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Study suggests potential prognostic value of enlarged perivascular spaces in MS
Key clinical point: The prevalence of enlarged perivascular spaces (EPVS) on magnetic resonance imaging is higher in patients with multiple sclerosis (MS), with higher EPVS burden vs. controls. This supports a potential role of EPVS in MS etiopathogenesis and its use as marker with prognostic potential.
Major finding: Whole brain EPVSs were more common in patients with MS vs. controls (odds ratio [OR], 4.61; P = .001). Patients with MS had a larger EPVS volume (standardized mean difference [SMD], 0.88; P = .01), area (SMD, 0.79; P = .06), and count (SMD, 0.46; P less than .0001) compared with controls.
Study details: Systematic review and meta-analysis of 9 studies including 457 patients with MS and 352 control participants.
Disclosures: This study was supported by grants of the Swiss National Science Foundation and the Region of Stockholm. The authors declared no conflict of interest.
Citation: Granberg T et al. J Neurol. 2020 Jun 13. doi: 10.1007/s00415-020-09971-5.
Key clinical point: The prevalence of enlarged perivascular spaces (EPVS) on magnetic resonance imaging is higher in patients with multiple sclerosis (MS), with higher EPVS burden vs. controls. This supports a potential role of EPVS in MS etiopathogenesis and its use as marker with prognostic potential.
Major finding: Whole brain EPVSs were more common in patients with MS vs. controls (odds ratio [OR], 4.61; P = .001). Patients with MS had a larger EPVS volume (standardized mean difference [SMD], 0.88; P = .01), area (SMD, 0.79; P = .06), and count (SMD, 0.46; P less than .0001) compared with controls.
Study details: Systematic review and meta-analysis of 9 studies including 457 patients with MS and 352 control participants.
Disclosures: This study was supported by grants of the Swiss National Science Foundation and the Region of Stockholm. The authors declared no conflict of interest.
Citation: Granberg T et al. J Neurol. 2020 Jun 13. doi: 10.1007/s00415-020-09971-5.
Key clinical point: The prevalence of enlarged perivascular spaces (EPVS) on magnetic resonance imaging is higher in patients with multiple sclerosis (MS), with higher EPVS burden vs. controls. This supports a potential role of EPVS in MS etiopathogenesis and its use as marker with prognostic potential.
Major finding: Whole brain EPVSs were more common in patients with MS vs. controls (odds ratio [OR], 4.61; P = .001). Patients with MS had a larger EPVS volume (standardized mean difference [SMD], 0.88; P = .01), area (SMD, 0.79; P = .06), and count (SMD, 0.46; P less than .0001) compared with controls.
Study details: Systematic review and meta-analysis of 9 studies including 457 patients with MS and 352 control participants.
Disclosures: This study was supported by grants of the Swiss National Science Foundation and the Region of Stockholm. The authors declared no conflict of interest.
Citation: Granberg T et al. J Neurol. 2020 Jun 13. doi: 10.1007/s00415-020-09971-5.
Effect of hookworm treatment on relapsing MS
Key clinical point: Treatment with hookworm was safe and possibly associated with an immunobiological effect in relapsing multiple sclerosis.
Major finding: During 3-9 months postinfection, no significant difference was detected between hookworm and placebo groups in total number of new T2 lesions, newly enhancing T1-weighted lesions, or T2 enlarging lesions. Hookworm group was somewhat less likely to have any magnetic resonance imaging activity (odds ratio, 0.33), higher percentage of CD4+CD25highCD127negT cells in peripheral blood (4.4% vs. 3.9%; P = .01), and lower relapse rate per patient (14.3% vs. 30.6%). No patients withdrew because of adverse effects. The only differing adverse event was more application-site skin discomfort in the hookworm group (82.86% vs. 27.78%).
Study details: In this phase 2 trial, 71 patients with relapsing MS without disease-modifying treatment were randomly assigned (1:1) to receive 25 Necator americanus larvae transcutaneously or placebo.
Disclosures: This study was supported by the MS Society of the Great Britain and Northern Ireland, the Forman Hardy Charitable Trust via the University of Nottingham, and an unrestricted grant from Bayer-Schering. Some of the investigators reported receiving grants and personal fees from multiple pharmaceutical companies.
Citation: Tanasescu R et al. JAMA Neurol. 2020 Jun 15. doi: 10.1001/jamaneurol.2020.1118.
Key clinical point: Treatment with hookworm was safe and possibly associated with an immunobiological effect in relapsing multiple sclerosis.
Major finding: During 3-9 months postinfection, no significant difference was detected between hookworm and placebo groups in total number of new T2 lesions, newly enhancing T1-weighted lesions, or T2 enlarging lesions. Hookworm group was somewhat less likely to have any magnetic resonance imaging activity (odds ratio, 0.33), higher percentage of CD4+CD25highCD127negT cells in peripheral blood (4.4% vs. 3.9%; P = .01), and lower relapse rate per patient (14.3% vs. 30.6%). No patients withdrew because of adverse effects. The only differing adverse event was more application-site skin discomfort in the hookworm group (82.86% vs. 27.78%).
