Multiple Sclerosis Hub

When it comes to SARS-CoV-2 infection among patients with multiple sclerosis (MS), disease-modifying therapies (DMTs) seem to have varying effects on risk of worse outcomes, according to a new analysis of an Italian cohort of patients with MS. The study confirmed that steroid exposure in the month before COVID-19 symptom onset is tied to more severe disease, and anti-CD20 therapy poses similar risks. But the researchers noted that interferon and possibly teriflunomide were associated with a protective effect in the multivariate analysis.

Maria Pia Sormani, PhD, who is a professor of biostatistics at the University of Genoa, presented the study at the 2021 annual meeting of the American Academy of Neurology.

The results confirm some previous analyses, and add to the body of evidence clinicians rely on, according to Jiwon Oh, MD, PhD, who moderated the session. “These data about the risk with the anti-CD20 therapies have been around for a while, but it seems that risk is pretty apparent, with this registry and other registries around the world. It affects counseling to patients on anti-CD20 therapies. We would counsel them to be cautious, obviously, follow public health precautions, but maybe be even more cautious. It affects our recommendations about the urgency of vaccination in these folks, how high priority they should be,” Dr. Oh said in an interview. She is the clinical director of the Barlo MS Center at St. Michael’s Unity Health in Toronto.

The analysis also hinted at complexities within demographics that might help explain some of the differing outcomes of infections. “We have learned that the course of the viral infection per se may not be the cause of severe outcomes, but the exaggerated inflammatory response to the virus is mainly responsible for intubations and deaths. The hypothesis we are investigating is whether anti-CD20 therapies can cause a more severe viral infection (that is something already known for other viral infections) but do not play a crucial role in causing the explosion of the inflammatory process,” said Dr. Sormani in an email.

The group plans to look at the risk of anti-CD20 therapies in different age groups, “to try to understand the underlying mechanism through which anti-CD20 increases the risk of more severe outcome,” she said.

Dr. Sormani presented an analysis of 3,274 patients with MS who contracted COVID-19 in Italy. The mean age was 44, the median Expanded Disability Status Scale (EDSS) score was 2, Among the study cohort, 68.6% were female; 14% had progressive MS and 26 patients died. Patients who died had a mean age of 63, 48% were female, 73% had progressive MS, and 50% were not on any DMT.

The researchers used ordinal logistic regression that “orders” outcome on a severity scale of 0 (mild disease, no pneumonia or hospitalization), 1 (pneumonia or hospitalization, n = 184), or 2 (ICU admission or death, n = 36). They calculated the odds ratio of moving from 0 to 1, or 1 to 2, and carried the assumption that the risk is the same. For example, an odds ratio of 2 for males versus females would mean that males are twice as likely to be hospitalized and twice as likely to go from being hospitalized to going to the ICU or dying.

The researchers found that older age, male sex, and comorbidities increase risk of worse COVID-19 outcomes. Exposure to methylprednisolone 1 month before COVID-19 symptom onset carried an increased risk (OR, 2.33; P = .03). Compared with no therapy, receiving interferon was associated with lower risk (OR, 0.34; P = .009) and teriflunomide trended towards an association with better outcomes (OR, 0.49; P = .054). Anti-CD20 treatment (ocrelizumab or rituximab) was linked to worse outcomes (OR, 1.89; P = .012) overall, which held up when ocrelizumab (OR, 1.71; P = .04) and rituximab (OR, 2.77; P = .03) were considered separately.

To understand why the risk of ocrelizumab might be lower, the researchers examined risk by duration of anti-CD20 treatment, and found that risk increased with increased duration of treatment, with the lowest risk at treatment duration less than 6 months (OR, 1.56; 95% CI, 0.65-3.77; not significant), followed by 6 months to 1 year (OR, 1.68; 95% CI, 0.69-4.03; P < .001), 1-2 years (OR, 1.74; 95% CI, 0.83-3.64; trend), and the highest risk at more than 2 years (OR, 2.75; 95% CI, 1.28-5.88).

Dr. Sormani suggested that the greater risk associated with rituximab may be because of a tendency towards longer treatment length, since patients treated with rituximab were more often treated for greater lengths of time; 11% had been treated for 6 months or less (vs. 24% of ocrelizumab patients); 26%, 6-12 months (vs. 18% ocrelizumab); 19%, 1-2 years (vs. 37% ocrelizumab); and 44%, 2 years or longer (vs. 21% ocrelizumab).

Dr. Sormani has received consulting fees from Biogen, GeNeuro, Genzyme, MedDay, Merck KGaA, Novartis, Roche, and Immunic. The platform for data collection was donated by Merck. Dr. Oh has consulted for Roche, Celgene, Biogen-Idec, EMD-Serono, Sanofi-Genzyme, Novartis, Alexion. She has been on a scientific advisory or data safety monitoring board for Roche, Biogen-Idec, and Sanofi-Genzyme.

When it comes to SARS-CoV-2 infection among patients with multiple sclerosis (MS), disease-modifying therapies (DMTs) seem to have varying effects on risk of worse outcomes, according to a new analysis of an Italian cohort of patients with MS. The study confirmed that steroid exposure in the month before COVID-19 symptom onset is tied to more severe disease, and anti-CD20 therapy poses similar risks. But the researchers noted that interferon and possibly teriflunomide were associated with a protective effect in the multivariate analysis.

Maria Pia Sormani, PhD, who is a professor of biostatistics at the University of Genoa, presented the study at the 2021 annual meeting of the American Academy of Neurology.

The results confirm some previous analyses, and add to the body of evidence clinicians rely on, according to Jiwon Oh, MD, PhD, who moderated the session. “These data about the risk with the anti-CD20 therapies have been around for a while, but it seems that risk is pretty apparent, with this registry and other registries around the world. It affects counseling to patients on anti-CD20 therapies. We would counsel them to be cautious, obviously, follow public health precautions, but maybe be even more cautious. It affects our recommendations about the urgency of vaccination in these folks, how high priority they should be,” Dr. Oh said in an interview. She is the clinical director of the Barlo MS Center at St. Michael’s Unity Health in Toronto.

The analysis also hinted at complexities within demographics that might help explain some of the differing outcomes of infections. “We have learned that the course of the viral infection per se may not be the cause of severe outcomes, but the exaggerated inflammatory response to the virus is mainly responsible for intubations and deaths. The hypothesis we are investigating is whether anti-CD20 therapies can cause a more severe viral infection (that is something already known for other viral infections) but do not play a crucial role in causing the explosion of the inflammatory process,” said Dr. Sormani in an email.

The group plans to look at the risk of anti-CD20 therapies in different age groups, “to try to understand the underlying mechanism through which anti-CD20 increases the risk of more severe outcome,” she said.

Dr. Sormani presented an analysis of 3,274 patients with MS who contracted COVID-19 in Italy. The mean age was 44, the median Expanded Disability Status Scale (EDSS) score was 2, Among the study cohort, 68.6% were female; 14% had progressive MS and 26 patients died. Patients who died had a mean age of 63, 48% were female, 73% had progressive MS, and 50% were not on any DMT.

The researchers used ordinal logistic regression that “orders” outcome on a severity scale of 0 (mild disease, no pneumonia or hospitalization), 1 (pneumonia or hospitalization, n = 184), or 2 (ICU admission or death, n = 36). They calculated the odds ratio of moving from 0 to 1, or 1 to 2, and carried the assumption that the risk is the same. For example, an odds ratio of 2 for males versus females would mean that males are twice as likely to be hospitalized and twice as likely to go from being hospitalized to going to the ICU or dying.

The researchers found that older age, male sex, and comorbidities increase risk of worse COVID-19 outcomes. Exposure to methylprednisolone 1 month before COVID-19 symptom onset carried an increased risk (OR, 2.33; P = .03). Compared with no therapy, receiving interferon was associated with lower risk (OR, 0.34; P = .009) and teriflunomide trended towards an association with better outcomes (OR, 0.49; P = .054). Anti-CD20 treatment (ocrelizumab or rituximab) was linked to worse outcomes (OR, 1.89; P = .012) overall, which held up when ocrelizumab (OR, 1.71; P = .04) and rituximab (OR, 2.77; P = .03) were considered separately.

To understand why the risk of ocrelizumab might be lower, the researchers examined risk by duration of anti-CD20 treatment, and found that risk increased with increased duration of treatment, with the lowest risk at treatment duration less than 6 months (OR, 1.56; 95% CI, 0.65-3.77; not significant), followed by 6 months to 1 year (OR, 1.68; 95% CI, 0.69-4.03; P < .001), 1-2 years (OR, 1.74; 95% CI, 0.83-3.64; trend), and the highest risk at more than 2 years (OR, 2.75; 95% CI, 1.28-5.88).

Dr. Sormani suggested that the greater risk associated with rituximab may be because of a tendency towards longer treatment length, since patients treated with rituximab were more often treated for greater lengths of time; 11% had been treated for 6 months or less (vs. 24% of ocrelizumab patients); 26%, 6-12 months (vs. 18% ocrelizumab); 19%, 1-2 years (vs. 37% ocrelizumab); and 44%, 2 years or longer (vs. 21% ocrelizumab).

Dr. Sormani has received consulting fees from Biogen, GeNeuro, Genzyme, MedDay, Merck KGaA, Novartis, Roche, and Immunic. The platform for data collection was donated by Merck. Dr. Oh has consulted for Roche, Celgene, Biogen-Idec, EMD-Serono, Sanofi-Genzyme, Novartis, Alexion. She has been on a scientific advisory or data safety monitoring board for Roche, Biogen-Idec, and Sanofi-Genzyme.

When it comes to SARS-CoV-2 infection among patients with multiple sclerosis (MS), disease-modifying therapies (DMTs) seem to have varying effects on risk of worse outcomes, according to a new analysis of an Italian cohort of patients with MS. The study confirmed that steroid exposure in the month before COVID-19 symptom onset is tied to more severe disease, and anti-CD20 therapy poses similar risks. But the researchers noted that interferon and possibly teriflunomide were associated with a protective effect in the multivariate analysis.

Maria Pia Sormani, PhD, who is a professor of biostatistics at the University of Genoa, presented the study at the 2021 annual meeting of the American Academy of Neurology.

The results confirm some previous analyses, and add to the body of evidence clinicians rely on, according to Jiwon Oh, MD, PhD, who moderated the session. “These data about the risk with the anti-CD20 therapies have been around for a while, but it seems that risk is pretty apparent, with this registry and other registries around the world. It affects counseling to patients on anti-CD20 therapies. We would counsel them to be cautious, obviously, follow public health precautions, but maybe be even more cautious. It affects our recommendations about the urgency of vaccination in these folks, how high priority they should be,” Dr. Oh said in an interview. She is the clinical director of the Barlo MS Center at St. Michael’s Unity Health in Toronto.

The analysis also hinted at complexities within demographics that might help explain some of the differing outcomes of infections. “We have learned that the course of the viral infection per se may not be the cause of severe outcomes, but the exaggerated inflammatory response to the virus is mainly responsible for intubations and deaths. The hypothesis we are investigating is whether anti-CD20 therapies can cause a more severe viral infection (that is something already known for other viral infections) but do not play a crucial role in causing the explosion of the inflammatory process,” said Dr. Sormani in an email.

The group plans to look at the risk of anti-CD20 therapies in different age groups, “to try to understand the underlying mechanism through which anti-CD20 increases the risk of more severe outcome,” she said.

