Multiple Sclerosis

Key clinical point: Toxoplasma gondii (T. gondii) is negatively associated with multiple sclerosis (MS), suggesting a possible protective role of the parasite in MS.

Major finding: Anti-T. gondii antibodies were detected in 38 MS patients (29.5%) and 130 healthy controls (45.4%). After adjustment, T. gondii seropositivity was significantly associated with a reduced risk of MS (adjusted odds ratio, 0.56; P = .02).

Study details: The data come from an Italian population‑based case-control study of 129 patients with MS and 287 age- and sex-matched controls.

Disclosures: This research was funded by the Department of Medical and Surgical Sciences and Advanced Technologies “G.F. Ingrassia,” University of Catania, Italy. The authors declared no conflicts of interest.

Source: Nicoletti A et al. Sci Rep. 2020 Nov 2. doi: 10.1038/s41598-020-75830-y.

Key clinical point: Toxoplasma gondii (T. gondii) is negatively associated with multiple sclerosis (MS), suggesting a possible protective role of the parasite in MS.

Major finding: Anti-T. gondii antibodies were detected in 38 MS patients (29.5%) and 130 healthy controls (45.4%). After adjustment, T. gondii seropositivity was significantly associated with a reduced risk of MS (adjusted odds ratio, 0.56; P = .02).

Study details: The data come from an Italian population‑based case-control study of 129 patients with MS and 287 age- and sex-matched controls.

Disclosures: This research was funded by the Department of Medical and Surgical Sciences and Advanced Technologies “G.F. Ingrassia,” University of Catania, Italy. The authors declared no conflicts of interest.

Source: Nicoletti A et al. Sci Rep. 2020 Nov 2. doi: 10.1038/s41598-020-75830-y.

Key clinical point: Toxoplasma gondii (T. gondii) is negatively associated with multiple sclerosis (MS), suggesting a possible protective role of the parasite in MS.

Major finding: Anti-T. gondii antibodies were detected in 38 MS patients (29.5%) and 130 healthy controls (45.4%). After adjustment, T. gondii seropositivity was significantly associated with a reduced risk of MS (adjusted odds ratio, 0.56; P = .02).

Study details: The data come from an Italian population‑based case-control study of 129 patients with MS and 287 age- and sex-matched controls.

Disclosures: This research was funded by the Department of Medical and Surgical Sciences and Advanced Technologies “G.F. Ingrassia,” University of Catania, Italy. The authors declared no conflicts of interest.

Source: Nicoletti A et al. Sci Rep. 2020 Nov 2. doi: 10.1038/s41598-020-75830-y.

Best of 2020: The MS Report  is a supplement to Neurology Reviews. 

In this supplement, Neurology Reviews collects the top MS research from 2020. Coverage includes MS highlights from the ACTRIMS, AAN, CMSC, and ECTRIMS annual meetings.

Read Now

Best of 2020: The MS Report  is a supplement to Neurology Reviews. 

In this supplement, Neurology Reviews collects the top MS research from 2020. Coverage includes MS highlights from the ACTRIMS, AAN, CMSC, and ECTRIMS annual meetings.

Read Now

Best of 2020: The MS Report  is a supplement to Neurology Reviews. 

In this supplement, Neurology Reviews collects the top MS research from 2020. Coverage includes MS highlights from the ACTRIMS, AAN, CMSC, and ECTRIMS annual meetings.

Read Now

Key clinical point: Nearly one third of patients with multiple sclerosis (MS) experience migraine.

Major finding: The pooled prevalence rate of migraine was 31% (P less than .001), which significantly varied across the continents (P less than .001).

Study details: A systematic review and meta-analysis of 11 articles and 12 conference abstracts including a total of 11,372 MS cases.

Disclosures: No funding source was identified. The authors declared no conflicts of interest.

Citation: Mirmosayyeb O et al. J Clin Neuroscience. 2020 Aug 4. doi: 10.1016/j.jocn.2020.06.021.

