Contributions
Abstract: P1082
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 22 OCT
Background: Progressive retinal atrophy has been shown in multiple sclerosis (MS) patients using optical coherence tomography (OCT), regardless of history of optic neuritis (ON), and has been correlated with clinical disability. Alemtuzumab has been shown to cause long-lasting suppression of disease activity and sustained improvement in disability in RRMS patients. We previously reported a cohort of RRMS patients who received alemtuzumab that demonstrated neuroprotection on OCT in both peripapillary retinal nerve fibre layer (pRNFL) and ganglion cell plus inner plexiform layers (GCIPL) over 2-years. The current study aims to evaluate whether this cohort has a continued long term benefit on retinal layers.
Objective: To determine the long term change in pRNFL thickness and GCIPL volume in RRMS patients who were treated with alemtuzumab.
Methods: This is a prospective, single centre, open label study of 20 patients (80% female, mean age 35y and mean disease duration 5y at baseline) out of a 26 RRMS patient cohort followed longitudinally and treated with alemtuzumab as necessary based on disease activity. Patient eyes with a pretreatment (≤3months) or new ON during the study were excluded (n=2). Using the Heidelberg Spectralis SD-OCT, the pRNFL thickness and GCIPL volume were measured at baseline (≤1week prior to the first infusion), every 6 months for 24 months, and subsequently at long term follow up (median 60 months, range 42-60 months).
Results: For all eyes, the mean RNFL thickness was 90.0µm at baseline and 89.0µm at long term follow up, with a mean change of -0.80µm (95% CI -2.3 to 0.7; p=0.49). The GCIPL mean volume for all eyes was 1.80mm3 at baseline and 1.80mm3 at long term follow up, a mean change of +0.02mm3 (95% CI -0.01 to 0.04; p=0.36). Thirteen patients (65% of cohort) required additional therapy with alemtuzumab during this follow up timeframe. When comparing all eyes there was no significant difference in RNFL and GCIPL between patients that received only 2 courses of medication and those that received >2 courses.
Conclusions: This study shows that over a longitudinal follow period (median 60 months) there is no evidence for a decrease in RNFL thickness and GCIPL volume compared to the natural history data suggesting that alemtuzumab may have a durable neuroprotective effect against injury to the retinal layers in MS patients, and those patients who required additional courses fared similar to those who only required 2 courses.
Disclosure:
JKC: grant support from Biogen; consulting for Roche.
CT: nothing to disclose.
AT: consulting for Chugai, Novartis, Roche, Sanofi Genzyme, EMD Serono, Teva innovation; PI on clinical trials with Biogen, Genzyme, Roche, Chugai.
AN: grant support from Novartis, Biogen, Merk Serono; consulting for EMD Serono.
EHML: grant support from Merck (Grant for MS Innovation); consulting from Genzyme. Travel and accommodation support from Roche and Genzyme. She is a member of the IMSVISUAL consortium.
RC: research support from Teva, consulting for Novartis, EMD Serono, Sanofi, Biogen, Roche; PI on clinical trials with MedImmune, Roche, Novartis.
Source of funding: Sanofi Genzyme
Abstract: P1082
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 22 OCT
Background: Progressive retinal atrophy has been shown in multiple sclerosis (MS) patients using optical coherence tomography (OCT), regardless of history of optic neuritis (ON), and has been correlated with clinical disability. Alemtuzumab has been shown to cause long-lasting suppression of disease activity and sustained improvement in disability in RRMS patients. We previously reported a cohort of RRMS patients who received alemtuzumab that demonstrated neuroprotection on OCT in both peripapillary retinal nerve fibre layer (pRNFL) and ganglion cell plus inner plexiform layers (GCIPL) over 2-years. The current study aims to evaluate whether this cohort has a continued long term benefit on retinal layers.
Objective: To determine the long term change in pRNFL thickness and GCIPL volume in RRMS patients who were treated with alemtuzumab.
Methods: This is a prospective, single centre, open label study of 20 patients (80% female, mean age 35y and mean disease duration 5y at baseline) out of a 26 RRMS patient cohort followed longitudinally and treated with alemtuzumab as necessary based on disease activity. Patient eyes with a pretreatment (≤3months) or new ON during the study were excluded (n=2). Using the Heidelberg Spectralis SD-OCT, the pRNFL thickness and GCIPL volume were measured at baseline (≤1week prior to the first infusion), every 6 months for 24 months, and subsequently at long term follow up (median 60 months, range 42-60 months).
Results: For all eyes, the mean RNFL thickness was 90.0µm at baseline and 89.0µm at long term follow up, with a mean change of -0.80µm (95% CI -2.3 to 0.7; p=0.49). The GCIPL mean volume for all eyes was 1.80mm3 at baseline and 1.80mm3 at long term follow up, a mean change of +0.02mm3 (95% CI -0.01 to 0.04; p=0.36). Thirteen patients (65% of cohort) required additional therapy with alemtuzumab during this follow up timeframe. When comparing all eyes there was no significant difference in RNFL and GCIPL between patients that received only 2 courses of medication and those that received >2 courses.
Conclusions: This study shows that over a longitudinal follow period (median 60 months) there is no evidence for a decrease in RNFL thickness and GCIPL volume compared to the natural history data suggesting that alemtuzumab may have a durable neuroprotective effect against injury to the retinal layers in MS patients, and those patients who required additional courses fared similar to those who only required 2 courses.
Disclosure:
JKC: grant support from Biogen; consulting for Roche.
CT: nothing to disclose.
AT: consulting for Chugai, Novartis, Roche, Sanofi Genzyme, EMD Serono, Teva innovation; PI on clinical trials with Biogen, Genzyme, Roche, Chugai.
AN: grant support from Novartis, Biogen, Merk Serono; consulting for EMD Serono.
EHML: grant support from Merck (Grant for MS Innovation); consulting from Genzyme. Travel and accommodation support from Roche and Genzyme. She is a member of the IMSVISUAL consortium.
RC: research support from Teva, consulting for Novartis, EMD Serono, Sanofi, Biogen, Roche; PI on clinical trials with MedImmune, Roche, Novartis.
Source of funding: Sanofi Genzyme