Dr. Sormani presented an analysis of 3,274 patients with MS who contracted COVID-19 in Italy. The mean age was 44, the median Expanded Disability Status Scale (EDSS) score was 2, Among the study cohort, 68.6% were female; 14% had progressive MS and 26 patients died. Patients who died had a mean age of 63, 48% were female, 73% had progressive MS, and 50% were not on any DMT.

The researchers used ordinal logistic regression that “orders” outcome on a severity scale of 0 (mild disease, no pneumonia or hospitalization), 1 (pneumonia or hospitalization, n = 184), or 2 (ICU admission or death, n = 36). They calculated the odds ratio of moving from 0 to 1, or 1 to 2, and carried the assumption that the risk is the same. For example, an odds ratio of 2 for males versus females would mean that males are twice as likely to be hospitalized and twice as likely to go from being hospitalized to going to the ICU or dying.

The researchers found that older age, male sex, and comorbidities increase risk of worse COVID-19 outcomes. Exposure to methylprednisolone 1 month before COVID-19 symptom onset carried an increased risk (OR, 2.33; P = .03). Compared with no therapy, receiving interferon was associated with lower risk (OR, 0.34; P = .009) and teriflunomide trended towards an association with better outcomes (OR, 0.49; P = .054). Anti-CD20 treatment (ocrelizumab or rituximab) was linked to worse outcomes (OR, 1.89; P = .012) overall, which held up when ocrelizumab (OR, 1.71; P = .04) and rituximab (OR, 2.77; P = .03) were considered separately.

To understand why the risk of ocrelizumab might be lower, the researchers examined risk by duration of anti-CD20 treatment, and found that risk increased with increased duration of treatment, with the lowest risk at treatment duration less than 6 months (OR, 1.56; 95% CI, 0.65-3.77; not significant), followed by 6 months to 1 year (OR, 1.68; 95% CI, 0.69-4.03; P < .001), 1-2 years (OR, 1.74; 95% CI, 0.83-3.64; trend), and the highest risk at more than 2 years (OR, 2.75; 95% CI, 1.28-5.88).

Dr. Sormani suggested that the greater risk associated with rituximab may be because of a tendency towards longer treatment length, since patients treated with rituximab were more often treated for greater lengths of time; 11% had been treated for 6 months or less (vs. 24% of ocrelizumab patients); 26%, 6-12 months (vs. 18% ocrelizumab); 19%, 1-2 years (vs. 37% ocrelizumab); and 44%, 2 years or longer (vs. 21% ocrelizumab).

Dr. Sormani has received consulting fees from Biogen, GeNeuro, Genzyme, MedDay, Merck KGaA, Novartis, Roche, and Immunic. The platform for data collection was donated by Merck. Dr. Oh has consulted for Roche, Celgene, Biogen-Idec, EMD-Serono, Sanofi-Genzyme, Novartis, Alexion. She has been on a scientific advisory or data safety monitoring board for Roche, Biogen-Idec, and Sanofi-Genzyme.

Oral evobrutinib, an investigational highly selective Bruton’s tyrosine kinase inhibitor, may have a beneficial effect on reducing nerve damage in multiple sclerosis (MS), based on how it’s been found to lower levels of a key blood biomarker, according to a post hoc analysis of a placebo-controlled clinical trial reported at the American Academy of Neurology’s 2021 annual meeting.

Jens Kuhle, MD, of the department of biomedicine at University Hospital Basel, Switzerland, said the conclusion was based on reductions in blood levels of neurofilament light chain (NfL), a biomarker of neuroaxonal damage, in treated patients. “These data on the effect of evobrutinib on NfL dynamics are the first to be reported for a BTK inhibitor investigated for MS,” Dr. Kuhle said. Evobrutinib targets beta cells and myeloid cells, including macrophages and microglia, to disrupt NfL production.

The analysis consisted of three treatment arms in addition to the placebo arm: 25 and 75 mg daily, and 75 mg twice daily. The post hoc analysis included 166 patients across all arms, with 148 being evaluated at week 24.

Dr. Kuhle said the 75-mg twice-daily group exhibited significantly lower blood NfL levels as early as week 12 with lowered levels maintained to week 24, the last time point the study evaluated – specifically reductions of 18.9% (P = .01) and 16.8% (P = .040) compared with placebo, respectively.

However, the 75-mg once daily dose also showed meaningful reductions when compared with placebo: 15.4% (P = .043) and 14.1% (P = .10) at 12 and 24 weeks, respectively, Dr. Kuhle said. “There were no significant differences seen with the 25-mg once-daily group,” he said.

“These results are promising and indicate evobrutinib at an efficacious dose of 75 mg twice daily has a beneficial effect on reducing neuroaxonal damage in MS,” he said.

In an interview, Dr. Kuhle explained the importance of lower NfL levels. “The hope is that detecting subclinical disease activity in a sensitive and comprehensive way will lead to more effective treatment of the individual MS patient,” he said.

The findings may also inform future studies of evobrutinib in MS, he said. “Neurofilaments and neurons are the key substrate of permanent disability in MS and other neurodegenerative diseases,” Dr. Kuhle said. “It is anticipated that normalization of NfL to levels in same-age healthy controls should be the adequate treatment target for individual patients.”

NfL could be an “easily accessible and modifiable biomarker” for use in clinical trials of relapsing and progressive MS, he said. The researchers plan to use NfL measurements in the extension phase of the trial.

“An important next step is the development of reliable and age-adjusted reference values for NfL measurements in blood to move this biomarker further toward individual application in clinical practice,” he added, noting that his group has already collected more than 10,000 serum samples from more than 5,000 healthy controls to do that.

The analysis adds to the growing body of evidence supporting the use of blood NfL levels to gauge the effectiveness of disease-modifying therapies on neuroaxonal degeneration in MS, said Fredrik Piehl, MD, PhD, a professor at Karolinska University Hospital in Stockholm.

Oral evobrutinib, an investigational highly selective Bruton’s tyrosine kinase inhibitor, may have a beneficial effect on reducing nerve damage in multiple sclerosis (MS), based on how it’s been found to lower levels of a key blood biomarker, according to a post hoc analysis of a placebo-controlled clinical trial reported at the American Academy of Neurology’s 2021 annual meeting.

Jens Kuhle, MD, of the department of biomedicine at University Hospital Basel, Switzerland, said the conclusion was based on reductions in blood levels of neurofilament light chain (NfL), a biomarker of neuroaxonal damage, in treated patients. “These data on the effect of evobrutinib on NfL dynamics are the first to be reported for a BTK inhibitor investigated for MS,” Dr. Kuhle said. Evobrutinib targets beta cells and myeloid cells, including macrophages and microglia, to disrupt NfL production.

The analysis consisted of three treatment arms in addition to the placebo arm: 25 and 75 mg daily, and 75 mg twice daily. The post hoc analysis included 166 patients across all arms, with 148 being evaluated at week 24.

Dr. Kuhle said the 75-mg twice-daily group exhibited significantly lower blood NfL levels as early as week 12 with lowered levels maintained to week 24, the last time point the study evaluated – specifically reductions of 18.9% (P = .01) and 16.8% (P = .040) compared with placebo, respectively.

However, the 75-mg once daily dose also showed meaningful reductions when compared with placebo: 15.4% (P = .043) and 14.1% (P = .10) at 12 and 24 weeks, respectively, Dr. Kuhle said. “There were no significant differences seen with the 25-mg once-daily group,” he said.

“These results are promising and indicate evobrutinib at an efficacious dose of 75 mg twice daily has a beneficial effect on reducing neuroaxonal damage in MS,” he said.

In an interview, Dr. Kuhle explained the importance of lower NfL levels. “The hope is that detecting subclinical disease activity in a sensitive and comprehensive way will lead to more effective treatment of the individual MS patient,” he said.

The findings may also inform future studies of evobrutinib in MS, he said. “Neurofilaments and neurons are the key substrate of permanent disability in MS and other neurodegenerative diseases,” Dr. Kuhle said. “It is anticipated that normalization of NfL to levels in same-age healthy controls should be the adequate treatment target for individual patients.”

NfL could be an “easily accessible and modifiable biomarker” for use in clinical trials of relapsing and progressive MS, he said. The researchers plan to use NfL measurements in the extension phase of the trial.

“An important next step is the development of reliable and age-adjusted reference values for NfL measurements in blood to move this biomarker further toward individual application in clinical practice,” he added, noting that his group has already collected more than 10,000 serum samples from more than 5,000 healthy controls to do that.

The analysis adds to the growing body of evidence supporting the use of blood NfL levels to gauge the effectiveness of disease-modifying therapies on neuroaxonal degeneration in MS, said Fredrik Piehl, MD, PhD, a professor at Karolinska University Hospital in Stockholm.

Oral evobrutinib, an investigational highly selective Bruton’s tyrosine kinase inhibitor, may have a beneficial effect on reducing nerve damage in multiple sclerosis (MS), based on how it’s been found to lower levels of a key blood biomarker, according to a post hoc analysis of a placebo-controlled clinical trial reported at the American Academy of Neurology’s 2021 annual meeting.

Jens Kuhle, MD, of the department of biomedicine at University Hospital Basel, Switzerland, said the conclusion was based on reductions in blood levels of neurofilament light chain (NfL), a biomarker of neuroaxonal damage, in treated patients. “These data on the effect of evobrutinib on NfL dynamics are the first to be reported for a BTK inhibitor investigated for MS,” Dr. Kuhle said. Evobrutinib targets beta cells and myeloid cells, including macrophages and microglia, to disrupt NfL production.

The analysis consisted of three treatment arms in addition to the placebo arm: 25 and 75 mg daily, and 75 mg twice daily. The post hoc analysis included 166 patients across all arms, with 148 being evaluated at week 24.

Dr. Kuhle said the 75-mg twice-daily group exhibited significantly lower blood NfL levels as early as week 12 with lowered levels maintained to week 24, the last time point the study evaluated – specifically reductions of 18.9% (P = .01) and 16.8% (P = .040) compared with placebo, respectively.

However, the 75-mg once daily dose also showed meaningful reductions when compared with placebo: 15.4% (P = .043) and 14.1% (P = .10) at 12 and 24 weeks, respectively, Dr. Kuhle said. “There were no significant differences seen with the 25-mg once-daily group,” he said.

“These results are promising and indicate evobrutinib at an efficacious dose of 75 mg twice daily has a beneficial effect on reducing neuroaxonal damage in MS,” he said.

In an interview, Dr. Kuhle explained the importance of lower NfL levels. “The hope is that detecting subclinical disease activity in a sensitive and comprehensive way will lead to more effective treatment of the individual MS patient,” he said.

The findings may also inform future studies of evobrutinib in MS, he said. “Neurofilaments and neurons are the key substrate of permanent disability in MS and other neurodegenerative diseases,” Dr. Kuhle said. “It is anticipated that normalization of NfL to levels in same-age healthy controls should be the adequate treatment target for individual patients.”

NfL could be an “easily accessible and modifiable biomarker” for use in clinical trials of relapsing and progressive MS, he said. The researchers plan to use NfL measurements in the extension phase of the trial.

“An important next step is the development of reliable and age-adjusted reference values for NfL measurements in blood to move this biomarker further toward individual application in clinical practice,” he added, noting that his group has already collected more than 10,000 serum samples from more than 5,000 healthy controls to do that.

The analysis adds to the growing body of evidence supporting the use of blood NfL levels to gauge the effectiveness of disease-modifying therapies on neuroaxonal degeneration in MS, said Fredrik Piehl, MD, PhD, a professor at Karolinska University Hospital in Stockholm.