Study details: In this phase 2 trial, 71 patients with relapsing MS without disease-modifying treatment were randomly assigned (1:1) to receive 25 Necator americanus larvae transcutaneously or placebo.
Disclosures: This study was supported by the MS Society of the Great Britain and Northern Ireland, the Forman Hardy Charitable Trust via the University of Nottingham, and an unrestricted grant from Bayer-Schering. Some of the investigators reported receiving grants and personal fees from multiple pharmaceutical companies.
Citation: Tanasescu R et al. JAMA Neurol. 2020 Jun 15. doi: 10.1001/jamaneurol.2020.1118.
Key clinical point: Treatment with hookworm was safe and possibly associated with an immunobiological effect in relapsing multiple sclerosis.
Major finding: During 3-9 months postinfection, no significant difference was detected between hookworm and placebo groups in total number of new T2 lesions, newly enhancing T1-weighted lesions, or T2 enlarging lesions. Hookworm group was somewhat less likely to have any magnetic resonance imaging activity (odds ratio, 0.33), higher percentage of CD4+CD25highCD127negT cells in peripheral blood (4.4% vs. 3.9%; P = .01), and lower relapse rate per patient (14.3% vs. 30.6%). No patients withdrew because of adverse effects. The only differing adverse event was more application-site skin discomfort in the hookworm group (82.86% vs. 27.78%).
Study details: In this phase 2 trial, 71 patients with relapsing MS without disease-modifying treatment were randomly assigned (1:1) to receive 25 Necator americanus larvae transcutaneously or placebo.
Disclosures: This study was supported by the MS Society of the Great Britain and Northern Ireland, the Forman Hardy Charitable Trust via the University of Nottingham, and an unrestricted grant from Bayer-Schering. Some of the investigators reported receiving grants and personal fees from multiple pharmaceutical companies.
Citation: Tanasescu R et al. JAMA Neurol. 2020 Jun 15. doi: 10.1001/jamaneurol.2020.1118.
MSBase study validates therapy for relapse in secondary progressive MS
An observational cohort study of a prospective international database of patients with multiple sclerosis has reported that medical therapy can reduce disability progression in patients with active secondary progressive MS (SPMS) who are prone to inflammatory relapses.
The international researchers, led by Nathanial Lizak, MMBS, of the University of Melbourne, conducted the cohort study of 1,621 patients with SPMS from the MSBase international registry, which prospectively collected the information from 1995 to 2018. Their findings were published in JAMA Neurology.
“ wrote Dr. Lizak and colleagues of the MSBase Study Group.
Therapy’s impact on disease progression
To ensure that they had timely data on the early disease course of all study patients, they researchers only included patients whose diagnosis and first documented Expanded Disability Status Scale (EDSS) score were no more than 24 months apart. At SPMS conversion, 1,494 patients had an EDSS score of less than 7 (on a scale of 0-10); during the follow-up period, 267 of them (17.9%) crossed over the threshold of 7.
Dr. Lizak and colleagues noted that early treatment during relapsing remitting MS didn’t impact outcomes after SPMS conversion.
For evaluating the MS Severity Score (MSSS), the study split the cohort into three groups depending on the efficacy of therapy: low-efficacy treatments, mostly consisting of interferon-beta and glatiramer acetate; medium-efficacy treatments, mostly fingolimod and dimethyl fumarate; and high-efficacy treatments, predominately natalizumab and mitoxantrone.
The MSSS progression slope in the cohort had an average reduction of 0.02 points per year. “For patients who experienced superimposed relapses during SPMS, a reduced MSSS progression slope during SPMS was observed among those who received disease-modifying therapies for a greater proportion of time during SPMS,” Dr. Lizak and colleagues wrote.
MSSS progression slope reduction was more pronounced in the medium- and high-efficacy groups, with a reduction of beta 0.22 (P = .06) and 0.034 (P = .002), respectively.
“Based on our models, the level of disability in patients with active SPMS who are continuously treated with high-efficacy immunotherapies would progress more slowly in comparison with the general population with MS by a mean (standard deviation) of 1.56 (4.60) deciles over 10 years,” Dr. Lizak and colleagues wrote.
While the researchers cited a number of studies that didn’t support immunotherapy for SPMS, they also did cite the EXPAND trial to support treatment with siponimod in SPMS patients (Lancet. 2018;391:1263-73). The ASCEND trial of natalizumab enrolled a largely relapse-free cohort and found no link between treatment and disability progression in SPMS (Lancet Neurol. 2018;17:405-15), and a previous report by the MSBase Study Group found no benefit of therapy when adjusted for SPMS relapse rates (Neurology. 2017;89:1050-9).
“Together with the present study, the existing data converge on the suggestion that relapses during SPMS provide a therapeutic target and a marker of future response to immunotherapy during SPMS,” Dr. Lizak and colleagues wrote.
Challenging dogma
Commenting on the research, Mark Freedman, HBSc, MSc, MD, said that the MSBase study makes an important contribution to the literature on management of SPMS. “Up until this point we’ve been basing our assumptions on secondary progressive MS on natural history studies, which are actually quite old, dating back 20-30 years.” Dr. Freedman is senior scientist in the Neuroscience Program at the Ottawa Hospital Research Institute and professor of medicine in neurology at the University of Ottawa.
