
Contributions
Abstract: EP1533
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - 21 Imaging
Purpose: Progressive multifocal leucoencephalopathy (PML) is a demyelinating disease of the central nervous system caused by reactivation of the JC polyomavirus. PML is most frequently associated with AIDS and emerges as a complication of Natalizumab (NAT) treatment of multiple sclerosis (MS). MRI presentation differs between HIV-positive individuals and MS patients treated with NAT. Rituximab (RITUX), a monoclonal antibody currently used for hematological malignancies and autoimmune disorders, is also associated with a moderately increased risk of PML. We compare the MRI presentation of RITUX-associated PML to NAT or HIV-associated PML.
Materials and methods: Brain MRI exams from 29 patients with a definite PML diagnosis including 12 after NAT treatment, 7 after RITUX treatment and 10 HIV-positive patients were analyzed using the following key MRI features: aspect in T1/T2/DWI and T2* weighted images, location of the lesion, enhancement, U fibers and cortex involvement.
Results: The three PML entities show hyperintensities on T2 weighted sequence with lesions affecting U fibers associated to low signal intensities in U fibers on T2* weighted sequence. Only NAT-associated PML shows a punctuate microcystic appearance in or in proximity to the lesion with a potential involvement of the cortex on T2, T2* and on diffusion weighted sequence and in some cases an early contrast enhancement. Similarly to HIV-associated PML, RITUX-associated PML shows a rim of hyperintensity on diffusion weighted sequence and no early enhancement. However, we observed no punctuate appearance and no cortex involvement.
Conclusion: Imaging features of RITUX-associated PML are different from those of NAT-associated PML and are close to those observed in HIV-associated PML. These differences may be due to the higher level of immunosuppression in HIV patients and patients treated with RITUX compared to patients treated with NAT.
Disclosure:
ALLEG Manel:nothing to disclose
Morgane SOLIS:nothing to discloseSamira FAFI-KREMER:nothing to disclose
Stéphane Kremer:nothing to disclose
Jérome DE SEZE:nothing to disclose
Guido AHLE:nothing to disclose
Hélène OESTERLE:nothing to disclose
Xavier LECLERC:nothing to disclose
Jean Pierre PRUVO:nothing to disclose
Patrick VERMERSCH:nothing to disclose
Fabrice BONNEVILLE:nothing to disclose
Jerome HODEL:nothing to disclose
David BRASSAT:nothing to disclose
Damien BIOTTI:nothing to disclose
Abstract: EP1533
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - 21 Imaging
Purpose: Progressive multifocal leucoencephalopathy (PML) is a demyelinating disease of the central nervous system caused by reactivation of the JC polyomavirus. PML is most frequently associated with AIDS and emerges as a complication of Natalizumab (NAT) treatment of multiple sclerosis (MS). MRI presentation differs between HIV-positive individuals and MS patients treated with NAT. Rituximab (RITUX), a monoclonal antibody currently used for hematological malignancies and autoimmune disorders, is also associated with a moderately increased risk of PML. We compare the MRI presentation of RITUX-associated PML to NAT or HIV-associated PML.
Materials and methods: Brain MRI exams from 29 patients with a definite PML diagnosis including 12 after NAT treatment, 7 after RITUX treatment and 10 HIV-positive patients were analyzed using the following key MRI features: aspect in T1/T2/DWI and T2* weighted images, location of the lesion, enhancement, U fibers and cortex involvement.
Results: The three PML entities show hyperintensities on T2 weighted sequence with lesions affecting U fibers associated to low signal intensities in U fibers on T2* weighted sequence. Only NAT-associated PML shows a punctuate microcystic appearance in or in proximity to the lesion with a potential involvement of the cortex on T2, T2* and on diffusion weighted sequence and in some cases an early contrast enhancement. Similarly to HIV-associated PML, RITUX-associated PML shows a rim of hyperintensity on diffusion weighted sequence and no early enhancement. However, we observed no punctuate appearance and no cortex involvement.
Conclusion: Imaging features of RITUX-associated PML are different from those of NAT-associated PML and are close to those observed in HIV-associated PML. These differences may be due to the higher level of immunosuppression in HIV patients and patients treated with RITUX compared to patients treated with NAT.
Disclosure:
ALLEG Manel:nothing to disclose
Morgane SOLIS:nothing to discloseSamira FAFI-KREMER:nothing to disclose
Stéphane Kremer:nothing to disclose
Jérome DE SEZE:nothing to disclose
Guido AHLE:nothing to disclose
Hélène OESTERLE:nothing to disclose
Xavier LECLERC:nothing to disclose
Jean Pierre PRUVO:nothing to disclose
Patrick VERMERSCH:nothing to disclose
Fabrice BONNEVILLE:nothing to disclose
Jerome HODEL:nothing to disclose
David BRASSAT:nothing to disclose
Damien BIOTTI:nothing to disclose