Black patients with multiple sclerosis (MS) or neuromyelitis optica spectrum disorder (NMOSD) may respond differently to common MS treatment compared to their White peers, new research suggests. In a study of almost 200 patients, Black participants with MS or NMOSD showed significantly more rapid B-cell repopulation 6-12 months after receiving anti-CD20 infusion therapy with rituximab or ocrelizumab (Rituxan, Ocrevus, Genentech) than did White participants.

“The results showed that this B-cell targeted therapy wore off more quickly in African Americans,” said study coinvestigator Gregg J. Silverman, MD, a professor at New York University.

He said that, although the study was more observational in design, “over time when people come back to the clinic, it gives you an idea of whether the agent is still working in their bodies.”

Overall, “our findings raise the question of whether the same therapy dose may be equally effective for all people,” coinvestigator Ilya Kister, MD, also from NYU, added in a press release.

Dr. Kister noted that this could have implications for the way Black patients with autoimmune diseases are treated in the future.

The findings were released ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology.
 

More severe disease in Black patients

Anti-CD20 infusion therapy, or B-cell depletion therapy, is commonly used to treat autoimmune diseases, including MS and NMOSD. “While previous research has shown that this type of infusion therapy is effective for people with these diseases, we also know that Black people tend to have more severe courses of MS,” Dr. Kister said.

“We wanted to compare how quickly the B cells came back in Black people and White people after treatment,” he added.

Dr. Silverman noted that he has been “studying this agent in autoimmune disease for many years. And from all the different studies, I don’t think we had the right population to ask this question. Demographics were just reviewed as they were.”

The current study included 168 participants (mean age, 44 years; 71% women) who had a diagnosis of MS (n = 134) or NMOSD (n = 32) or who were considered to have MS or NMOSD (n = 2). In addition, 36% of the participants self-identified as Black or African American, 36% self-identified as White, and 28% self-identified as another race.

Flow cytometry results were available for all patients after undergoing anti-CD20 infusions at the NYU MS Care Center. Cluster analyses were conducted on the following B-cell subsets: CD19, CD20, IgD, and CD27. “B-cell repopulation was defined as any detectable number of CD19+ cells on flow cytometry,” the investigators reported.
 

Clinical implications?

Results showed that 29.8% of the full study group showed B-cell repopulation a mean of 6.8 months after infusion. In those with B-cell repopulation, 80.3% had IgD+/CD27– subsets, 11.6% had IgD–/CD27+, 6.2% had IgD–/CD27–, and 1.8% had IgD+/CD27+. These B-cell subset ratios did not differ significantly between the Black and White participants.

Interestingly, no patients showed B-cell repopulation before 4 months after infusion. From 4 to 6 months after infusion, there were no significant differences between the Black and White participants in terms of frequency of B-cell repopulation (20.8% vs. 17.9%, respectively; P = .79).

However, repopulation was significantly more frequent in the Black patients 6-12 months after infusion (76.2% vs. 33.3%; P = .02).

Overall, the findings “may have implications for clinical management of MS/NMOSD” in Black individuals, the investigators wrote.

“I was impressed by the differences we saw in responses of patients that were self-declaring as African Americans versus those who were Whites,” Dr. Silverman said. However, “as we say in science: it gives us an answer but it raises even more questions, which may well be important for helping us understand how the agent works and how the disease affects different people.”

Still, Dr. Silverman noted that the findings give clinicians using the agent “a signal that they should be very vigilant. It was an observation at one center, but we’re asking our colleagues [at other clinics] to think about being more careful as they review data with their patients.”

He added that future multicenter studies will allow these issues to be assessed more comprehensively. “This was a discovery study; it now needs validation; and maybe the next step would be looking into the mechanism.”

Dr. Silverman pointed out that the Food and Drug Administration–approved label for this type of therapy “allows for somewhat more frequent dosing. So that might be indicated if it’s found that it’s wearing off in an individual. Perhaps they should be treated more frequently?”

“At a minimum, this has raised our vigilance – and we’re interested to see what the feedback will be at the [AAN] meeting,” he added.
 

Real-world data

Commenting on the findings, Eric Klawiter, MD, associate professor of neurology at Harvard Medical School and director of the Multiple Sclerosis and NMO unit at Massachusetts General Hospital, both in Boston, noted that an important study factor was the focus on repopulation to identify specific groups “who may be early repopulators” as it relates to disease activity and disability progression in MS.

“I thought this was a nicely designed study that made good use of real-world data in MS and NMOSD,” added Dr. Klawiter, who was not involved with the research. He pointed out that timing was another interesting aspect of the study. “As we typically use these cell-depleting agents on an ‘every-6-month’ basis, the most pertinent time frame surrounds those that repopulate prior to 6 months.”

If the current study would have shown differences between the Black and White participants at that time point, “I think that would have been most pertinent from a clinical standpoint and a greater opportunity for intervention,” Dr. Klawiter said. “But we saw that, before 4 and 6 months, [the difference] wasn’t significant.”

Still, “after 6 months, the study demonstrates that Black people with MS and NMOSD may repopulate faster,” he added.

“The only real change a clinician could make would be to modify the frequency of the dosing. So if we can identify certain characteristics that would lead you to want to evaluate for the need of redosing sooner, I think that would be useful,” he said.

Specific characteristics identified in previous research include body mass index. “If there are also ethnicity factors, that would be an additional demographic factor that a clinician should pay close attention to,” said Dr. Klawiter.

He noted that his current practice is to check flow cytometry and B-cell counts at the time of a patient’s next infusion. “And if I’m seeing that B-cell levels are repleting at that time point, I am already then making adjustments with their next infusion as to the dosing frequency,” he added.

“This [study] may elucidate some of the potential reasons why we see some people replete their B cells faster than others, but I think additional studies are necessary to make that determination,” Dr. Klawiter concluded.

Genentech provided funding for the study. Dr. Silverman reported no relevant financial relationships. Dr. Klawiter reported having received research funds and consulting fees from Genentech.

A version of this article first appeared on Medscape.com.

Black patients with multiple sclerosis (MS) or neuromyelitis optica spectrum disorder (NMOSD) may respond differently to common MS treatment compared to their White peers, new research suggests. In a study of almost 200 patients, Black participants with MS or NMOSD showed significantly more rapid B-cell repopulation 6-12 months after receiving anti-CD20 infusion therapy with rituximab or ocrelizumab (Rituxan, Ocrevus, Genentech) than did White participants.

“The results showed that this B-cell targeted therapy wore off more quickly in African Americans,” said study coinvestigator Gregg J. Silverman, MD, a professor at New York University.

He said that, although the study was more observational in design, “over time when people come back to the clinic, it gives you an idea of whether the agent is still working in their bodies.”

Overall, “our findings raise the question of whether the same therapy dose may be equally effective for all people,” coinvestigator Ilya Kister, MD, also from NYU, added in a press release.

Dr. Kister noted that this could have implications for the way Black patients with autoimmune diseases are treated in the future.

The findings were released ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology.
 

More severe disease in Black patients

Anti-CD20 infusion therapy, or B-cell depletion therapy, is commonly used to treat autoimmune diseases, including MS and NMOSD. “While previous research has shown that this type of infusion therapy is effective for people with these diseases, we also know that Black people tend to have more severe courses of MS,” Dr. Kister said.

“We wanted to compare how quickly the B cells came back in Black people and White people after treatment,” he added.

Dr. Silverman noted that he has been “studying this agent in autoimmune disease for many years. And from all the different studies, I don’t think we had the right population to ask this question. Demographics were just reviewed as they were.”

The current study included 168 participants (mean age, 44 years; 71% women) who had a diagnosis of MS (n = 134) or NMOSD (n = 32) or who were considered to have MS or NMOSD (n = 2). In addition, 36% of the participants self-identified as Black or African American, 36% self-identified as White, and 28% self-identified as another race.

Flow cytometry results were available for all patients after undergoing anti-CD20 infusions at the NYU MS Care Center. Cluster analyses were conducted on the following B-cell subsets: CD19, CD20, IgD, and CD27. “B-cell repopulation was defined as any detectable number of CD19+ cells on flow cytometry,” the investigators reported.
 

Clinical implications?

Results showed that 29.8% of the full study group showed B-cell repopulation a mean of 6.8 months after infusion. In those with B-cell repopulation, 80.3% had IgD+/CD27– subsets, 11.6% had IgD–/CD27+, 6.2% had IgD–/CD27–, and 1.8% had IgD+/CD27+. These B-cell subset ratios did not differ significantly between the Black and White participants.

Interestingly, no patients showed B-cell repopulation before 4 months after infusion. From 4 to 6 months after infusion, there were no significant differences between the Black and White participants in terms of frequency of B-cell repopulation (20.8% vs. 17.9%, respectively; P = .79).

However, repopulation was significantly more frequent in the Black patients 6-12 months after infusion (76.2% vs. 33.3%; P = .02).

Overall, the findings “may have implications for clinical management of MS/NMOSD” in Black individuals, the investigators wrote.

“I was impressed by the differences we saw in responses of patients that were self-declaring as African Americans versus those who were Whites,” Dr. Silverman said. However, “as we say in science: it gives us an answer but it raises even more questions, which may well be important for helping us understand how the agent works and how the disease affects different people.”

Still, Dr. Silverman noted that the findings give clinicians using the agent “a signal that they should be very vigilant. It was an observation at one center, but we’re asking our colleagues [at other clinics] to think about being more careful as they review data with their patients.”

He added that future multicenter studies will allow these issues to be assessed more comprehensively. “This was a discovery study; it now needs validation; and maybe the next step would be looking into the mechanism.”

Dr. Silverman pointed out that the Food and Drug Administration–approved label for this type of therapy “allows for somewhat more frequent dosing. So that might be indicated if it’s found that it’s wearing off in an individual. Perhaps they should be treated more frequently?”

“At a minimum, this has raised our vigilance – and we’re interested to see what the feedback will be at the [AAN] meeting,” he added.
 

Real-world data

Commenting on the findings, Eric Klawiter, MD, associate professor of neurology at Harvard Medical School and director of the Multiple Sclerosis and NMO unit at Massachusetts General Hospital, both in Boston, noted that an important study factor was the focus on repopulation to identify specific groups “who may be early repopulators” as it relates to disease activity and disability progression in MS.

“I thought this was a nicely designed study that made good use of real-world data in MS and NMOSD,” added Dr. Klawiter, who was not involved with the research. He pointed out that timing was another interesting aspect of the study. “As we typically use these cell-depleting agents on an ‘every-6-month’ basis, the most pertinent time frame surrounds those that repopulate prior to 6 months.”

If the current study would have shown differences between the Black and White participants at that time point, “I think that would have been most pertinent from a clinical standpoint and a greater opportunity for intervention,” Dr. Klawiter said. “But we saw that, before 4 and 6 months, [the difference] wasn’t significant.”

Still, “after 6 months, the study demonstrates that Black people with MS and NMOSD may repopulate faster,” he added.

“The only real change a clinician could make would be to modify the frequency of the dosing. So if we can identify certain characteristics that would lead you to want to evaluate for the need of redosing sooner, I think that would be useful,” he said.

Specific characteristics identified in previous research include body mass index. “If there are also ethnicity factors, that would be an additional demographic factor that a clinician should pay close attention to,” said Dr. Klawiter.

He noted that his current practice is to check flow cytometry and B-cell counts at the time of a patient’s next infusion. “And if I’m seeing that B-cell levels are repleting at that time point, I am already then making adjustments with their next infusion as to the dosing frequency,” he added.

“This [study] may elucidate some of the potential reasons why we see some people replete their B cells faster than others, but I think additional studies are necessary to make that determination,” Dr. Klawiter concluded.