He said “the most damaging” of those studies was by the late Christian Confavreaux, MD, and colleagues in Lyon, France (N Engl J Med. 2000;343:1430-8), that reported relapses didn’t alter the progression of disability. “In other words, once you’re in EDSS of 4, it’s a runaway train; it doesn’t matter what you do,” Dr. Freedman said.
“That was kind of dogma for years,” he said. “The reason this publication is important is because it’s suggesting that’s not the case.” In other words, the MSBase cohort study is validating what neurologists have been doing in the real world for years: treating patients with SPMS who have relapses.
Dr Lizak reported receiving travel compensation from Merck outside the scope of the study. His coauthors reported numerous financial relationships.
SOURCE: Lizak N et al. JAMA Neurol. 2020 Jul 27. doi: 10.1001/jamaneurol.2020.2453
An observational cohort study of a prospective international database of patients with multiple sclerosis has reported that medical therapy can reduce disability progression in patients with active secondary progressive MS (SPMS) who are prone to inflammatory relapses.
The international researchers, led by Nathanial Lizak, MMBS, of the University of Melbourne, conducted the cohort study of 1,621 patients with SPMS from the MSBase international registry, which prospectively collected the information from 1995 to 2018. Their findings were published in JAMA Neurology.
“ wrote Dr. Lizak and colleagues of the MSBase Study Group.
Therapy’s impact on disease progression
To ensure that they had timely data on the early disease course of all study patients, they researchers only included patients whose diagnosis and first documented Expanded Disability Status Scale (EDSS) score were no more than 24 months apart. At SPMS conversion, 1,494 patients had an EDSS score of less than 7 (on a scale of 0-10); during the follow-up period, 267 of them (17.9%) crossed over the threshold of 7.
Dr. Lizak and colleagues noted that early treatment during relapsing remitting MS didn’t impact outcomes after SPMS conversion.
For evaluating the MS Severity Score (MSSS), the study split the cohort into three groups depending on the efficacy of therapy: low-efficacy treatments, mostly consisting of interferon-beta and glatiramer acetate; medium-efficacy treatments, mostly fingolimod and dimethyl fumarate; and high-efficacy treatments, predominately natalizumab and mitoxantrone.
The MSSS progression slope in the cohort had an average reduction of 0.02 points per year. “For patients who experienced superimposed relapses during SPMS, a reduced MSSS progression slope during SPMS was observed among those who received disease-modifying therapies for a greater proportion of time during SPMS,” Dr. Lizak and colleagues wrote.
MSSS progression slope reduction was more pronounced in the medium- and high-efficacy groups, with a reduction of beta 0.22 (P = .06) and 0.034 (P = .002), respectively.
“Based on our models, the level of disability in patients with active SPMS who are continuously treated with high-efficacy immunotherapies would progress more slowly in comparison with the general population with MS by a mean (standard deviation) of 1.56 (4.60) deciles over 10 years,” Dr. Lizak and colleagues wrote.
While the researchers cited a number of studies that didn’t support immunotherapy for SPMS, they also did cite the EXPAND trial to support treatment with siponimod in SPMS patients (Lancet. 2018;391:1263-73). The ASCEND trial of natalizumab enrolled a largely relapse-free cohort and found no link between treatment and disability progression in SPMS (Lancet Neurol. 2018;17:405-15), and a previous report by the MSBase Study Group found no benefit of therapy when adjusted for SPMS relapse rates (Neurology. 2017;89:1050-9).
“Together with the present study, the existing data converge on the suggestion that relapses during SPMS provide a therapeutic target and a marker of future response to immunotherapy during SPMS,” Dr. Lizak and colleagues wrote.
Challenging dogma
Commenting on the research, Mark Freedman, HBSc, MSc, MD, said that the MSBase study makes an important contribution to the literature on management of SPMS. “Up until this point we’ve been basing our assumptions on secondary progressive MS on natural history studies, which are actually quite old, dating back 20-30 years.” Dr. Freedman is senior scientist in the Neuroscience Program at the Ottawa Hospital Research Institute and professor of medicine in neurology at the University of Ottawa.
He said “the most damaging” of those studies was by the late Christian Confavreaux, MD, and colleagues in Lyon, France (N Engl J Med. 2000;343:1430-8), that reported relapses didn’t alter the progression of disability. “In other words, once you’re in EDSS of 4, it’s a runaway train; it doesn’t matter what you do,” Dr. Freedman said.
“That was kind of dogma for years,” he said. “The reason this publication is important is because it’s suggesting that’s not the case.” In other words, the MSBase cohort study is validating what neurologists have been doing in the real world for years: treating patients with SPMS who have relapses.
Dr Lizak reported receiving travel compensation from Merck outside the scope of the study. His coauthors reported numerous financial relationships.
SOURCE: Lizak N et al. JAMA Neurol. 2020 Jul 27. doi: 10.1001/jamaneurol.2020.2453
An observational cohort study of a prospective international database of patients with multiple sclerosis has reported that medical therapy can reduce disability progression in patients with active secondary progressive MS (SPMS) who are prone to inflammatory relapses.