Key clinical point: Nearly one third of patients with multiple sclerosis (MS) experience migraine.

Major finding: The pooled prevalence rate of migraine was 31% (P less than .001), which significantly varied across the continents (P less than .001).

Study details: A systematic review and meta-analysis of 11 articles and 12 conference abstracts including a total of 11,372 MS cases.

Disclosures: No funding source was identified. The authors declared no conflicts of interest.

Citation: Mirmosayyeb O et al. J Clin Neuroscience. 2020 Aug 4. doi: 10.1016/j.jocn.2020.06.021.

Key clinical point: Nearly one third of patients with multiple sclerosis (MS) experience migraine.

Major finding: The pooled prevalence rate of migraine was 31% (P less than .001), which significantly varied across the continents (P less than .001).

Study details: A systematic review and meta-analysis of 11 articles and 12 conference abstracts including a total of 11,372 MS cases.

Disclosures: No funding source was identified. The authors declared no conflicts of interest.

Citation: Mirmosayyeb O et al. J Clin Neuroscience. 2020 Aug 4. doi: 10.1016/j.jocn.2020.06.021.

Key clinical point: In patients with progressive multiple sclerosis (MS), impaired odor identification is associated with a greater clinical decline and higher risk for death.

Major finding: Impaired Brief-Smell Identification (B-SIT) was associated with higher risk for death (adjusted hazard ratio [aHR], 14.9; P less than .001). Among patients with progressive MS, impaired B-SIT vs normal B-SIT showed greater clinical change per month in terms of Multiple Sclerosis Severity scores (median, 0.62 vs. –0.08; P =.004) and Age-Related Multiple Sclerosis Severity scores (median, 0.54 vs. –0.07; P =.004).

Study details: Findings from a retrospective review on 149 patients with MS during a median follow-up of 121 months.

Disclosures: No funding source was identified. The authors declared no conflicts of interest.

Citation: da Silva AM et al. Mult Scler Relat Disord. 2020 Sep 3. doi: 10.1016/j.msard.2020.102486.

Key clinical point: In patients with progressive multiple sclerosis (MS), impaired odor identification is associated with a greater clinical decline and higher risk for death.

Major finding: Impaired Brief-Smell Identification (B-SIT) was associated with higher risk for death (adjusted hazard ratio [aHR], 14.9; P less than .001). Among patients with progressive MS, impaired B-SIT vs normal B-SIT showed greater clinical change per month in terms of Multiple Sclerosis Severity scores (median, 0.62 vs. –0.08; P =.004) and Age-Related Multiple Sclerosis Severity scores (median, 0.54 vs. –0.07; P =.004).

Study details: Findings from a retrospective review on 149 patients with MS during a median follow-up of 121 months.

Disclosures: No funding source was identified. The authors declared no conflicts of interest.

Citation: da Silva AM et al. Mult Scler Relat Disord. 2020 Sep 3. doi: 10.1016/j.msard.2020.102486.

Key clinical point: In patients with progressive multiple sclerosis (MS), impaired odor identification is associated with a greater clinical decline and higher risk for death.

Major finding: Impaired Brief-Smell Identification (B-SIT) was associated with higher risk for death (adjusted hazard ratio [aHR], 14.9; P less than .001). Among patients with progressive MS, impaired B-SIT vs normal B-SIT showed greater clinical change per month in terms of Multiple Sclerosis Severity scores (median, 0.62 vs. –0.08; P =.004) and Age-Related Multiple Sclerosis Severity scores (median, 0.54 vs. –0.07; P =.004).

Study details: Findings from a retrospective review on 149 patients with MS during a median follow-up of 121 months.

Disclosures: No funding source was identified. The authors declared no conflicts of interest.

Citation: da Silva AM et al. Mult Scler Relat Disord. 2020 Sep 3. doi: 10.1016/j.msard.2020.102486.

Key clinical point: Impaired respiratory muscle functions are linked to sleep disturbance and cognitive impairment in patients with multiple sclerosis (MS), warranting early evaluation of respiratory muscle strength.

