Rituximab’s modulating effects on retinal atrophy in RRMS more significant after 12 months
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Rituximab modulated retinal atrophy in relapsing-remitting MS, with attenuating effects that may be more significant after 12 months of treatment, according to results of an observational study published in Neurology.
“Many experts purport that therapeutic optimization occurs rapidly following the commencement of B-cell-depleting disease-modifying treatment of relapsing-remitting MS [RRMS],” Shiv Saidha, MBBCh, MD, MRCPI, lead author and professor of neurology at the Johns Hopkins University School of Medicine, told Healio Neurology. “However, there is a suggestion in the data, particularly regarding phase 3 clinical trial data of ocrelizumab (an FDA-approved treatment for MS that is closely related to the compound rituximab investigated in the current study), that there may be differential therapeutic effects at years 1 and 2 following the commencement of treatment. Therefore, it has been unclear how long it takes for the inflammatory therapeutic effect following the commencement of B-cell-depleting therapies to become optimized, and the lag between this and slowing the consequential effects of inflammation-triggered neurodegeneration.”
The present study examined “the association between rituximab (Rituxan; Genentech, Biogen) use and rates of change in retinal atrophy (specifically, the composite ganglion-cell inner plexiform layer) among people with MS, which had not been evaluated in prior studies,” Kathryn Cauley Fitzgerald, ScD, PhD, study author and assistant professor of neurology at Johns Hopkins University School of Medicine, also told Healio Neurology.
“We also wanted to compare rates of retinal atrophy for people with MS taking rituximab relative to other MS disease modifying therapies,” she said.
The researchers conducted serial optical coherence tomography (OCT) scans on 35 patients on rituximab and compared ganglion cell-inner plexiform layer (GCIPL) atrophy rates in these patients to those seen among patients with RRMS treated with glatiramer acetate (n = 49) and Tsyabri (natalizumab, Biogen; n = 88) whom the researchers matched according to age and sex, as well as with 78 healthy controls. They conducted serial OCT for a median duration of 2.8 years and excluded individuals with uncontrolled hypertension, diabetes mellitus or glaucoma, and those whose eyes had optic neuritis for 6 months or less before baseline OCT or during follow-up. They employed linear mixed-effects regression to conduct statistical analyses.
Results showed GCIPL atrophy rates of -0.28±0.11µm per year among those treated with rituximab, -0.33±0.05µm (P = .69) per year among those treated with glatiramer acetate, -0.17±0.10µm (P = .13) per year among those treated with natalizumab and -0.15±0.03µm (P = .006) per year among healthy controls, representing similar results among patients treated with rituximab compared with glatiramer acetate and natalizumab and quicker rates compared with healthy controls. Saidha and colleagues reported 0.55±0.23µm per year faster GCIPL atrophy rates among patients treated with rituximab during the first 12 months of treatment compared with afterward (n = 25; P = .02), during which they reported GCIPL atrophy rates of -0.14±0.13µm per year.
The study results demonstrated that “rituximab may modulate retinal atrophy rates in people with MS, and the effect may vary by the duration of rituximab treatment,” according to Fitzgerald, who noted that the results should be confirmed in larger studies.
“Our findings should make physicians aware that the neuroprotective effects of rituximab may not be as rapid as previously considered following the commencement of treatment in RRMS,” Saidha said.