PMC6696829_01
Magnetic resonance imaging (MRI) data. (a) Initial Cerebral MRI (cMRI) before rituximab treatment: symmetric hyperintense T2 FLAIR signal in the parieto-occipital white matter (age 7 years, 10 months; Philips 1.5T T2 FLAIR axial). (b) Last cMRI 4 months after rituximab treatment: symmetric hyperintense T2 FLAIR signal in the parieto-occipital white matter with progression of inflammatory demyelination extending to the frontal lobe (age 8 years, 3 months; SIEMENS 1.5T T2 FLAIR axial). (c) Initial cMRI before rituximab treatment: symmetric hypointense T1 signal in the parieto-occipital region with contrast enhancement at the advancing margin (age 7 years, 10 months; Philips 1.5T T1 post gadolinium axial). (d) Last cMRI 4 months after rituximab treatment: symmetric hypointense T1 signal in the parieto-occipital region with contrast enhancement at the advancing margin extending to the frontal lobe (age 8 years, 3 months; SIEMENS 1.5T T1 post gadolinium axial).
10.1177_1756286419868133-fig1.jpg
PMC6696829_04_10.1177_1756286419868133-fig1.jpg
fig1-1756286419868133
Despite this treatment, the clinical course of the patient was rapidly progressive, showing deterioration in motor and cognitive functions. cMRIs performed 2 and 4 months after the first rituximab treatment displayed progressive inflammatory demyelination extending to the frontal lobe (Figure 1b+d).
PMC6696829_02
PMC6696829_03
Analysis of peripheral immune cell subtypes: peripheral blood immune cell subtypes including CD19+ B cells and CD3+ T cells were evaluated prior to the first, second, third and fourth as well as after the fourth rituximab infusion. Normal percentages of CD19+ B cells and CD3+ T before the first rituximab infusion. CD19+ B cells decreased markedly after the first rituximab cycle, with further reduction to zero after the fourth rituximab infusion.
10.1177_1756286419868133-fig2.jpg
PMC6696829_03_10.1177_1756286419868133-fig2.jpg
fig2-1756286419868133
After the second infusion of rituximab, total depletion of B cells in the peripheral blood B-cell counts was demonstrated with fluorescence-activated cell sorting (FACS) analysis (Figure 2).
PMC6696829_04
Magnetic resonance imaging (MRI) data. (a) Initial Cerebral MRI (cMRI) before rituximab treatment: symmetric hyperintense T2 FLAIR signal in the parieto-occipital white matter (age 7 years, 10 months; Philips 1.5T T2 FLAIR axial). (b) Last cMRI 4 months after rituximab treatment: symmetric hyperintense T2 FLAIR signal in the parieto-occipital white matter with progression of inflammatory demyelination extending to the frontal lobe (age 8 years, 3 months; SIEMENS 1.5T T2 FLAIR axial). (c) Initial cMRI before rituximab treatment: symmetric hypointense T1 signal in the parieto-occipital region with contrast enhancement at the advancing margin (age 7 years, 10 months; Philips 1.5T T1 post gadolinium axial). (d) Last cMRI 4 months after rituximab treatment: symmetric hypointense T1 signal in the parieto-occipital region with contrast enhancement at the advancing margin extending to the frontal lobe (age 8 years, 3 months; SIEMENS 1.5T T1 post gadolinium axial).
10.1177_1756286419868133-fig1.jpg
PMC6696829_04_10.1177_1756286419868133-fig1.jpg
fig1-1756286419868133
Despite this treatment, the clinical course of the patient was rapidly progressive, showing deterioration in motor and cognitive functions. cMRIs performed 2 and 4 months after the first rituximab treatment displayed progressive inflammatory demyelination extending to the frontal lobe (Figure 1b+d).