Major finding: The respiratory muscle function test negatively correlated with the scores of Epworth Sleepiness Scale (ESS) and Perceived Deficits Questionnaire (PDQ) and showed a positive correlation with the Brief International Cognitive Assessment for Multiple Sclerosis (BICAMS) scale score (P less than .001 for all).

Study details: The study assessed 146 MS patients with a mean age of 29.3 years and a mean Expanded Disability Status Scale (EDSS) score of 4.11.

Disclosures: This study did not receive any external funding. The authors declared no conflicts of interests.

Citation: Hashim NA et al. Mult Scler Relat Dis. 2020 Sep 16. doi: 10.1016/j.msard.2020.102514.

Key clinical point: Impaired respiratory muscle functions are linked to sleep disturbance and cognitive impairment in patients with multiple sclerosis (MS), warranting early evaluation of respiratory muscle strength.

Major finding: The respiratory muscle function test negatively correlated with the scores of Epworth Sleepiness Scale (ESS) and Perceived Deficits Questionnaire (PDQ) and showed a positive correlation with the Brief International Cognitive Assessment for Multiple Sclerosis (BICAMS) scale score (P less than .001 for all).

Study details: The study assessed 146 MS patients with a mean age of 29.3 years and a mean Expanded Disability Status Scale (EDSS) score of 4.11.

Disclosures: This study did not receive any external funding. The authors declared no conflicts of interests.

Citation: Hashim NA et al. Mult Scler Relat Dis. 2020 Sep 16. doi: 10.1016/j.msard.2020.102514.

Key clinical point: Impaired respiratory muscle functions are linked to sleep disturbance and cognitive impairment in patients with multiple sclerosis (MS), warranting early evaluation of respiratory muscle strength.

Major finding: The respiratory muscle function test negatively correlated with the scores of Epworth Sleepiness Scale (ESS) and Perceived Deficits Questionnaire (PDQ) and showed a positive correlation with the Brief International Cognitive Assessment for Multiple Sclerosis (BICAMS) scale score (P less than .001 for all).

Study details: The study assessed 146 MS patients with a mean age of 29.3 years and a mean Expanded Disability Status Scale (EDSS) score of 4.11.

Disclosures: This study did not receive any external funding. The authors declared no conflicts of interests.

Citation: Hashim NA et al. Mult Scler Relat Dis. 2020 Sep 16. doi: 10.1016/j.msard.2020.102514.

Key clinical point: Teriflunomide as a long-term immunomodulatory therapy in patients with relapsing multiple sclerosis (MS) has a favorable benefit-risk profile.

Major finding: The safety profile of teriflunomide 14 mg in the extension study was consistent with that in the core study, with similar incidences of adverse events (AEs) and serious AEs. There were differences in serious AE incidences between the placebo and teriflunomide 14 mg groups (6.4% vs. 12.4%). Teriflunomide was associated with reduction in annualized relapse rates in all treatment groups, irrespective of when treatment was initiated.

Study details: Long-term extension of the phase 3 TOWER study: Patients who received teriflunomide 14 mg in the core study were assigned to their original dose (14 mg/14 mg group); patients who received placebo or teriflunomide 7 mg in the core study were reassigned to teriflunomide 14 mg (placebo/14 mg and 7 mg/14 mg groups, respectively).

Disclosures: Development of the manuscript was supported by Sanofi. AL Lublin, P Truffinet, J Chavin, J Delhay, and A Purvis are employees of Sanofi, with ownership interest. M Benamor is an employee of Sanofi. The remaining authors reported ties with various pharmaceutical companies, including Sanofi.

Citation: Miller AE et al. Mult Scler Relat Disord. 2020 Aug 1. doi: 10.1016/j.msard.2020.102438.

Key clinical point: Teriflunomide as a long-term immunomodulatory therapy in patients with relapsing multiple sclerosis (MS) has a favorable benefit-risk profile.