Genentech provided funding for the study. Dr. Silverman reported no relevant financial relationships. Dr. Klawiter reported having received research funds and consulting fees from Genentech.

A version of this article first appeared on Medscape.com.

Black patients with multiple sclerosis (MS) or neuromyelitis optica spectrum disorder (NMOSD) may respond differently to common MS treatment compared to their White peers, new research suggests. In a study of almost 200 patients, Black participants with MS or NMOSD showed significantly more rapid B-cell repopulation 6-12 months after receiving anti-CD20 infusion therapy with rituximab or ocrelizumab (Rituxan, Ocrevus, Genentech) than did White participants.

“The results showed that this B-cell targeted therapy wore off more quickly in African Americans,” said study coinvestigator Gregg J. Silverman, MD, a professor at New York University.

He said that, although the study was more observational in design, “over time when people come back to the clinic, it gives you an idea of whether the agent is still working in their bodies.”

Overall, “our findings raise the question of whether the same therapy dose may be equally effective for all people,” coinvestigator Ilya Kister, MD, also from NYU, added in a press release.

Dr. Kister noted that this could have implications for the way Black patients with autoimmune diseases are treated in the future.

The findings were released ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology.
 

More severe disease in Black patients

Anti-CD20 infusion therapy, or B-cell depletion therapy, is commonly used to treat autoimmune diseases, including MS and NMOSD. “While previous research has shown that this type of infusion therapy is effective for people with these diseases, we also know that Black people tend to have more severe courses of MS,” Dr. Kister said.

“We wanted to compare how quickly the B cells came back in Black people and White people after treatment,” he added.

Dr. Silverman noted that he has been “studying this agent in autoimmune disease for many years. And from all the different studies, I don’t think we had the right population to ask this question. Demographics were just reviewed as they were.”

The current study included 168 participants (mean age, 44 years; 71% women) who had a diagnosis of MS (n = 134) or NMOSD (n = 32) or who were considered to have MS or NMOSD (n = 2). In addition, 36% of the participants self-identified as Black or African American, 36% self-identified as White, and 28% self-identified as another race.

Flow cytometry results were available for all patients after undergoing anti-CD20 infusions at the NYU MS Care Center. Cluster analyses were conducted on the following B-cell subsets: CD19, CD20, IgD, and CD27. “B-cell repopulation was defined as any detectable number of CD19+ cells on flow cytometry,” the investigators reported.
 

Clinical implications?

Results showed that 29.8% of the full study group showed B-cell repopulation a mean of 6.8 months after infusion. In those with B-cell repopulation, 80.3% had IgD+/CD27– subsets, 11.6% had IgD–/CD27+, 6.2% had IgD–/CD27–, and 1.8% had IgD+/CD27+. These B-cell subset ratios did not differ significantly between the Black and White participants.

Interestingly, no patients showed B-cell repopulation before 4 months after infusion. From 4 to 6 months after infusion, there were no significant differences between the Black and White participants in terms of frequency of B-cell repopulation (20.8% vs. 17.9%, respectively; P = .79).

However, repopulation was significantly more frequent in the Black patients 6-12 months after infusion (76.2% vs. 33.3%; P = .02).

Overall, the findings “may have implications for clinical management of MS/NMOSD” in Black individuals, the investigators wrote.

“I was impressed by the differences we saw in responses of patients that were self-declaring as African Americans versus those who were Whites,” Dr. Silverman said. However, “as we say in science: it gives us an answer but it raises even more questions, which may well be important for helping us understand how the agent works and how the disease affects different people.”

Still, Dr. Silverman noted that the findings give clinicians using the agent “a signal that they should be very vigilant. It was an observation at one center, but we’re asking our colleagues [at other clinics] to think about being more careful as they review data with their patients.”

He added that future multicenter studies will allow these issues to be assessed more comprehensively. “This was a discovery study; it now needs validation; and maybe the next step would be looking into the mechanism.”

Dr. Silverman pointed out that the Food and Drug Administration–approved label for this type of therapy “allows for somewhat more frequent dosing. So that might be indicated if it’s found that it’s wearing off in an individual. Perhaps they should be treated more frequently?”

“At a minimum, this has raised our vigilance – and we’re interested to see what the feedback will be at the [AAN] meeting,” he added.
 

Real-world data

Commenting on the findings, Eric Klawiter, MD, associate professor of neurology at Harvard Medical School and director of the Multiple Sclerosis and NMO unit at Massachusetts General Hospital, both in Boston, noted that an important study factor was the focus on repopulation to identify specific groups “who may be early repopulators” as it relates to disease activity and disability progression in MS.

“I thought this was a nicely designed study that made good use of real-world data in MS and NMOSD,” added Dr. Klawiter, who was not involved with the research. He pointed out that timing was another interesting aspect of the study. “As we typically use these cell-depleting agents on an ‘every-6-month’ basis, the most pertinent time frame surrounds those that repopulate prior to 6 months.”

If the current study would have shown differences between the Black and White participants at that time point, “I think that would have been most pertinent from a clinical standpoint and a greater opportunity for intervention,” Dr. Klawiter said. “But we saw that, before 4 and 6 months, [the difference] wasn’t significant.”

Still, “after 6 months, the study demonstrates that Black people with MS and NMOSD may repopulate faster,” he added.

“The only real change a clinician could make would be to modify the frequency of the dosing. So if we can identify certain characteristics that would lead you to want to evaluate for the need of redosing sooner, I think that would be useful,” he said.

Specific characteristics identified in previous research include body mass index. “If there are also ethnicity factors, that would be an additional demographic factor that a clinician should pay close attention to,” said Dr. Klawiter.

He noted that his current practice is to check flow cytometry and B-cell counts at the time of a patient’s next infusion. “And if I’m seeing that B-cell levels are repleting at that time point, I am already then making adjustments with their next infusion as to the dosing frequency,” he added.

“This [study] may elucidate some of the potential reasons why we see some people replete their B cells faster than others, but I think additional studies are necessary to make that determination,” Dr. Klawiter concluded.

Genentech provided funding for the study. Dr. Silverman reported no relevant financial relationships. Dr. Klawiter reported having received research funds and consulting fees from Genentech.

A version of this article first appeared on Medscape.com.

It’s time for a large-scale phase 2 study into whether supplementary estrogen can relieve multiple sclerosis (MS) symptoms in menopausal women with the disease, a neurologist told colleagues at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

This kind of research should explore the effects of aging, including in the brain, and “focus on what is preventable – this dramatic and abrupt loss of estrogen in women with MS,” said Rhonda Voskuhl, MD, of the Brain Research Institute at the University of California, Los Angeles.

“This is a call to action. There’s a huge gap that needs to be filled,” she added in an interview. “Not enough attention has been paid to menopause and cognitive issues in MS and even in healthy women.”

Research has found that many women with MS experience a decline in function during menopause, she said. “They’re having a worsening of their preexisting disabilities,” she noted, due to neurodegeneration.

Dr. Voskuhl highlighted a 2016 study, for instance, that found postmenopausal women with MS on hormone replacement therapy reported better physical function and quality of life than did their counterparts after adjustment for covariates. She also pointed to a 2019 study that concluded that “natural menopause seems to be a turning point to a more progressive phase of MS.”

Estrogen appears to play a significant role. “It’s involved in synaptic plasticity,” she said. “That’s why the disabilities are worsening.”

Dr. Voskuhl supports a year-long, randomized and controlled study of estrogen supplementation in 150-200 participants. The goal, she said, is “not just to prevent loss and bad things from happening but also make improvements.”

In healthy patients, she said, outcomes should include cognitive decline in menopause, cognitive domain outcomes, and region-specific biomarkers in the frontal cortex and hippocampus instead of global cognition and global brain volume. In patients with MS, she said, the focus should be on worsening of disability with emphasis on specific disabilities such as walking and region-specific biomarkers for the motor cortex and spinal cord.

“We need to be looking at cortical gray matter, which we know is responsive to estrogen,” Dr. Voskuhl said. She led a 2018 placebo-controlled study that found women with MS who took estrogen supplements appeared to experience localized sparing of progressive gray matter, which the researchers linked to improved results in cognitive testing. The findings, the study authors wrote, suggest “a clinically relevant, disability-specific biomarker for clinical trials of candidate neuroprotective treatments in MS.”

What about men? Does hormone loss worsen their MS? Dr. Voskuhl said there seems to be a connection between lower levels of testosterone and more disability in men with MS. But their situation is different. Loss of testosterone in men is gradual and happens over decades instead of over the short period of menopause in women, she said.

Jennifer Graves, MD, a neurologist at the University of California, San Diego, agreed that it’s time for further research into estrogen supplementation in MS. As she noted, “we don’t know the exact biological mechanism that might link perimenopause with developing a more progressive type of MS.”

She added: “An overall decrease in estrogen may be at play but there are other biological changes around menopause. We must also take care in studies to try to separate out what might be due to ovarian aging versus other types of aging processes that might be happening at the same time.”

Dr. Voskuhl disclosed that she is an inventor on university patents for use of estriol and estrogen receptor–beta ligands as treatments. Dr. Graves reports no relevant disclosures.

It’s time for a large-scale phase 2 study into whether supplementary estrogen can relieve multiple sclerosis (MS) symptoms in menopausal women with the disease, a neurologist told colleagues at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

This kind of research should explore the effects of aging, including in the brain, and “focus on what is preventable – this dramatic and abrupt loss of estrogen in women with MS,” said Rhonda Voskuhl, MD, of the Brain Research Institute at the University of California, Los Angeles.

“This is a call to action. There’s a huge gap that needs to be filled,” she added in an interview. “Not enough attention has been paid to menopause and cognitive issues in MS and even in healthy women.”

Research has found that many women with MS experience a decline in function during menopause, she said. “They’re having a worsening of their preexisting disabilities,” she noted, due to neurodegeneration.

Dr. Voskuhl highlighted a 2016 study, for instance, that found postmenopausal women with MS on hormone replacement therapy reported better physical function and quality of life than did their counterparts after adjustment for covariates. She also pointed to a 2019 study that concluded that “natural menopause seems to be a turning point to a more progressive phase of MS.”

Estrogen appears to play a significant role. “It’s involved in synaptic plasticity,” she said. “That’s why the disabilities are worsening.”

Dr. Voskuhl supports a year-long, randomized and controlled study of estrogen supplementation in 150-200 participants. The goal, she said, is “not just to prevent loss and bad things from happening but also make improvements.”

In healthy patients, she said, outcomes should include cognitive decline in menopause, cognitive domain outcomes, and region-specific biomarkers in the frontal cortex and hippocampus instead of global cognition and global brain volume. In patients with MS, she said, the focus should be on worsening of disability with emphasis on specific disabilities such as walking and region-specific biomarkers for the motor cortex and spinal cord.

“We need to be looking at cortical gray matter, which we know is responsive to estrogen,” Dr. Voskuhl said. She led a 2018 placebo-controlled study that found women with MS who took estrogen supplements appeared to experience localized sparing of progressive gray matter, which the researchers linked to improved results in cognitive testing. The findings, the study authors wrote, suggest “a clinically relevant, disability-specific biomarker for clinical trials of candidate neuroprotective treatments in MS.”

What about men? Does hormone loss worsen their MS? Dr. Voskuhl said there seems to be a connection between lower levels of testosterone and more disability in men with MS. But their situation is different. Loss of testosterone in men is gradual and happens over decades instead of over the short period of menopause in women, she said.

Jennifer Graves, MD, a neurologist at the University of California, San Diego, agreed that it’s time for further research into estrogen supplementation in MS. As she noted, “we don’t know the exact biological mechanism that might link perimenopause with developing a more progressive type of MS.”