The international researchers, led by Nathanial Lizak, MMBS, of the University of Melbourne, conducted the cohort study of 1,621 patients with SPMS from the MSBase international registry, which prospectively collected the information from 1995 to 2018. Their findings were published in JAMA Neurology.
“ wrote Dr. Lizak and colleagues of the MSBase Study Group.
Therapy’s impact on disease progression
To ensure that they had timely data on the early disease course of all study patients, they researchers only included patients whose diagnosis and first documented Expanded Disability Status Scale (EDSS) score were no more than 24 months apart. At SPMS conversion, 1,494 patients had an EDSS score of less than 7 (on a scale of 0-10); during the follow-up period, 267 of them (17.9%) crossed over the threshold of 7.
Dr. Lizak and colleagues noted that early treatment during relapsing remitting MS didn’t impact outcomes after SPMS conversion.
For evaluating the MS Severity Score (MSSS), the study split the cohort into three groups depending on the efficacy of therapy: low-efficacy treatments, mostly consisting of interferon-beta and glatiramer acetate; medium-efficacy treatments, mostly fingolimod and dimethyl fumarate; and high-efficacy treatments, predominately natalizumab and mitoxantrone.
The MSSS progression slope in the cohort had an average reduction of 0.02 points per year. “For patients who experienced superimposed relapses during SPMS, a reduced MSSS progression slope during SPMS was observed among those who received disease-modifying therapies for a greater proportion of time during SPMS,” Dr. Lizak and colleagues wrote.
MSSS progression slope reduction was more pronounced in the medium- and high-efficacy groups, with a reduction of beta 0.22 (P = .06) and 0.034 (P = .002), respectively.
“Based on our models, the level of disability in patients with active SPMS who are continuously treated with high-efficacy immunotherapies would progress more slowly in comparison with the general population with MS by a mean (standard deviation) of 1.56 (4.60) deciles over 10 years,” Dr. Lizak and colleagues wrote.
While the researchers cited a number of studies that didn’t support immunotherapy for SPMS, they also did cite the EXPAND trial to support treatment with siponimod in SPMS patients (Lancet. 2018;391:1263-73). The ASCEND trial of natalizumab enrolled a largely relapse-free cohort and found no link between treatment and disability progression in SPMS (Lancet Neurol. 2018;17:405-15), and a previous report by the MSBase Study Group found no benefit of therapy when adjusted for SPMS relapse rates (Neurology. 2017;89:1050-9).
“Together with the present study, the existing data converge on the suggestion that relapses during SPMS provide a therapeutic target and a marker of future response to immunotherapy during SPMS,” Dr. Lizak and colleagues wrote.
Challenging dogma
Commenting on the research, Mark Freedman, HBSc, MSc, MD, said that the MSBase study makes an important contribution to the literature on management of SPMS. “Up until this point we’ve been basing our assumptions on secondary progressive MS on natural history studies, which are actually quite old, dating back 20-30 years.” Dr. Freedman is senior scientist in the Neuroscience Program at the Ottawa Hospital Research Institute and professor of medicine in neurology at the University of Ottawa.
He said “the most damaging” of those studies was by the late Christian Confavreaux, MD, and colleagues in Lyon, France (N Engl J Med. 2000;343:1430-8), that reported relapses didn’t alter the progression of disability. “In other words, once you’re in EDSS of 4, it’s a runaway train; it doesn’t matter what you do,” Dr. Freedman said.
“That was kind of dogma for years,” he said. “The reason this publication is important is because it’s suggesting that’s not the case.” In other words, the MSBase cohort study is validating what neurologists have been doing in the real world for years: treating patients with SPMS who have relapses.
Dr Lizak reported receiving travel compensation from Merck outside the scope of the study. His coauthors reported numerous financial relationships.
SOURCE: Lizak N et al. JAMA Neurol. 2020 Jul 27. doi: 10.1001/jamaneurol.2020.2453
FROM JAMA NEUROLOGY
Higher incidence of depression in patients with MS
Key clinical point: Patients with multiple sclerosis (MS) in the United States (US) and the United Kingdom (UK) have a 2- to 3-fold higher incidence of depression than those without MS.
Major finding: A significantly higher incidence of depression was observed among patients with MS vs. non-MS control individuals in the US (incidence rate ratio [IRR], 3.20; 95% confidence interval [CI], 3.05-3.35) and the UK (IRR, 1.90; 95% CI, 1.74-2.06).
Study details: This cohort study included individuals with a first recorded diagnosis of MS and matched non-MS individuals identified from the US Department of Defense military healthcare system and the UK’s Clinical Practice Research Datalink GOLD.
Disclosures: The study was funded by Celgene Corporation, a wholly owned subsidiary of Bristol-Myers Squibb. Sally Lee, Neil Minton, Steve Niemcryk, and Anders Lindholm are employees of Bristol-Myers Squibb. Amber M Evans is an employee of Health ResearchTx LLC, which has a business relationship with Celgene Corporation.
Citation: Persson R et al. Eur J Neurol. 2020 May 12. doi: 10.1111/ene.14314.
Key clinical point: Patients with multiple sclerosis (MS) in the United States (US) and the United Kingdom (UK) have a 2- to 3-fold higher incidence of depression than those without MS.