Major finding: The safety profile of teriflunomide 14 mg in the extension study was consistent with that in the core study, with similar incidences of adverse events (AEs) and serious AEs. There were differences in serious AE incidences between the placebo and teriflunomide 14 mg groups (6.4% vs. 12.4%). Teriflunomide was associated with reduction in annualized relapse rates in all treatment groups, irrespective of when treatment was initiated.

Study details: Long-term extension of the phase 3 TOWER study: Patients who received teriflunomide 14 mg in the core study were assigned to their original dose (14 mg/14 mg group); patients who received placebo or teriflunomide 7 mg in the core study were reassigned to teriflunomide 14 mg (placebo/14 mg and 7 mg/14 mg groups, respectively).

Disclosures: Development of the manuscript was supported by Sanofi. AL Lublin, P Truffinet, J Chavin, J Delhay, and A Purvis are employees of Sanofi, with ownership interest. M Benamor is an employee of Sanofi. The remaining authors reported ties with various pharmaceutical companies, including Sanofi.

Citation: Miller AE et al. Mult Scler Relat Disord. 2020 Aug 1. doi: 10.1016/j.msard.2020.102438.

Key clinical point: Teriflunomide as a long-term immunomodulatory therapy in patients with relapsing multiple sclerosis (MS) has a favorable benefit-risk profile.

Major finding: The safety profile of teriflunomide 14 mg in the extension study was consistent with that in the core study, with similar incidences of adverse events (AEs) and serious AEs. There were differences in serious AE incidences between the placebo and teriflunomide 14 mg groups (6.4% vs. 12.4%). Teriflunomide was associated with reduction in annualized relapse rates in all treatment groups, irrespective of when treatment was initiated.

Study details: Long-term extension of the phase 3 TOWER study: Patients who received teriflunomide 14 mg in the core study were assigned to their original dose (14 mg/14 mg group); patients who received placebo or teriflunomide 7 mg in the core study were reassigned to teriflunomide 14 mg (placebo/14 mg and 7 mg/14 mg groups, respectively).

Disclosures: Development of the manuscript was supported by Sanofi. AL Lublin, P Truffinet, J Chavin, J Delhay, and A Purvis are employees of Sanofi, with ownership interest. M Benamor is an employee of Sanofi. The remaining authors reported ties with various pharmaceutical companies, including Sanofi.

Citation: Miller AE et al. Mult Scler Relat Disord. 2020 Aug 1. doi: 10.1016/j.msard.2020.102438.

In 1993 I graduated from medical school. That same year Betaseron (interferon beta-1b) came to market as the first treatment specifically approved for multiple sclerosis (MS). This was a groundbreaker at the time, as there’d been little besides steroids and other potent immunosuppressants to try. Now we had a real drug to offer patients.

The demand for Betaseron was huge, so much so that a lottery system was used to determine which patients would get it first, as there simply wasn’t enough to go around. In the next several years a few more agents jumped into the ring – Avonex (interferon beta-1a), Copaxone (glatiramer acetate), Novantrone (mitoxantrone), and Rebif (interferon beta-1a) – before things went quiet for a while.

In 2006 the first monoclonal antibody for MS – Tysabri (natalizumab) – came out, then almost just as quickly vanished again, not returning until 2009.

Since then we’ve had a gradual explosion of new treatments for MS – like watching kernels become popcorn – first one, then two, then a deluge filling up the basket.

So here we are, approaching the end of 2020, with a remarkable collection of monoclonal antibodies, S1P modulators, fumarates, immunosuppressants, and one symptomatic treatment, many of which weren’t even imagined in 1993. Not to mention the original ABCR (Avonex, Betaseron, Copaxone, Rebif) agents, though they’re riding into the sunset.

A friend and I were talking about this remarkable success story. MS certainly hasn’t been cured, but its treatments have had a dramatic improvement in efficacy over the last quarter century.

He made a point though: that this selection of treatments may be relegating MS from the province of a general neurologist to that of the fellowship-trained MS subspecialist.