She added: “An overall decrease in estrogen may be at play but there are other biological changes around menopause. We must also take care in studies to try to separate out what might be due to ovarian aging versus other types of aging processes that might be happening at the same time.”

Dr. Voskuhl disclosed that she is an inventor on university patents for use of estriol and estrogen receptor–beta ligands as treatments. Dr. Graves reports no relevant disclosures.

It’s time for a large-scale phase 2 study into whether supplementary estrogen can relieve multiple sclerosis (MS) symptoms in menopausal women with the disease, a neurologist told colleagues at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

This kind of research should explore the effects of aging, including in the brain, and “focus on what is preventable – this dramatic and abrupt loss of estrogen in women with MS,” said Rhonda Voskuhl, MD, of the Brain Research Institute at the University of California, Los Angeles.

“This is a call to action. There’s a huge gap that needs to be filled,” she added in an interview. “Not enough attention has been paid to menopause and cognitive issues in MS and even in healthy women.”

Research has found that many women with MS experience a decline in function during menopause, she said. “They’re having a worsening of their preexisting disabilities,” she noted, due to neurodegeneration.

Dr. Voskuhl highlighted a 2016 study, for instance, that found postmenopausal women with MS on hormone replacement therapy reported better physical function and quality of life than did their counterparts after adjustment for covariates. She also pointed to a 2019 study that concluded that “natural menopause seems to be a turning point to a more progressive phase of MS.”

Estrogen appears to play a significant role. “It’s involved in synaptic plasticity,” she said. “That’s why the disabilities are worsening.”

Dr. Voskuhl supports a year-long, randomized and controlled study of estrogen supplementation in 150-200 participants. The goal, she said, is “not just to prevent loss and bad things from happening but also make improvements.”

In healthy patients, she said, outcomes should include cognitive decline in menopause, cognitive domain outcomes, and region-specific biomarkers in the frontal cortex and hippocampus instead of global cognition and global brain volume. In patients with MS, she said, the focus should be on worsening of disability with emphasis on specific disabilities such as walking and region-specific biomarkers for the motor cortex and spinal cord.

“We need to be looking at cortical gray matter, which we know is responsive to estrogen,” Dr. Voskuhl said. She led a 2018 placebo-controlled study that found women with MS who took estrogen supplements appeared to experience localized sparing of progressive gray matter, which the researchers linked to improved results in cognitive testing. The findings, the study authors wrote, suggest “a clinically relevant, disability-specific biomarker for clinical trials of candidate neuroprotective treatments in MS.”

What about men? Does hormone loss worsen their MS? Dr. Voskuhl said there seems to be a connection between lower levels of testosterone and more disability in men with MS. But their situation is different. Loss of testosterone in men is gradual and happens over decades instead of over the short period of menopause in women, she said.

Jennifer Graves, MD, a neurologist at the University of California, San Diego, agreed that it’s time for further research into estrogen supplementation in MS. As she noted, “we don’t know the exact biological mechanism that might link perimenopause with developing a more progressive type of MS.”

She added: “An overall decrease in estrogen may be at play but there are other biological changes around menopause. We must also take care in studies to try to separate out what might be due to ovarian aging versus other types of aging processes that might be happening at the same time.”

Dr. Voskuhl disclosed that she is an inventor on university patents for use of estriol and estrogen receptor–beta ligands as treatments. Dr. Graves reports no relevant disclosures.

Medicare payments for branded neurologic drugs jumped 50% over a 5-year period, while claims for these medications increased by just 8%, new research shows. Results of the retrospective study also showed that most of the increased costs for these agents were due to rising costs for neuroimmunology drugs, mainly for those used to treat multiple sclerosis (MS).

“The same brand name medication in 2017 cost approximately 50% more than in 2013,” said Adam de Havenon, MD, assistant professor of neurology, University of Utah, Salt Lake City.

“An analogy would be if you bought an iPhone 5 in 2013 for $500, and then in 2017, you were asked to pay $750 for the exact same iPhone 5,” Dr. de Havenon added.

The study findings were published online March 10 in the journal Neurology.
 

$26 billion in payments

Both neurologists and patients are concerned about the high cost of prescription drugs for neurologic diseases, and Medicare Part D data indicate that these drugs are the most expensive component of neurologic care, the researchers noted. In addition, out-of-pocket costs have increased significantly for patients with neurologic disease such as Parkinson’s disease, epilepsy, and MS.

To understand trends in payments for neurologic drugs, Dr. de Havenon and colleagues analyzed Medicare Part D claims filed from 2013 to 2017. The payments include costs paid by Medicare, the patient, government subsidies, and other third-party payers.

In addition to examining more current Medicare Part D data than previous studies, the current analysis examined all medications prescribed by neurologists that consistently remained branded or generic during the 5-year study period, said Dr. de Havenon. This approach resulted in a large number of claims and a large total cost.

To calculate the percentage change in annual payment claims, the researchers used 2013 prices as a reference point. They identified drugs named in 2013 claims and classified them as generic, brand-name only, or brand-name with generic equivalent. Researchers also divided the drugs by neurologic subspecialty.

The analysis included 520 drugs, all of which were available in each year of the study period. Of these drugs, 322 were generic, 61 were brand-name only, and 137 were brand-name with a generic equivalent. There were 90.7 million total claims.

Results showed total payments amounted to $26.65 billion. Yearly total payments increased from $4.05 billion in 2013 to $6.09 billion in 2017, representing a 50.4% increase, even after adjusting for inflation. Total claims increased by 7.6% – from 17.1 million in 2013 to 18.4 million in 2017.

From 2013 to 2017, claim payments increased by 0.6% for generic drugs, 42.4% for brand-name only drugs, and 45% for brand-name drugs with generic equivalents. The proportion of claims increased from 81.9% to 88% for generic drugs and from 4.9% to 6.2% for brand-name only drugs.

However, the proportion of claims for brand-name drugs with generic equivalents decreased from 13.3% to 5.8%.
 

Treatment barrier

Neuroimmunologic drugs, most of which were prescribed for MS, had exceptional cost, the researchers noted. These drugs accounted for more than 50% of payments but only 4.3% of claims. Claim payment for these drugs increased by 46.9% during the study period, from $3,337 to $4,902.

When neuroimmunologic drugs were removed from the analysis there was still significant increase in claim payments for brand-name only drugs (50.4%) and brand-name drugs with generic equivalents (45.6%).

Although neuroimmunologic medicines, including monoclonal antibodies, are more expensive to produce, this factor alone does not explain their exceptional cost, said Dr. de Havenon. “The high cost of brand-name drugs in this speciality is likely because the market bears it,” he added. “In other words, MS is a disabling disease and the medications work, so historically the Centers for Medicare & Medicaid Services have been willing to tolerate the high cost of these primarily brand-name medications.”

Several countries have controlled drug costs by negotiating with pharmaceutical companies and through legislation, Dr. de Havenon noted.

“My intent with this article was to raise awareness on the topic, which I struggle with frequently as a clinician. I know I want my patients to have a medication, but the cost prevents it,” he said.
 

‘Unfettered’ price-setting

Commenting on the findings, Robert J. Fox, MD, vice chair for research at the Neurological Institute of the Cleveland Clinic, said the study “brings into clear light” what neurologists, particularly those who treat MS, have long suspected but did not really know. These neurologists “are typically distanced from the payment aspects of the medications they prescribe,” said Dr. Fox, who was not involved with the research.

Although a particular strength of the study was its comprehensiveness, the researchers excluded infusion claims – which account for a large portion of total patient care costs for many disorders, he noted.

Drugs for MS historically have been expensive, ostensibly because of their high cost of development. In addition, the large and continued price increase that occurs long after these drugs have been approved remains unexplained, said Dr. Fox.

He noted that the study findings might not directly affect clinical practice because neurologists will continue prescribing medications they think are best for their patients. “Instead, I think this is a lesson to lawmakers about the massive error in the Medicare Modernization Act of 2003, where the federal government was prohibited from negotiating drug prices. If the seller is unfettered in setting a price, then no one should be surprised when the price rises,” Dr. Fox said.

Because many new drugs and new generic formulations for treating MS have become available during the past year, “repeating these types of economic studies for the period 2020-2025 will help us understand if generic competition – as well as new laws if they are passed – alter price,” he concluded.

The study was funded by the American Academy of Neurology, which publishes Neurology. Dr. de Havenon has received clinical research funding from AMAG Pharmaceuticals and Regeneron Pharmaceuticals. Dr. Fox receives consulting fees from many pharmaceutical companies involved in the development of therapies for MS.

A version of this article first appeared on Medscape.com.

Medicare payments for branded neurologic drugs jumped 50% over a 5-year period, while claims for these medications increased by just 8%, new research shows. Results of the retrospective study also showed that most of the increased costs for these agents were due to rising costs for neuroimmunology drugs, mainly for those used to treat multiple sclerosis (MS).

“The same brand name medication in 2017 cost approximately 50% more than in 2013,” said Adam de Havenon, MD, assistant professor of neurology, University of Utah, Salt Lake City.

“An analogy would be if you bought an iPhone 5 in 2013 for $500, and then in 2017, you were asked to pay $750 for the exact same iPhone 5,” Dr. de Havenon added.

The study findings were published online March 10 in the journal Neurology.
 

$26 billion in payments

Both neurologists and patients are concerned about the high cost of prescription drugs for neurologic diseases, and Medicare Part D data indicate that these drugs are the most expensive component of neurologic care, the researchers noted. In addition, out-of-pocket costs have increased significantly for patients with neurologic disease such as Parkinson’s disease, epilepsy, and MS.

To understand trends in payments for neurologic drugs, Dr. de Havenon and colleagues analyzed Medicare Part D claims filed from 2013 to 2017. The payments include costs paid by Medicare, the patient, government subsidies, and other third-party payers.

In addition to examining more current Medicare Part D data than previous studies, the current analysis examined all medications prescribed by neurologists that consistently remained branded or generic during the 5-year study period, said Dr. de Havenon. This approach resulted in a large number of claims and a large total cost.

To calculate the percentage change in annual payment claims, the researchers used 2013 prices as a reference point. They identified drugs named in 2013 claims and classified them as generic, brand-name only, or brand-name with generic equivalent. Researchers also divided the drugs by neurologic subspecialty.

The analysis included 520 drugs, all of which were available in each year of the study period. Of these drugs, 322 were generic, 61 were brand-name only, and 137 were brand-name with a generic equivalent. There were 90.7 million total claims.

Results showed total payments amounted to $26.65 billion. Yearly total payments increased from $4.05 billion in 2013 to $6.09 billion in 2017, representing a 50.4% increase, even after adjusting for inflation. Total claims increased by 7.6% – from 17.1 million in 2013 to 18.4 million in 2017.

From 2013 to 2017, claim payments increased by 0.6% for generic drugs, 42.4% for brand-name only drugs, and 45% for brand-name drugs with generic equivalents. The proportion of claims increased from 81.9% to 88% for generic drugs and from 4.9% to 6.2% for brand-name only drugs.

However, the proportion of claims for brand-name drugs with generic equivalents decreased from 13.3% to 5.8%.
 

Treatment barrier

Neuroimmunologic drugs, most of which were prescribed for MS, had exceptional cost, the researchers noted. These drugs accounted for more than 50% of payments but only 4.3% of claims. Claim payment for these drugs increased by 46.9% during the study period, from $3,337 to $4,902.

When neuroimmunologic drugs were removed from the analysis there was still significant increase in claim payments for brand-name only drugs (50.4%) and brand-name drugs with generic equivalents (45.6%).

