years. Previous medical hystory was negative. Routine white blood cell count showed a lymphocytopenia with a variable value from to 700/mmc and 300/mmc.
In May 2016 pts presented a minimal worsening of paraparesis with more fatigue and slowness . We plan a strict clinical-radiological follow-up. One mounth later patient presented inability to control movement. Brain MRI revealed multifocal non enhancing white matter (WM) T2 hyperintensity, involves subcortical U-fibers in frontal and parieto-occipital areas. Cerebrospinal JCV viral load was 1000 copies/ml. White blood cell count showed a leucocytopenia (3600/mmc) and lymphocytopenia (400/mmc). Stratify JCV was positive (3,82). We immediatly stopped treatment; other immunocompromission causes were excluded. Neuropsycological tests revealed cognitive impairment focused on attentional systems and ideomotor/ideational apraxia. We planned monthly MRI in order to identify immune reconstitution inflammatory syndrome. Clinical progress was insidious and reached the nadir in september when patient presented constructional/spatial defects, dressing apraxia, dysgraphia, dyscalculia and worsening of motor weakness. Serial MRI showed progression of the patchy WM lesions without enhancement; increased signal intensity on T2-weighted and diffusion-weighted images suggested an active inflammatory process. We never prescribed steroids. Four month after drug discontinuation cerebrospinal JCV viral load was negative.
Since october 2016 clinical status slowly improved and MRI showed stabilized lesions. Patient underwent to rehabilitation: now she required unilateral assistance to walk and retains most self-care functions.
Actually 9 cases of PML are reported in MS patients on Fingolimod treatment; all patients are over 50 years old, suggesting immunosenescence as main promoting factor. No one has been fatal. MRI and neuropsycological assessment are precious tools to recognize PML in subclinical phase in order to optimize the management of disease.
Disclosure: Francesca Rossi: nothing to disclose
Abstract: EP1723
Type: ePoster
Abstract Category: Therapy - disease modifying - 29 Risk management for disease modifying treatments
Awareness of Progressive multifocal leucoencephalopathy (PML) has increased in recent years, with the description of cases related to disease modifying therapy in multiple sclerosis (MS).
We present a case of PML affecting a patient with MS treated with fingolimod.
A 60 year-old female patient affected by MS since 1993, presented in June 2016 subacute onset of apraxia. She took fingolimod uneventfully since march 2012. She had previously received treatment with interferon Beta 1a for 3 years. Previous medical hystory was negative. Routine white blood cell count showed a lymphocytopenia with a variable value from to 700/mmc and 300/mmc.
In May 2016 pts presented a minimal worsening of paraparesis with more fatigue and slowness . We plan a strict clinical-radiological follow-up. One mounth later patient presented inability to control movement. Brain MRI revealed multifocal non enhancing white matter (WM) T2 hyperintensity, involves subcortical U-fibers in frontal and parieto-occipital areas. Cerebrospinal JCV viral load was 1000 copies/ml. White blood cell count showed a leucocytopenia (3600/mmc) and lymphocytopenia (400/mmc). Stratify JCV was positive (3,82). We immediatly stopped treatment; other immunocompromission causes were excluded. Neuropsycological tests revealed cognitive impairment focused on attentional systems and ideomotor/ideational apraxia. We planned monthly MRI in order to identify immune reconstitution inflammatory syndrome. Clinical progress was insidious and reached the nadir in september when patient presented constructional/spatial defects, dressing apraxia, dysgraphia, dyscalculia and worsening of motor weakness. Serial MRI showed progression of the patchy WM lesions without enhancement; increased signal intensity on T2-weighted and diffusion-weighted images suggested an active inflammatory process. We never prescribed steroids. Four month after drug discontinuation cerebrospinal JCV viral load was negative.
Since october 2016 clinical status slowly improved and MRI showed stabilized lesions. Patient underwent to rehabilitation: now she required unilateral assistance to walk and retains most self-care functions.
Actually 9 cases of PML are reported in MS patients on Fingolimod treatment; all patients are over 50 years old, suggesting immunosenescence as main promoting factor. No one has been fatal. MRI and neuropsycological assessment are precious tools to recognize PML in subclinical phase in order to optimize the management of disease.
Disclosure: Francesca Rossi: nothing to disclose