Not that that is such a bad thing, as MS is a very challenging disease. But the point is well taken. As treatments become increasingly complicated, and numerous, it becomes harder to know which one is best. Most of us likely choose orals first and monoclonal antibodies second, but the question of “which one?” arises for each category. They each have their own risks, side effects, initiation protocols, and peculiarities. In a disease of heterogeneous presentations and courses, there are no clear data on which agent to start first for what patient type. To a general neurologist, also juggling migraines, strokes, Parkinson’s disease, dementia, and neuropathy (and many other disorders) in the course of a day, it becomes tricky to keep up on such.

At some point do general neurologists become a victim of this success? Maybe, but probably not. Just as there are more general practitioners than neurologists, there are more general neurologists than MS subspecialists. Their knowledge and training should be reserved for those patients not responding to our first- (and second-) line treatments, presentations that are atypical, and more complex issues outside the scope of those of us practicing whatever-comes-to-the-door neurology.

It would, however, be nice to have a good consensus on how to best use this array of treatments. Solid guidelines, breaking disease subtypes and treatments down by patient types, drugs, and mechanisms of action, would help those of us on the neurology frontlines to better care for those who need us.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

In 1993 I graduated from medical school. That same year Betaseron (interferon beta-1b) came to market as the first treatment specifically approved for multiple sclerosis (MS). This was a groundbreaker at the time, as there’d been little besides steroids and other potent immunosuppressants to try. Now we had a real drug to offer patients.

The demand for Betaseron was huge, so much so that a lottery system was used to determine which patients would get it first, as there simply wasn’t enough to go around. In the next several years a few more agents jumped into the ring – Avonex (interferon beta-1a), Copaxone (glatiramer acetate), Novantrone (mitoxantrone), and Rebif (interferon beta-1a) – before things went quiet for a while.

In 2006 the first monoclonal antibody for MS – Tysabri (natalizumab) – came out, then almost just as quickly vanished again, not returning until 2009.

Since then we’ve had a gradual explosion of new treatments for MS – like watching kernels become popcorn – first one, then two, then a deluge filling up the basket.

So here we are, approaching the end of 2020, with a remarkable collection of monoclonal antibodies, S1P modulators, fumarates, immunosuppressants, and one symptomatic treatment, many of which weren’t even imagined in 1993. Not to mention the original ABCR (Avonex, Betaseron, Copaxone, Rebif) agents, though they’re riding into the sunset.

A friend and I were talking about this remarkable success story. MS certainly hasn’t been cured, but its treatments have had a dramatic improvement in efficacy over the last quarter century.

He made a point though: that this selection of treatments may be relegating MS from the province of a general neurologist to that of the fellowship-trained MS subspecialist.

Not that that is such a bad thing, as MS is a very challenging disease. But the point is well taken. As treatments become increasingly complicated, and numerous, it becomes harder to know which one is best. Most of us likely choose orals first and monoclonal antibodies second, but the question of “which one?” arises for each category. They each have their own risks, side effects, initiation protocols, and peculiarities. In a disease of heterogeneous presentations and courses, there are no clear data on which agent to start first for what patient type. To a general neurologist, also juggling migraines, strokes, Parkinson’s disease, dementia, and neuropathy (and many other disorders) in the course of a day, it becomes tricky to keep up on such.

At some point do general neurologists become a victim of this success? Maybe, but probably not. Just as there are more general practitioners than neurologists, there are more general neurologists than MS subspecialists. Their knowledge and training should be reserved for those patients not responding to our first- (and second-) line treatments, presentations that are atypical, and more complex issues outside the scope of those of us practicing whatever-comes-to-the-door neurology.

It would, however, be nice to have a good consensus on how to best use this array of treatments. Solid guidelines, breaking disease subtypes and treatments down by patient types, drugs, and mechanisms of action, would help those of us on the neurology frontlines to better care for those who need us.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

In 1993 I graduated from medical school. That same year Betaseron (interferon beta-1b) came to market as the first treatment specifically approved for multiple sclerosis (MS). This was a groundbreaker at the time, as there’d been little besides steroids and other potent immunosuppressants to try. Now we had a real drug to offer patients.