Although neuroimmunologic medicines, including monoclonal antibodies, are more expensive to produce, this factor alone does not explain their exceptional cost, said Dr. de Havenon. “The high cost of brand-name drugs in this speciality is likely because the market bears it,” he added. “In other words, MS is a disabling disease and the medications work, so historically the Centers for Medicare & Medicaid Services have been willing to tolerate the high cost of these primarily brand-name medications.”

Several countries have controlled drug costs by negotiating with pharmaceutical companies and through legislation, Dr. de Havenon noted.

“My intent with this article was to raise awareness on the topic, which I struggle with frequently as a clinician. I know I want my patients to have a medication, but the cost prevents it,” he said.
 

‘Unfettered’ price-setting

Commenting on the findings, Robert J. Fox, MD, vice chair for research at the Neurological Institute of the Cleveland Clinic, said the study “brings into clear light” what neurologists, particularly those who treat MS, have long suspected but did not really know. These neurologists “are typically distanced from the payment aspects of the medications they prescribe,” said Dr. Fox, who was not involved with the research.

Although a particular strength of the study was its comprehensiveness, the researchers excluded infusion claims – which account for a large portion of total patient care costs for many disorders, he noted.

Drugs for MS historically have been expensive, ostensibly because of their high cost of development. In addition, the large and continued price increase that occurs long after these drugs have been approved remains unexplained, said Dr. Fox.

He noted that the study findings might not directly affect clinical practice because neurologists will continue prescribing medications they think are best for their patients. “Instead, I think this is a lesson to lawmakers about the massive error in the Medicare Modernization Act of 2003, where the federal government was prohibited from negotiating drug prices. If the seller is unfettered in setting a price, then no one should be surprised when the price rises,” Dr. Fox said.

Because many new drugs and new generic formulations for treating MS have become available during the past year, “repeating these types of economic studies for the period 2020-2025 will help us understand if generic competition – as well as new laws if they are passed – alter price,” he concluded.

The study was funded by the American Academy of Neurology, which publishes Neurology. Dr. de Havenon has received clinical research funding from AMAG Pharmaceuticals and Regeneron Pharmaceuticals. Dr. Fox receives consulting fees from many pharmaceutical companies involved in the development of therapies for MS.

A version of this article first appeared on Medscape.com.

Medicare payments for branded neurologic drugs jumped 50% over a 5-year period, while claims for these medications increased by just 8%, new research shows. Results of the retrospective study also showed that most of the increased costs for these agents were due to rising costs for neuroimmunology drugs, mainly for those used to treat multiple sclerosis (MS).

“The same brand name medication in 2017 cost approximately 50% more than in 2013,” said Adam de Havenon, MD, assistant professor of neurology, University of Utah, Salt Lake City.

“An analogy would be if you bought an iPhone 5 in 2013 for $500, and then in 2017, you were asked to pay $750 for the exact same iPhone 5,” Dr. de Havenon added.

The study findings were published online March 10 in the journal Neurology.
 

$26 billion in payments

Both neurologists and patients are concerned about the high cost of prescription drugs for neurologic diseases, and Medicare Part D data indicate that these drugs are the most expensive component of neurologic care, the researchers noted. In addition, out-of-pocket costs have increased significantly for patients with neurologic disease such as Parkinson’s disease, epilepsy, and MS.

To understand trends in payments for neurologic drugs, Dr. de Havenon and colleagues analyzed Medicare Part D claims filed from 2013 to 2017. The payments include costs paid by Medicare, the patient, government subsidies, and other third-party payers.

In addition to examining more current Medicare Part D data than previous studies, the current analysis examined all medications prescribed by neurologists that consistently remained branded or generic during the 5-year study period, said Dr. de Havenon. This approach resulted in a large number of claims and a large total cost.

To calculate the percentage change in annual payment claims, the researchers used 2013 prices as a reference point. They identified drugs named in 2013 claims and classified them as generic, brand-name only, or brand-name with generic equivalent. Researchers also divided the drugs by neurologic subspecialty.

The analysis included 520 drugs, all of which were available in each year of the study period. Of these drugs, 322 were generic, 61 were brand-name only, and 137 were brand-name with a generic equivalent. There were 90.7 million total claims.

Results showed total payments amounted to $26.65 billion. Yearly total payments increased from $4.05 billion in 2013 to $6.09 billion in 2017, representing a 50.4% increase, even after adjusting for inflation. Total claims increased by 7.6% – from 17.1 million in 2013 to 18.4 million in 2017.

From 2013 to 2017, claim payments increased by 0.6% for generic drugs, 42.4% for brand-name only drugs, and 45% for brand-name drugs with generic equivalents. The proportion of claims increased from 81.9% to 88% for generic drugs and from 4.9% to 6.2% for brand-name only drugs.

However, the proportion of claims for brand-name drugs with generic equivalents decreased from 13.3% to 5.8%.
 

Treatment barrier

Neuroimmunologic drugs, most of which were prescribed for MS, had exceptional cost, the researchers noted. These drugs accounted for more than 50% of payments but only 4.3% of claims. Claim payment for these drugs increased by 46.9% during the study period, from $3,337 to $4,902.

When neuroimmunologic drugs were removed from the analysis there was still significant increase in claim payments for brand-name only drugs (50.4%) and brand-name drugs with generic equivalents (45.6%).

Although neuroimmunologic medicines, including monoclonal antibodies, are more expensive to produce, this factor alone does not explain their exceptional cost, said Dr. de Havenon. “The high cost of brand-name drugs in this speciality is likely because the market bears it,” he added. “In other words, MS is a disabling disease and the medications work, so historically the Centers for Medicare & Medicaid Services have been willing to tolerate the high cost of these primarily brand-name medications.”

Several countries have controlled drug costs by negotiating with pharmaceutical companies and through legislation, Dr. de Havenon noted.

“My intent with this article was to raise awareness on the topic, which I struggle with frequently as a clinician. I know I want my patients to have a medication, but the cost prevents it,” he said.
 

‘Unfettered’ price-setting

Commenting on the findings, Robert J. Fox, MD, vice chair for research at the Neurological Institute of the Cleveland Clinic, said the study “brings into clear light” what neurologists, particularly those who treat MS, have long suspected but did not really know. These neurologists “are typically distanced from the payment aspects of the medications they prescribe,” said Dr. Fox, who was not involved with the research.

Although a particular strength of the study was its comprehensiveness, the researchers excluded infusion claims – which account for a large portion of total patient care costs for many disorders, he noted.

Drugs for MS historically have been expensive, ostensibly because of their high cost of development. In addition, the large and continued price increase that occurs long after these drugs have been approved remains unexplained, said Dr. Fox.

He noted that the study findings might not directly affect clinical practice because neurologists will continue prescribing medications they think are best for their patients. “Instead, I think this is a lesson to lawmakers about the massive error in the Medicare Modernization Act of 2003, where the federal government was prohibited from negotiating drug prices. If the seller is unfettered in setting a price, then no one should be surprised when the price rises,” Dr. Fox said.

Because many new drugs and new generic formulations for treating MS have become available during the past year, “repeating these types of economic studies for the period 2020-2025 will help us understand if generic competition – as well as new laws if they are passed – alter price,” he concluded.

The study was funded by the American Academy of Neurology, which publishes Neurology. Dr. de Havenon has received clinical research funding from AMAG Pharmaceuticals and Regeneron Pharmaceuticals. Dr. Fox receives consulting fees from many pharmaceutical companies involved in the development of therapies for MS.

A version of this article first appeared on Medscape.com.

Children who have higher levels of sun exposure appear to have a substantially lower risk of developing pediatric multiple sclerosis (MS) than children who are less exposed to the sun, research shows. The use of sunscreen does not appear to affect the risk.

“This is the first study, as far as we are aware, to investigate the effect of sun exposure in pediatric MS,” first author Prince Sebastian, of the ANU Medical School, Australian National University, Canberra, said during a presentation at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

“In order to reduce the incidence of MS, parents should be encouraged to allow their children to spend at least 30 minutes outdoors in the sun every day, while using adequate sun protection,” Mr. Sebastian said.

“This is especially important for children with a family history of MS,” he said. As the findings show, “you can use adequate sun protection and still get the benefit of sun exposure in terms of MS risk reduction.”

Low sun exposure, exposure to ultraviolet light, and vitamin D have been well established as modifiable risk factors for MS in adults. However, research is lacking on the effect of these factors upon patients younger than 18 years who have pediatric MS, a less common form of the disease. Pediatric MS constitutes about 5% of all MS cases.

To investigate the issue, Mr. Sebastian and colleagues evaluated data on 332 patients with pediatric MS who were between the ages of 4 and 22 years. The patients were enrolled at 16 MS centers around the United States. They were compared by sex and age with 534 control persons aged 3-22 years who did not have MS.

For the patients with MS, the median disease duration was 7.3 months, and 63% were female. The median age of the patients was 15.9 years.

Compared with those who did not have MS, patients with MS were significantly less likely to have been exposed to cigarette smoke (17.8% vs. 14.2%). They were significantly more likely to be overweight (23.8% vs. 14.2%), and the median anti-VCA level was higher (3.7 vs. 2.2).

Those who were exposed to the sun during the most recent summer for a duration of 30 minutes to 1 hour daily, as determined on the basis of self-report or parent report, had a 2.6-fold reduced risk of having MS, compared with those who spent less than 30 minutes outdoors daily (odds ratio, 0.39; P < .05), after adjusting for age, sex, birth season, the child’s skin color, the mother’s education, smoke exposure, being overweight, and Epstein-Barr virus infection.

Sun exposure for 1-2 hours daily was associated with a 7.4-fold reduced risk for MS, compared with exposure of 30 minutes or less (OR, 0.13; P < .001).

The odds were similar for those with 2-3 hours of sun exposure (OR, 0.21; P < .001) and for those with more than 3 hours of daily exposure (OR, 0.14; P < .001), versus less than 30 minutes.

Mr. Sebastian and his team also assessed the role of summer ambient levels of UV light and whether such exposure conferred a similar degree of protection. The risk for MS was lower among those who were exposed to higher summer ambient UV levels than among those exposed to lower levels (OR, 0.80; P = .046).

He noted, “Based on the results, individuals residing in Florida (28° N) would have 20% lower odds of MS, compared with an individual residing in New York (40° N).”

Interestingly, median rates of the use of sun protection were similar for the participants with MS and those without MS (OR, 0.95), suggesting that the use of sunscreen did not reduce the protective effect of sun exposure.

“We predicted that greater use of protection would limit effective sun exposure and would therefore increase MS risk,” Mr. Sebastian said, “but we don’t see that, and it’s probably because someone who uses sun protection likely gets more sun exposure anyway.”

“Our results suggest that you can use adequate sun protection and still get most of the benefit in terms of MS prevention, which is quite encouraging,” he added.

For those with MS, median serum 25(OH)D levels were higher (27.7 ng/mL vs. 23.7 ng/mL; P < .001), but Mr. Sebastian noted that this difference was likely attributable to the use of vitamin D supplementation after an MS diagnosis. An important limitation of the study was a lack of data on supplementation.
 

Stronger effect of frequent sun protection

Previous studies have shown a link between sun exposure and MS. A study published in 2018 compared 2,251 patients with MS with 4,028 control persons who did not have MS. The participants were in Canada, Italy, and Norway.

In that study, for most of the patients with MS, the age of onset was older than 18 years. In that study, there was a nearly 50% increased risk among those with the lowest degree of summer sun exposure in comparison with those who had the highest level of exposure (risk ratio, 1.47).