Major finding: A significantly higher incidence of depression was observed among patients with MS vs. non-MS control individuals in the US (incidence rate ratio [IRR], 3.20; 95% confidence interval [CI], 3.05-3.35) and the UK (IRR, 1.90; 95% CI, 1.74-2.06).
Study details: This cohort study included individuals with a first recorded diagnosis of MS and matched non-MS individuals identified from the US Department of Defense military healthcare system and the UK’s Clinical Practice Research Datalink GOLD.
Disclosures: The study was funded by Celgene Corporation, a wholly owned subsidiary of Bristol-Myers Squibb. Sally Lee, Neil Minton, Steve Niemcryk, and Anders Lindholm are employees of Bristol-Myers Squibb. Amber M Evans is an employee of Health ResearchTx LLC, which has a business relationship with Celgene Corporation.
Citation: Persson R et al. Eur J Neurol. 2020 May 12. doi: 10.1111/ene.14314.
Key clinical point: Patients with multiple sclerosis (MS) in the United States (US) and the United Kingdom (UK) have a 2- to 3-fold higher incidence of depression than those without MS.
Major finding: A significantly higher incidence of depression was observed among patients with MS vs. non-MS control individuals in the US (incidence rate ratio [IRR], 3.20; 95% confidence interval [CI], 3.05-3.35) and the UK (IRR, 1.90; 95% CI, 1.74-2.06).
Study details: This cohort study included individuals with a first recorded diagnosis of MS and matched non-MS individuals identified from the US Department of Defense military healthcare system and the UK’s Clinical Practice Research Datalink GOLD.
Disclosures: The study was funded by Celgene Corporation, a wholly owned subsidiary of Bristol-Myers Squibb. Sally Lee, Neil Minton, Steve Niemcryk, and Anders Lindholm are employees of Bristol-Myers Squibb. Amber M Evans is an employee of Health ResearchTx LLC, which has a business relationship with Celgene Corporation.
Citation: Persson R et al. Eur J Neurol. 2020 May 12. doi: 10.1111/ene.14314.
MS: Gadolinium enhancement decreases with advancing age
Key clinical point: Inflammatory activity declines with age in patients with multiple sclerosis (MS), as evidenced by decreased gadolinium enhancement with advancing age.
Major finding: The odds for gadolinium enhancement decreased with advancing age up to 60 years (31-40 years: odds ratio [OR], 0.55; 41-50 years: OR, 0.42; and 51-60 years: OR, 0.24; P less than .0001 for all).
Study details: A cohort study of 1,543 patients with clinically isolated syndrome and MS assessed the association of risk factors, including age, with gadolinium enhancement on cranial magnetic resonance imaging scans.
Disclosures: The study did not receive any funding. Marcus W Koch and Wei-Qiao Liu reported relationships with multiple pharmaceutical companies. Jop Mostert, Jamie Greenfield, and Prof Luanne Metz have declared no conflicts of interest.
Citation: Koch MW et al. J Neurol. 2020 May 09. doi: 10.1007/s00415-020-09895-0.
Key clinical point: Inflammatory activity declines with age in patients with multiple sclerosis (MS), as evidenced by decreased gadolinium enhancement with advancing age.
Major finding: The odds for gadolinium enhancement decreased with advancing age up to 60 years (31-40 years: odds ratio [OR], 0.55; 41-50 years: OR, 0.42; and 51-60 years: OR, 0.24; P less than .0001 for all).
Study details: A cohort study of 1,543 patients with clinically isolated syndrome and MS assessed the association of risk factors, including age, with gadolinium enhancement on cranial magnetic resonance imaging scans.
Disclosures: The study did not receive any funding. Marcus W Koch and Wei-Qiao Liu reported relationships with multiple pharmaceutical companies. Jop Mostert, Jamie Greenfield, and Prof Luanne Metz have declared no conflicts of interest.
Citation: Koch MW et al. J Neurol. 2020 May 09. doi: 10.1007/s00415-020-09895-0.
Key clinical point: Inflammatory activity declines with age in patients with multiple sclerosis (MS), as evidenced by decreased gadolinium enhancement with advancing age.
Major finding: The odds for gadolinium enhancement decreased with advancing age up to 60 years (31-40 years: odds ratio [OR], 0.55; 41-50 years: OR, 0.42; and 51-60 years: OR, 0.24; P less than .0001 for all).
Study details: A cohort study of 1,543 patients with clinically isolated syndrome and MS assessed the association of risk factors, including age, with gadolinium enhancement on cranial magnetic resonance imaging scans.
Disclosures: The study did not receive any funding. Marcus W Koch and Wei-Qiao Liu reported relationships with multiple pharmaceutical companies. Jop Mostert, Jamie Greenfield, and Prof Luanne Metz have declared no conflicts of interest.
Citation: Koch MW et al. J Neurol. 2020 May 09. doi: 10.1007/s00415-020-09895-0.
Relapsing-remitting MS: Dimethyl fumarate slows cognitive impairment
Key clinical point: Dimethyl fumarate (DMF) may slow down cognitive impairment in patients with relapsing-remitting multiple sclerosis (RRMS).
Major finding: Of 34 patients with cognitive impairment at baseline, 55.9% of patients did not show evidence of cognitive worsening at 2 years.