The demand for Betaseron was huge, so much so that a lottery system was used to determine which patients would get it first, as there simply wasn’t enough to go around. In the next several years a few more agents jumped into the ring – Avonex (interferon beta-1a), Copaxone (glatiramer acetate), Novantrone (mitoxantrone), and Rebif (interferon beta-1a) – before things went quiet for a while.

In 2006 the first monoclonal antibody for MS – Tysabri (natalizumab) – came out, then almost just as quickly vanished again, not returning until 2009.

Since then we’ve had a gradual explosion of new treatments for MS – like watching kernels become popcorn – first one, then two, then a deluge filling up the basket.

So here we are, approaching the end of 2020, with a remarkable collection of monoclonal antibodies, S1P modulators, fumarates, immunosuppressants, and one symptomatic treatment, many of which weren’t even imagined in 1993. Not to mention the original ABCR (Avonex, Betaseron, Copaxone, Rebif) agents, though they’re riding into the sunset.

A friend and I were talking about this remarkable success story. MS certainly hasn’t been cured, but its treatments have had a dramatic improvement in efficacy over the last quarter century.

He made a point though: that this selection of treatments may be relegating MS from the province of a general neurologist to that of the fellowship-trained MS subspecialist.

Not that that is such a bad thing, as MS is a very challenging disease. But the point is well taken. As treatments become increasingly complicated, and numerous, it becomes harder to know which one is best. Most of us likely choose orals first and monoclonal antibodies second, but the question of “which one?” arises for each category. They each have their own risks, side effects, initiation protocols, and peculiarities. In a disease of heterogeneous presentations and courses, there are no clear data on which agent to start first for what patient type. To a general neurologist, also juggling migraines, strokes, Parkinson’s disease, dementia, and neuropathy (and many other disorders) in the course of a day, it becomes tricky to keep up on such.

At some point do general neurologists become a victim of this success? Maybe, but probably not. Just as there are more general practitioners than neurologists, there are more general neurologists than MS subspecialists. Their knowledge and training should be reserved for those patients not responding to our first- (and second-) line treatments, presentations that are atypical, and more complex issues outside the scope of those of us practicing whatever-comes-to-the-door neurology.

It would, however, be nice to have a good consensus on how to best use this array of treatments. Solid guidelines, breaking disease subtypes and treatments down by patient types, drugs, and mechanisms of action, would help those of us on the neurology frontlines to better care for those who need us.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

Key clinical point: Fingolimod is superior to glatiramer acetate in reducing the relapse rates for relapsing-remitting multiple sclerosis (RRMS), and 0.5 mg is the optimal dose.

Major finding: Fingolimod 0.5 mg vs. glatiramer acetate treatment showed a 40.7% relative reduction in annualized relapse rate (P = .01). No statistically significant difference was seen with fingolimod 0.25 mg vs. glatiramer acetate (14.6% reduction in annualized relapse rate; P = .42).

Study details: Phase 3b ASSESS trial: Patients with RRMS were randomly assigned to fingolimod 0.5 mg (n = 352), fingolimod 0.25 mg (n = 370), or to glatiramer acetate 20 mg (n = 342) groups for 12 months.

Disclosures: The study was funded by Novartis Pharma AG, Basel, Switzerland. The authors reported ties with various pharmaceutical companies, including Novartis.

Citation: Cree BAC et al. JAMA Neurol. 2020 Aug 24. doi: 10.1001/jamaneurol.2020.2950

Key clinical point: Fingolimod is superior to glatiramer acetate in reducing the relapse rates for relapsing-remitting multiple sclerosis (RRMS), and 0.5 mg is the optimal dose.

Major finding: Fingolimod 0.5 mg vs. glatiramer acetate treatment showed a 40.7% relative reduction in annualized relapse rate (P = .01). No statistically significant difference was seen with fingolimod 0.25 mg vs. glatiramer acetate (14.6% reduction in annualized relapse rate; P = .42).