Contrary to the current study, that study did show an effect of the use of sun protection – those with the lowest degree of sun exposure during summer and winter and the highest use of sun protection had the highest risk for MS. They had a 76% increased risk, compared with those who had the highest degree of sun exposure and the least use of sun protection (RR, 1.76).

Sandra Magalhaes, PhD, of the University of New Brunswick, Fredericton, Canada, who was first author on that study, noted that the new study of pediatric MS adds valuable evidence on the issue.

“This study is important, as it adds to the etiological literature on MS implicating relevance of sun exposure,” Dr. Magalhaes said.

“We have a number of studies that have demonstrated an important effect of reduced levels of sun exposure and increased risk of MS. However, these studies focus on adult-onset MS populations; rather, the new study adds to the existing literature, as it also implicates sun exposure in etiology of pediatric-onset MS,” she said.

Notably, their previous work, unlike the current study, showed that, among those who experienced low levels of sun exposure, the risk for MS was higher for those who used sunscreen frequently.

“Overall, in their limited time outdoors, use of sunscreen may further increase risk of MS, which makes sense, since limited time outdoors in less sun, adding sun protection means [exposure to] even less sun.”

The findings of both studies support the bulk of research indicating that sun exposure is beneficial with regard to MS.

“There is a need for promoting balanced safe sun practices to reduce disease burden, especially in countries and cultures where children spend a lot of time indoors,” Dr. Magalhaes said. “Sun exposure has a number of important physiological roles, including vitamin D synthesis but also immune system functioning.”

Mr. Sebastian and Dr. Magalhaes have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Children who have higher levels of sun exposure appear to have a substantially lower risk of developing pediatric multiple sclerosis (MS) than children who are less exposed to the sun, research shows. The use of sunscreen does not appear to affect the risk.

“This is the first study, as far as we are aware, to investigate the effect of sun exposure in pediatric MS,” first author Prince Sebastian, of the ANU Medical School, Australian National University, Canberra, said during a presentation at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

“In order to reduce the incidence of MS, parents should be encouraged to allow their children to spend at least 30 minutes outdoors in the sun every day, while using adequate sun protection,” Mr. Sebastian said.

“This is especially important for children with a family history of MS,” he said. As the findings show, “you can use adequate sun protection and still get the benefit of sun exposure in terms of MS risk reduction.”

Low sun exposure, exposure to ultraviolet light, and vitamin D have been well established as modifiable risk factors for MS in adults. However, research is lacking on the effect of these factors upon patients younger than 18 years who have pediatric MS, a less common form of the disease. Pediatric MS constitutes about 5% of all MS cases.

To investigate the issue, Mr. Sebastian and colleagues evaluated data on 332 patients with pediatric MS who were between the ages of 4 and 22 years. The patients were enrolled at 16 MS centers around the United States. They were compared by sex and age with 534 control persons aged 3-22 years who did not have MS.

For the patients with MS, the median disease duration was 7.3 months, and 63% were female. The median age of the patients was 15.9 years.

Compared with those who did not have MS, patients with MS were significantly less likely to have been exposed to cigarette smoke (17.8% vs. 14.2%). They were significantly more likely to be overweight (23.8% vs. 14.2%), and the median anti-VCA level was higher (3.7 vs. 2.2).

Those who were exposed to the sun during the most recent summer for a duration of 30 minutes to 1 hour daily, as determined on the basis of self-report or parent report, had a 2.6-fold reduced risk of having MS, compared with those who spent less than 30 minutes outdoors daily (odds ratio, 0.39; P < .05), after adjusting for age, sex, birth season, the child’s skin color, the mother’s education, smoke exposure, being overweight, and Epstein-Barr virus infection.

Sun exposure for 1-2 hours daily was associated with a 7.4-fold reduced risk for MS, compared with exposure of 30 minutes or less (OR, 0.13; P < .001).

The odds were similar for those with 2-3 hours of sun exposure (OR, 0.21; P < .001) and for those with more than 3 hours of daily exposure (OR, 0.14; P < .001), versus less than 30 minutes.

Mr. Sebastian and his team also assessed the role of summer ambient levels of UV light and whether such exposure conferred a similar degree of protection. The risk for MS was lower among those who were exposed to higher summer ambient UV levels than among those exposed to lower levels (OR, 0.80; P = .046).

He noted, “Based on the results, individuals residing in Florida (28° N) would have 20% lower odds of MS, compared with an individual residing in New York (40° N).”

Interestingly, median rates of the use of sun protection were similar for the participants with MS and those without MS (OR, 0.95), suggesting that the use of sunscreen did not reduce the protective effect of sun exposure.

“We predicted that greater use of protection would limit effective sun exposure and would therefore increase MS risk,” Mr. Sebastian said, “but we don’t see that, and it’s probably because someone who uses sun protection likely gets more sun exposure anyway.”

“Our results suggest that you can use adequate sun protection and still get most of the benefit in terms of MS prevention, which is quite encouraging,” he added.

For those with MS, median serum 25(OH)D levels were higher (27.7 ng/mL vs. 23.7 ng/mL; P < .001), but Mr. Sebastian noted that this difference was likely attributable to the use of vitamin D supplementation after an MS diagnosis. An important limitation of the study was a lack of data on supplementation.
 

Stronger effect of frequent sun protection

Previous studies have shown a link between sun exposure and MS. A study published in 2018 compared 2,251 patients with MS with 4,028 control persons who did not have MS. The participants were in Canada, Italy, and Norway.

In that study, for most of the patients with MS, the age of onset was older than 18 years. In that study, there was a nearly 50% increased risk among those with the lowest degree of summer sun exposure in comparison with those who had the highest level of exposure (risk ratio, 1.47).

Contrary to the current study, that study did show an effect of the use of sun protection – those with the lowest degree of sun exposure during summer and winter and the highest use of sun protection had the highest risk for MS. They had a 76% increased risk, compared with those who had the highest degree of sun exposure and the least use of sun protection (RR, 1.76).

Sandra Magalhaes, PhD, of the University of New Brunswick, Fredericton, Canada, who was first author on that study, noted that the new study of pediatric MS adds valuable evidence on the issue.

“This study is important, as it adds to the etiological literature on MS implicating relevance of sun exposure,” Dr. Magalhaes said.

“We have a number of studies that have demonstrated an important effect of reduced levels of sun exposure and increased risk of MS. However, these studies focus on adult-onset MS populations; rather, the new study adds to the existing literature, as it also implicates sun exposure in etiology of pediatric-onset MS,” she said.

Notably, their previous work, unlike the current study, showed that, among those who experienced low levels of sun exposure, the risk for MS was higher for those who used sunscreen frequently.

“Overall, in their limited time outdoors, use of sunscreen may further increase risk of MS, which makes sense, since limited time outdoors in less sun, adding sun protection means [exposure to] even less sun.”

The findings of both studies support the bulk of research indicating that sun exposure is beneficial with regard to MS.

“There is a need for promoting balanced safe sun practices to reduce disease burden, especially in countries and cultures where children spend a lot of time indoors,” Dr. Magalhaes said. “Sun exposure has a number of important physiological roles, including vitamin D synthesis but also immune system functioning.”

Mr. Sebastian and Dr. Magalhaes have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Children who have higher levels of sun exposure appear to have a substantially lower risk of developing pediatric multiple sclerosis (MS) than children who are less exposed to the sun, research shows. The use of sunscreen does not appear to affect the risk.

“This is the first study, as far as we are aware, to investigate the effect of sun exposure in pediatric MS,” first author Prince Sebastian, of the ANU Medical School, Australian National University, Canberra, said during a presentation at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

“In order to reduce the incidence of MS, parents should be encouraged to allow their children to spend at least 30 minutes outdoors in the sun every day, while using adequate sun protection,” Mr. Sebastian said.

“This is especially important for children with a family history of MS,” he said. As the findings show, “you can use adequate sun protection and still get the benefit of sun exposure in terms of MS risk reduction.”

Low sun exposure, exposure to ultraviolet light, and vitamin D have been well established as modifiable risk factors for MS in adults. However, research is lacking on the effect of these factors upon patients younger than 18 years who have pediatric MS, a less common form of the disease. Pediatric MS constitutes about 5% of all MS cases.

To investigate the issue, Mr. Sebastian and colleagues evaluated data on 332 patients with pediatric MS who were between the ages of 4 and 22 years. The patients were enrolled at 16 MS centers around the United States. They were compared by sex and age with 534 control persons aged 3-22 years who did not have MS.

For the patients with MS, the median disease duration was 7.3 months, and 63% were female. The median age of the patients was 15.9 years.

Compared with those who did not have MS, patients with MS were significantly less likely to have been exposed to cigarette smoke (17.8% vs. 14.2%). They were significantly more likely to be overweight (23.8% vs. 14.2%), and the median anti-VCA level was higher (3.7 vs. 2.2).

Those who were exposed to the sun during the most recent summer for a duration of 30 minutes to 1 hour daily, as determined on the basis of self-report or parent report, had a 2.6-fold reduced risk of having MS, compared with those who spent less than 30 minutes outdoors daily (odds ratio, 0.39; P < .05), after adjusting for age, sex, birth season, the child’s skin color, the mother’s education, smoke exposure, being overweight, and Epstein-Barr virus infection.

Sun exposure for 1-2 hours daily was associated with a 7.4-fold reduced risk for MS, compared with exposure of 30 minutes or less (OR, 0.13; P < .001).

The odds were similar for those with 2-3 hours of sun exposure (OR, 0.21; P < .001) and for those with more than 3 hours of daily exposure (OR, 0.14; P < .001), versus less than 30 minutes.

Mr. Sebastian and his team also assessed the role of summer ambient levels of UV light and whether such exposure conferred a similar degree of protection. The risk for MS was lower among those who were exposed to higher summer ambient UV levels than among those exposed to lower levels (OR, 0.80; P = .046).

He noted, “Based on the results, individuals residing in Florida (28° N) would have 20% lower odds of MS, compared with an individual residing in New York (40° N).”

Interestingly, median rates of the use of sun protection were similar for the participants with MS and those without MS (OR, 0.95), suggesting that the use of sunscreen did not reduce the protective effect of sun exposure.

“We predicted that greater use of protection would limit effective sun exposure and would therefore increase MS risk,” Mr. Sebastian said, “but we don’t see that, and it’s probably because someone who uses sun protection likely gets more sun exposure anyway.”

“Our results suggest that you can use adequate sun protection and still get most of the benefit in terms of MS prevention, which is quite encouraging,” he added.

For those with MS, median serum 25(OH)D levels were higher (27.7 ng/mL vs. 23.7 ng/mL; P < .001), but Mr. Sebastian noted that this difference was likely attributable to the use of vitamin D supplementation after an MS diagnosis. An important limitation of the study was a lack of data on supplementation.
 

Stronger effect of frequent sun protection

Previous studies have shown a link between sun exposure and MS. A study published in 2018 compared 2,251 patients with MS with 4,028 control persons who did not have MS. The participants were in Canada, Italy, and Norway.

In that study, for most of the patients with MS, the age of onset was older than 18 years. In that study, there was a nearly 50% increased risk among those with the lowest degree of summer sun exposure in comparison with those who had the highest level of exposure (risk ratio, 1.47).

Contrary to the current study, that study did show an effect of the use of sun protection – those with the lowest degree of sun exposure during summer and winter and the highest use of sun protection had the highest risk for MS. They had a 76% increased risk, compared with those who had the highest degree of sun exposure and the least use of sun protection (RR, 1.76).

Sandra Magalhaes, PhD, of the University of New Brunswick, Fredericton, Canada, who was first author on that study, noted that the new study of pediatric MS adds valuable evidence on the issue.