Study details: This prospective single-arm study enrolled patients with RRMS (n=217) treated with DMF for 2 years.
Disclosures: This study was funded by Biogen. The authors reported relationships with multiple pharmaceutical companies.
Citation: Amato MP et al. Neurol Sci. 2020 May 01. doi: 10.1007/s10072-020-04320-w.
Key clinical point: Dimethyl fumarate (DMF) may slow down cognitive impairment in patients with relapsing-remitting multiple sclerosis (RRMS).
Major finding: Of 34 patients with cognitive impairment at baseline, 55.9% of patients did not show evidence of cognitive worsening at 2 years.
Study details: This prospective single-arm study enrolled patients with RRMS (n=217) treated with DMF for 2 years.
Disclosures: This study was funded by Biogen. The authors reported relationships with multiple pharmaceutical companies.
Citation: Amato MP et al. Neurol Sci. 2020 May 01. doi: 10.1007/s10072-020-04320-w.
Key clinical point: Dimethyl fumarate (DMF) may slow down cognitive impairment in patients with relapsing-remitting multiple sclerosis (RRMS).
Major finding: Of 34 patients with cognitive impairment at baseline, 55.9% of patients did not show evidence of cognitive worsening at 2 years.
Study details: This prospective single-arm study enrolled patients with RRMS (n=217) treated with DMF for 2 years.
Disclosures: This study was funded by Biogen. The authors reported relationships with multiple pharmaceutical companies.
Citation: Amato MP et al. Neurol Sci. 2020 May 01. doi: 10.1007/s10072-020-04320-w.
MS: Ocrelizumab can stabilize treatment-naïve and pretreated patients
Key clinical point: Ocrelizumab is a potential stabilizing treatment option for both treatment-naïve and pretreated patients with multiple sclerosis (MS).
Major finding: Among all patients, 24% were treatment naïve and 76% had previously received immune therapies. After initiating ocrelizumab, 13% of patients with relapsing-remitting multiple sclerosis (RRMS) or active secondary progressive multiple sclerosis (aSPMS) had a relapse (annualized relapse rate, 0.17). Among all patients with MS, 5% experienced a 12-week confirmed disability progression. Side effects were mostly mild and reported in 22% of the patients.
Study details: A retrospective analysis of real-world data on patients with MS who had received 2 ocrelizumab (300 mg) cycles at 2-week intervals. Of 210 patients, 55 had primary progressive MS and 155 had RRMS or aSPMS.
Disclosures: This study was supported by the German Research Council. The authors reported relationships with multiple pharmaceutical companies.
Citation: Nicholas J et al. J Med Econ. 2020 Apr 26. doi: 10.1212/NXI.0000000000000719.
Key clinical point: Ocrelizumab is a potential stabilizing treatment option for both treatment-naïve and pretreated patients with multiple sclerosis (MS).
Major finding: Among all patients, 24% were treatment naïve and 76% had previously received immune therapies. After initiating ocrelizumab, 13% of patients with relapsing-remitting multiple sclerosis (RRMS) or active secondary progressive multiple sclerosis (aSPMS) had a relapse (annualized relapse rate, 0.17). Among all patients with MS, 5% experienced a 12-week confirmed disability progression. Side effects were mostly mild and reported in 22% of the patients.
Study details: A retrospective analysis of real-world data on patients with MS who had received 2 ocrelizumab (300 mg) cycles at 2-week intervals. Of 210 patients, 55 had primary progressive MS and 155 had RRMS or aSPMS.
Disclosures: This study was supported by the German Research Council. The authors reported relationships with multiple pharmaceutical companies.
Citation: Nicholas J et al. J Med Econ. 2020 Apr 26. doi: 10.1212/NXI.0000000000000719.
Key clinical point: Ocrelizumab is a potential stabilizing treatment option for both treatment-naïve and pretreated patients with multiple sclerosis (MS).
Major finding: Among all patients, 24% were treatment naïve and 76% had previously received immune therapies. After initiating ocrelizumab, 13% of patients with relapsing-remitting multiple sclerosis (RRMS) or active secondary progressive multiple sclerosis (aSPMS) had a relapse (annualized relapse rate, 0.17). Among all patients with MS, 5% experienced a 12-week confirmed disability progression. Side effects were mostly mild and reported in 22% of the patients.
Study details: A retrospective analysis of real-world data on patients with MS who had received 2 ocrelizumab (300 mg) cycles at 2-week intervals. Of 210 patients, 55 had primary progressive MS and 155 had RRMS or aSPMS.
Disclosures: This study was supported by the German Research Council. The authors reported relationships with multiple pharmaceutical companies.
Citation: Nicholas J et al. J Med Econ. 2020 Apr 26. doi: 10.1212/NXI.0000000000000719.
Relapsing MS: Lower disability progression in long-term users of fingolimod
Key clinical point: Long-term exposure to fingolimod is associated with lower disability progression in patients with relapsing multiple sclerosis (MS).
Major finding: The high (≥8 years) vs. low (<8 years) exposure groups showed a smaller increase in the mean Expanded Disability Status Scale (+0.55 vs. +1.21) and lower frequencies of disability progression (34.7% vs. 56.1%; P less than .01) and wheelchair use (4.9% vs. 16.9%; P less than .0276) at 10 years.