Study details: Phase 3b ASSESS trial: Patients with RRMS were randomly assigned to fingolimod 0.5 mg (n = 352), fingolimod 0.25 mg (n = 370), or to glatiramer acetate 20 mg (n = 342) groups for 12 months.

Disclosures: The study was funded by Novartis Pharma AG, Basel, Switzerland. The authors reported ties with various pharmaceutical companies, including Novartis.

Citation: Cree BAC et al. JAMA Neurol. 2020 Aug 24. doi: 10.1001/jamaneurol.2020.2950

Key clinical point: Fingolimod is superior to glatiramer acetate in reducing the relapse rates for relapsing-remitting multiple sclerosis (RRMS), and 0.5 mg is the optimal dose.

Major finding: Fingolimod 0.5 mg vs. glatiramer acetate treatment showed a 40.7% relative reduction in annualized relapse rate (P = .01). No statistically significant difference was seen with fingolimod 0.25 mg vs. glatiramer acetate (14.6% reduction in annualized relapse rate; P = .42).

Study details: Phase 3b ASSESS trial: Patients with RRMS were randomly assigned to fingolimod 0.5 mg (n = 352), fingolimod 0.25 mg (n = 370), or to glatiramer acetate 20 mg (n = 342) groups for 12 months.

Disclosures: The study was funded by Novartis Pharma AG, Basel, Switzerland. The authors reported ties with various pharmaceutical companies, including Novartis.

Citation: Cree BAC et al. JAMA Neurol. 2020 Aug 24. doi: 10.1001/jamaneurol.2020.2950

Key clinical point: This meta-analysis suggests that the risk for cancer in patients with multiple sclerosis (MS) is less than the general population.

Major finding: The pooled relative risk (RR) of developing cancer was estimated as 0.83 (P less than .001), which shows that risk for cancer was 17% less in patients with MS than the general population. The RR of developing cancer in MS individuals differed between studies ranging from 0.7 to 1.67.

Study details: A systematic review and meta-analysis of 5 studies.

Disclosures: The study received no funding. The authors declared no conflicts of interest.

Citation: Ghajarzadeh M et al. Autoimmun Rev. 2020 Aug 13. doi: 10.1016/j.autrev.2020.102650.

Key clinical point: This meta-analysis suggests that the risk for cancer in patients with multiple sclerosis (MS) is less than the general population.

Major finding: The pooled relative risk (RR) of developing cancer was estimated as 0.83 (P less than .001), which shows that risk for cancer was 17% less in patients with MS than the general population. The RR of developing cancer in MS individuals differed between studies ranging from 0.7 to 1.67.

Study details: A systematic review and meta-analysis of 5 studies.

Disclosures: The study received no funding. The authors declared no conflicts of interest.

Citation: Ghajarzadeh M et al. Autoimmun Rev. 2020 Aug 13. doi: 10.1016/j.autrev.2020.102650.

Key clinical point: This meta-analysis suggests that the risk for cancer in patients with multiple sclerosis (MS) is less than the general population.

Major finding: The pooled relative risk (RR) of developing cancer was estimated as 0.83 (P less than .001), which shows that risk for cancer was 17% less in patients with MS than the general population. The RR of developing cancer in MS individuals differed between studies ranging from 0.7 to 1.67.

Study details: A systematic review and meta-analysis of 5 studies.

Disclosures: The study received no funding. The authors declared no conflicts of interest.

Citation: Ghajarzadeh M et al. Autoimmun Rev. 2020 Aug 13. doi: 10.1016/j.autrev.2020.102650.

Key clinical point: Cladribine tablets had lower annualized relapse rate (ARR) vs. interferon, glatiramer acetate, and dimethyl fumarate for relapsing-remitting multiple sclerosis (RRMS) in the first 2 years; a similar ARR vs. fingolimod; and a higher ARR vs. natalizumab.