Study details: ACROSS was a cross-sectional follow-up study of patients with relapsing MS enrolled in a phase 2 proof-of-concept study. Disability outcomes were assessed in patients grouped as per fingolimod exposure: high exposure (n=104) and low exposure (n=71).
Disclosures: The study was funded by Novartis Pharma AG, Basel, Switzerland. Amin Azmon and Davorka Tomic are employees of Novartis. The other authors reported relationships with multiple pharmaceutical companies.
Citation: Derfuss T et al. Mult Scler J Exp Transl Clin. 2020 Mar 30. doi: 10.1177/2055217320907951.
Key clinical point: Long-term exposure to fingolimod is associated with lower disability progression in patients with relapsing multiple sclerosis (MS).
Major finding: The high (≥8 years) vs. low (<8 years) exposure groups showed a smaller increase in the mean Expanded Disability Status Scale (+0.55 vs. +1.21) and lower frequencies of disability progression (34.7% vs. 56.1%; P less than .01) and wheelchair use (4.9% vs. 16.9%; P less than .0276) at 10 years.
Study details: ACROSS was a cross-sectional follow-up study of patients with relapsing MS enrolled in a phase 2 proof-of-concept study. Disability outcomes were assessed in patients grouped as per fingolimod exposure: high exposure (n=104) and low exposure (n=71).
Disclosures: The study was funded by Novartis Pharma AG, Basel, Switzerland. Amin Azmon and Davorka Tomic are employees of Novartis. The other authors reported relationships with multiple pharmaceutical companies.
Citation: Derfuss T et al. Mult Scler J Exp Transl Clin. 2020 Mar 30. doi: 10.1177/2055217320907951.
Key clinical point: Long-term exposure to fingolimod is associated with lower disability progression in patients with relapsing multiple sclerosis (MS).
Major finding: The high (≥8 years) vs. low (<8 years) exposure groups showed a smaller increase in the mean Expanded Disability Status Scale (+0.55 vs. +1.21) and lower frequencies of disability progression (34.7% vs. 56.1%; P less than .01) and wheelchair use (4.9% vs. 16.9%; P less than .0276) at 10 years.
Study details: ACROSS was a cross-sectional follow-up study of patients with relapsing MS enrolled in a phase 2 proof-of-concept study. Disability outcomes were assessed in patients grouped as per fingolimod exposure: high exposure (n=104) and low exposure (n=71).
Disclosures: The study was funded by Novartis Pharma AG, Basel, Switzerland. Amin Azmon and Davorka Tomic are employees of Novartis. The other authors reported relationships with multiple pharmaceutical companies.
Citation: Derfuss T et al. Mult Scler J Exp Transl Clin. 2020 Mar 30. doi: 10.1177/2055217320907951.
Obesity tied to accelerated retinal atrophy in MS
Key clinical point: Elevated body mass index (BMI) is independently associated with an accelerated rate of ganglion cell+inner plexiform layer (GCIPL) atrophy in patients with multiple sclerosis (MS).
Major findings: Obese (n=146; BMI, ≥30 kg/m2) vs. normal weight (n=214; BMI, 18.5-24.9 kg/m2) patients showed accelerated rate of GCIPL atrophy (−0.57%/year vs. −0.42%/year; P = .012). Atrophy rates were not significantly different between overweight (n=153; BMI, 25-29.9 kg/m2) and normal weight patients (−0.47%/year vs. −0.42%/year; P = .41). GCIPL atrophy rate accelerated by −0.011% per year with each 1 kg/m2 higher BMI (P =.003).
Study details: This observational study included 522 patients with MS from Johns Hopkins MS Center who were followed with retinal imaging for a median of 4.4 years.
Disclosures: The study was funded by the National MS Society, Race to Erase MS, and NIH/NINDS. The presenting author had no disclosures. One coauthor reported receiving support from the Race to Erase MS foundation.
Citation: Filippatou AG et al. Mult Scler. 2020 Apr 16. doi: 10.1177/1352458519900942.
Key clinical point: Elevated body mass index (BMI) is independently associated with an accelerated rate of ganglion cell+inner plexiform layer (GCIPL) atrophy in patients with multiple sclerosis (MS).
Major findings: Obese (n=146; BMI, ≥30 kg/m2) vs. normal weight (n=214; BMI, 18.5-24.9 kg/m2) patients showed accelerated rate of GCIPL atrophy (−0.57%/year vs. −0.42%/year; P = .012). Atrophy rates were not significantly different between overweight (n=153; BMI, 25-29.9 kg/m2) and normal weight patients (−0.47%/year vs. −0.42%/year; P = .41). GCIPL atrophy rate accelerated by −0.011% per year with each 1 kg/m2 higher BMI (P =.003).
Study details: This observational study included 522 patients with MS from Johns Hopkins MS Center who were followed with retinal imaging for a median of 4.4 years.
Disclosures: The study was funded by the National MS Society, Race to Erase MS, and NIH/NINDS. The presenting author had no disclosures. One coauthor reported receiving support from the Race to Erase MS foundation.