Major finding: Cladribine demonstrated significantly lower ARR vs. interferon (relapse ratio [RR], 0.48; P less than .001), glatiramer acetate (RR, 0.49; P less than .001), and dimethyl fumarate (RR, 0.6; P = .001). No significant differences in ARR were observed when compared with fingolimod (RR = 0.74; P = .24), whereas higher ARR was observed vs. natalizumab (RR, 2.13; P = .014).

Study details: This study compared the efficacy of cladribine vs. other approved drugs in patients with RRMS by matching randomized controlled trial (CLARITY trial; cladribine tablets vs. placebo; n = 945) to observational data (Italian multicenter database i-MuST; n = 2,204).

Disclosures: The study was sponsored by Merck Serono S.p.A., Rome, Italy; an affiliate of Merck KGaA, Darmstadt, Germany. Dr. Signori had no disclosures. Dr. Visconti is an employee at Merck Serono, Italy, and Dr. Sormani received consulting fees from various pharmaceutical companies including Merck KGaA.

Citation: Signori A et al. Neurol Neuroimmunol Neuroinflamm. 2020 Aug 14. doi: 10.1212/NXI.0000000000000878.

Key clinical point: Cladribine tablets had lower annualized relapse rate (ARR) vs. interferon, glatiramer acetate, and dimethyl fumarate for relapsing-remitting multiple sclerosis (RRMS) in the first 2 years; a similar ARR vs. fingolimod; and a higher ARR vs. natalizumab.

Major finding: Cladribine demonstrated significantly lower ARR vs. interferon (relapse ratio [RR], 0.48; P less than .001), glatiramer acetate (RR, 0.49; P less than .001), and dimethyl fumarate (RR, 0.6; P = .001). No significant differences in ARR were observed when compared with fingolimod (RR = 0.74; P = .24), whereas higher ARR was observed vs. natalizumab (RR, 2.13; P = .014).

Study details: This study compared the efficacy of cladribine vs. other approved drugs in patients with RRMS by matching randomized controlled trial (CLARITY trial; cladribine tablets vs. placebo; n = 945) to observational data (Italian multicenter database i-MuST; n = 2,204).

Disclosures: The study was sponsored by Merck Serono S.p.A., Rome, Italy; an affiliate of Merck KGaA, Darmstadt, Germany. Dr. Signori had no disclosures. Dr. Visconti is an employee at Merck Serono, Italy, and Dr. Sormani received consulting fees from various pharmaceutical companies including Merck KGaA.

Citation: Signori A et al. Neurol Neuroimmunol Neuroinflamm. 2020 Aug 14. doi: 10.1212/NXI.0000000000000878.

Key clinical point: Cladribine tablets had lower annualized relapse rate (ARR) vs. interferon, glatiramer acetate, and dimethyl fumarate for relapsing-remitting multiple sclerosis (RRMS) in the first 2 years; a similar ARR vs. fingolimod; and a higher ARR vs. natalizumab.

Major finding: Cladribine demonstrated significantly lower ARR vs. interferon (relapse ratio [RR], 0.48; P less than .001), glatiramer acetate (RR, 0.49; P less than .001), and dimethyl fumarate (RR, 0.6; P = .001). No significant differences in ARR were observed when compared with fingolimod (RR = 0.74; P = .24), whereas higher ARR was observed vs. natalizumab (RR, 2.13; P = .014).

Study details: This study compared the efficacy of cladribine vs. other approved drugs in patients with RRMS by matching randomized controlled trial (CLARITY trial; cladribine tablets vs. placebo; n = 945) to observational data (Italian multicenter database i-MuST; n = 2,204).

Disclosures: The study was sponsored by Merck Serono S.p.A., Rome, Italy; an affiliate of Merck KGaA, Darmstadt, Germany. Dr. Signori had no disclosures. Dr. Visconti is an employee at Merck Serono, Italy, and Dr. Sormani received consulting fees from various pharmaceutical companies including Merck KGaA.

Citation: Signori A et al. Neurol Neuroimmunol Neuroinflamm. 2020 Aug 14. doi: 10.1212/NXI.0000000000000878.