Citation: Filippatou AG et al. Mult Scler. 2020 Apr 16. doi: 10.1177/1352458519900942.
Key clinical point: Elevated body mass index (BMI) is independently associated with an accelerated rate of ganglion cell+inner plexiform layer (GCIPL) atrophy in patients with multiple sclerosis (MS).
Major findings: Obese (n=146; BMI, ≥30 kg/m2) vs. normal weight (n=214; BMI, 18.5-24.9 kg/m2) patients showed accelerated rate of GCIPL atrophy (−0.57%/year vs. −0.42%/year; P = .012). Atrophy rates were not significantly different between overweight (n=153; BMI, 25-29.9 kg/m2) and normal weight patients (−0.47%/year vs. −0.42%/year; P = .41). GCIPL atrophy rate accelerated by −0.011% per year with each 1 kg/m2 higher BMI (P =.003).
Study details: This observational study included 522 patients with MS from Johns Hopkins MS Center who were followed with retinal imaging for a median of 4.4 years.
Disclosures: The study was funded by the National MS Society, Race to Erase MS, and NIH/NINDS. The presenting author had no disclosures. One coauthor reported receiving support from the Race to Erase MS foundation.
Citation: Filippatou AG et al. Mult Scler. 2020 Apr 16. doi: 10.1177/1352458519900942.
Low fish consumption linked to small increased MS risk
Key clinical point: Low fish consumption is associated with an increased risk of developing multiple sclerosis (MS); vitamin D does not mediate this association.
Major finding: Regardless of sun exposure habits, MS risk was higher with low fish consumption, including both lean and fatty fish (odds ratio, 1.2; 95% confidence interval, 1.1-1.4). The mediation analysis revealed that the effect mediated by vitamin D deficiency on this association was very small. A significant interaction was noted between DRB1*15:01 allele and both low sun exposure and low fish consumption.
Study details: The data come from 2 Swedish population-based case-control studies (6,914 patients with MS and 6,590 control participants).
Disclosures: The study was supported by grants from the Swedish Medical Research Council, the Swedish Research Council for Health, Working Life and Welfare, the Swedish Brain Foundation, and the Swedish Society for Medical Research. Dr Olsson reported receiving grants from the Swedish Research Council, the Knut and Alice Wallenberg Foundation, and the Swedish Brain Foundation. Dr Alfredsson reported receiving grants from the Swedish Research Council, the Swedish
Research Council for Health Working Life and Welfare, and the Swedish Brain Foundation.
Citation: Hedström AK et al. Neurol Neuroimmunol Neuroinflamm. 2020 Apr 10. doi: 10.1212/NXI.0000000000000717.
Key clinical point: Low fish consumption is associated with an increased risk of developing multiple sclerosis (MS); vitamin D does not mediate this association.
Major finding: Regardless of sun exposure habits, MS risk was higher with low fish consumption, including both lean and fatty fish (odds ratio, 1.2; 95% confidence interval, 1.1-1.4). The mediation analysis revealed that the effect mediated by vitamin D deficiency on this association was very small. A significant interaction was noted between DRB1*15:01 allele and both low sun exposure and low fish consumption.
Study details: The data come from 2 Swedish population-based case-control studies (6,914 patients with MS and 6,590 control participants).
Disclosures: The study was supported by grants from the Swedish Medical Research Council, the Swedish Research Council for Health, Working Life and Welfare, the Swedish Brain Foundation, and the Swedish Society for Medical Research. Dr Olsson reported receiving grants from the Swedish Research Council, the Knut and Alice Wallenberg Foundation, and the Swedish Brain Foundation. Dr Alfredsson reported receiving grants from the Swedish Research Council, the Swedish
Research Council for Health Working Life and Welfare, and the Swedish Brain Foundation.
Citation: Hedström AK et al. Neurol Neuroimmunol Neuroinflamm. 2020 Apr 10. doi: 10.1212/NXI.0000000000000717.
Key clinical point: Low fish consumption is associated with an increased risk of developing multiple sclerosis (MS); vitamin D does not mediate this association.
Major finding: Regardless of sun exposure habits, MS risk was higher with low fish consumption, including both lean and fatty fish (odds ratio, 1.2; 95% confidence interval, 1.1-1.4). The mediation analysis revealed that the effect mediated by vitamin D deficiency on this association was very small. A significant interaction was noted between DRB1*15:01 allele and both low sun exposure and low fish consumption.
Study details: The data come from 2 Swedish population-based case-control studies (6,914 patients with MS and 6,590 control participants).
Disclosures: The study was supported by grants from the Swedish Medical Research Council, the Swedish Research Council for Health, Working Life and Welfare, the Swedish Brain Foundation, and the Swedish Society for Medical Research. Dr Olsson reported receiving grants from the Swedish Research Council, the Knut and Alice Wallenberg Foundation, and the Swedish Brain Foundation. Dr Alfredsson reported receiving grants from the Swedish Research Council, the Swedish
Research Council for Health Working Life and Welfare, and the Swedish Brain Foundation.
Citation: Hedström AK et al. Neurol Neuroimmunol Neuroinflamm. 2020 Apr 10. doi: 10.1212/NXI.0000000000000717.