“This study is important, as it adds to the etiological literature on MS implicating relevance of sun exposure,” Dr. Magalhaes said.

“We have a number of studies that have demonstrated an important effect of reduced levels of sun exposure and increased risk of MS. However, these studies focus on adult-onset MS populations; rather, the new study adds to the existing literature, as it also implicates sun exposure in etiology of pediatric-onset MS,” she said.

Notably, their previous work, unlike the current study, showed that, among those who experienced low levels of sun exposure, the risk for MS was higher for those who used sunscreen frequently.

“Overall, in their limited time outdoors, use of sunscreen may further increase risk of MS, which makes sense, since limited time outdoors in less sun, adding sun protection means [exposure to] even less sun.”

The findings of both studies support the bulk of research indicating that sun exposure is beneficial with regard to MS.

“There is a need for promoting balanced safe sun practices to reduce disease burden, especially in countries and cultures where children spend a lot of time indoors,” Dr. Magalhaes said. “Sun exposure has a number of important physiological roles, including vitamin D synthesis but also immune system functioning.”

Mr. Sebastian and Dr. Magalhaes have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Erythropoietin (EPO), shown in early studies to potentially provide neuroprotection for patients with optic neuritis, failed to provide any significant neuroprotection in comparison with placebo in a phase 3 randomized controlled trial.

“EPO conveyed neither functional nor structural neuroprotection in the visual pathways after optic neuritis as a clinically isolated syndrome,” said first author Wolf A. Lagreze, MD, of the University of Freiburg (Germany), in presenting the results at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

There are currently no treatments that provide neuroprotection for patients with optic neuritis, which can result in the degeneration of retinal ganglion cells, the axons of which form the optic nerve.

Although methylprednisolone, the standard treatment, can be of benefit, it has no effect in preventing neurodegeneration or subsequent vision impairment.

Importantly, optic neuritis, which can be a first sign of multiple sclerosis (MS), is considered an ideal model for an acute inflammatory attack on the nervous system and resulting neurodegeneration. Therefore, any treatment that provides neuroprotection for patients with optic neuritis could have potentially exciting broader implications.
 

The TONE trial

Preclinical studies have shown that EPO provides a small, potential degree of neuroprotection. To further evaluate EPO in this setting, Dr. Lagreze and colleagues conducted the TONE trial (Treatment of Optic Neuritis With Erythropoietin) in Germany between 2014 and 2017, in which they enrolled 108 patients with optic neuritis.

Inclusion criteria were having only unilateral optic neuritis as a clinically isolated syndrome that presented within 10 days of the first symptoms and having moderate to severe loss of visual acuity.

Persons with known MS were excluded; however, patients who were diagnosed with MS at the beginning of the study during the workup evaluation were included. Hence, about 20% of patients did have newly diagnosed MS, Dr. Lagreze noted.

The participants were randomly assigned in double-blind 1:1 ratio to receive treatment with either 33,000 IU EPO or placebo intravenously for 3 days as an adjunct to high-dose intravenous methylprednisolone (1,000 mg/day).

The final analysis included 52 patients who received EPO and 51 patients who received placebo. There were no significant differences between the groups in the first primary outcome of retinal nerve fiber layer atrophy, assessed with optic coherence tomography at week 26 (P = .76).

Likewise, no significant difference between groups was observed in the second primary outcome of low-contrast visual acuity at week 26, assessed using the 2.5% Sloan chart score of the affected eye (P = .38).

In addition, there were no significant differences between the groups in the rates of optic neuritis relapse.

In terms of safety measures, one patient in the EPO group developed sinus venous thrombosis, which was treated with anticoagulants and resolved without complications.
 

Reduced conversion to MS?

Interestingly, after 6 months, significantly fewer patients in the EPO arm (36%) had converted from clinically isolated syndrome to MS, compared with 57% in the placebo arm (P = .032). The difference became apparent as early as week 4.

Although those findings suggest that EPO provided some neuroprotection, there are notable caveats, Philippe Albrecht, MD, of the department of neurology at the University Hospital Dusseldorf (Germany), and a coauthor on the study, said.

“The significant separation of EPO and placebo group regarding MS conversion was observed very early on in the course and did not change thereafter,” Dr. Albrecht noted.

“One would expect a true disease-modifying effect of EPO on MS conversion to take longer to develop, and this early separation may very well have been due to an imbalance in the treatment groups, [for example] regarding MRI imaging findings such as gadolinium enhancement at baseline,” he said.

Dr. Lagreze said that it was a surprise to see no benefit from the drug, and a closer look at certain subgroups may still be worthwhile. Factors that could have a bearing on results include a shorter time interval for inclusion, having no concomitant use of steroids, and longer duration of treatment with EPO.

“If I could do the study again, I would do the treatment for longer than 3 days – that was based on experiences in previous EPO trials,” he said. “I would also love to do the trial without the concomitant methylprednisolone, but that is not possible from an ethical point of view.”
 

Trial nevertheless important

Commenting on the study, E. Anne Yeh, MD, of the division of neurology at the Hospital for Sick Children, Toronto, agreed that a challenge in evaluating therapies for optic neuritis is the potential for confounding from existing therapies that patients need to take.

“This agent could not be evaluated alone for its protective effect in comparison to no treatment at all,” she said.

In addition, improved metrics for gauging outcomes are needed to better determine the true effects, she added.

“The development of newer vision-related outcome metrics is important for future studies, and many are hard at work on both structural and functional metrics that may help us to understand the benefits of any protective therapies in a more nuanced manner than we are currently able to,” she said.

However, results of any kind – negative or positive – are valuable in improving understanding, Dr. Yeh underscored.

“Negative results can be disappointing in any trial, especially one in which alternative therapeutic pathways are being sought,” Dr. Yeh said. “I want to emphasize, however, that the fact that we are even considering and completing trials in this area is important.”

Dr. Yeh noted that she is currently involved in a trial that is evaluating the diabetes drug metformin for its remyelinating potential. “We hope to have some pilot data on MS in a few years,” she said.

Dr. Lagreze, Dr. Albrecht, and Dr. Yeh have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Erythropoietin (EPO), shown in early studies to potentially provide neuroprotection for patients with optic neuritis, failed to provide any significant neuroprotection in comparison with placebo in a phase 3 randomized controlled trial.

“EPO conveyed neither functional nor structural neuroprotection in the visual pathways after optic neuritis as a clinically isolated syndrome,” said first author Wolf A. Lagreze, MD, of the University of Freiburg (Germany), in presenting the results at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

There are currently no treatments that provide neuroprotection for patients with optic neuritis, which can result in the degeneration of retinal ganglion cells, the axons of which form the optic nerve.

Although methylprednisolone, the standard treatment, can be of benefit, it has no effect in preventing neurodegeneration or subsequent vision impairment.

Importantly, optic neuritis, which can be a first sign of multiple sclerosis (MS), is considered an ideal model for an acute inflammatory attack on the nervous system and resulting neurodegeneration. Therefore, any treatment that provides neuroprotection for patients with optic neuritis could have potentially exciting broader implications.
 

The TONE trial

Preclinical studies have shown that EPO provides a small, potential degree of neuroprotection. To further evaluate EPO in this setting, Dr. Lagreze and colleagues conducted the TONE trial (Treatment of Optic Neuritis With Erythropoietin) in Germany between 2014 and 2017, in which they enrolled 108 patients with optic neuritis.

Inclusion criteria were having only unilateral optic neuritis as a clinically isolated syndrome that presented within 10 days of the first symptoms and having moderate to severe loss of visual acuity.

Persons with known MS were excluded; however, patients who were diagnosed with MS at the beginning of the study during the workup evaluation were included. Hence, about 20% of patients did have newly diagnosed MS, Dr. Lagreze noted.

The participants were randomly assigned in double-blind 1:1 ratio to receive treatment with either 33,000 IU EPO or placebo intravenously for 3 days as an adjunct to high-dose intravenous methylprednisolone (1,000 mg/day).

The final analysis included 52 patients who received EPO and 51 patients who received placebo. There were no significant differences between the groups in the first primary outcome of retinal nerve fiber layer atrophy, assessed with optic coherence tomography at week 26 (P = .76).

Likewise, no significant difference between groups was observed in the second primary outcome of low-contrast visual acuity at week 26, assessed using the 2.5% Sloan chart score of the affected eye (P = .38).

In addition, there were no significant differences between the groups in the rates of optic neuritis relapse.

In terms of safety measures, one patient in the EPO group developed sinus venous thrombosis, which was treated with anticoagulants and resolved without complications.
 

Reduced conversion to MS?

Interestingly, after 6 months, significantly fewer patients in the EPO arm (36%) had converted from clinically isolated syndrome to MS, compared with 57% in the placebo arm (P = .032). The difference became apparent as early as week 4.

Although those findings suggest that EPO provided some neuroprotection, there are notable caveats, Philippe Albrecht, MD, of the department of neurology at the University Hospital Dusseldorf (Germany), and a coauthor on the study, said.

“The significant separation of EPO and placebo group regarding MS conversion was observed very early on in the course and did not change thereafter,” Dr. Albrecht noted.

“One would expect a true disease-modifying effect of EPO on MS conversion to take longer to develop, and this early separation may very well have been due to an imbalance in the treatment groups, [for example] regarding MRI imaging findings such as gadolinium enhancement at baseline,” he said.

Dr. Lagreze said that it was a surprise to see no benefit from the drug, and a closer look at certain subgroups may still be worthwhile. Factors that could have a bearing on results include a shorter time interval for inclusion, having no concomitant use of steroids, and longer duration of treatment with EPO.

“If I could do the study again, I would do the treatment for longer than 3 days – that was based on experiences in previous EPO trials,” he said. “I would also love to do the trial without the concomitant methylprednisolone, but that is not possible from an ethical point of view.”
 

Trial nevertheless important

Commenting on the study, E. Anne Yeh, MD, of the division of neurology at the Hospital for Sick Children, Toronto, agreed that a challenge in evaluating therapies for optic neuritis is the potential for confounding from existing therapies that patients need to take.

“This agent could not be evaluated alone for its protective effect in comparison to no treatment at all,” she said.

In addition, improved metrics for gauging outcomes are needed to better determine the true effects, she added.

“The development of newer vision-related outcome metrics is important for future studies, and many are hard at work on both structural and functional metrics that may help us to understand the benefits of any protective therapies in a more nuanced manner than we are currently able to,” she said.

However, results of any kind – negative or positive – are valuable in improving understanding, Dr. Yeh underscored.

“Negative results can be disappointing in any trial, especially one in which alternative therapeutic pathways are being sought,” Dr. Yeh said. “I want to emphasize, however, that the fact that we are even considering and completing trials in this area is important.”

Dr. Yeh noted that she is currently involved in a trial that is evaluating the diabetes drug metformin for its remyelinating potential. “We hope to have some pilot data on MS in a few years,” she said.

Dr. Lagreze, Dr. Albrecht, and Dr. Yeh have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Erythropoietin (EPO), shown in early studies to potentially provide neuroprotection for patients with optic neuritis, failed to provide any significant neuroprotection in comparison with placebo in a phase 3 randomized controlled trial.

“EPO conveyed neither functional nor structural neuroprotection in the visual pathways after optic neuritis as a clinically isolated syndrome,” said first author Wolf A. Lagreze, MD, of the University of Freiburg (Germany), in presenting the results at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis.

There are currently no treatments that provide neuroprotection for patients with optic neuritis, which can result in the degeneration of retinal ganglion cells, the axons of which form the optic nerve.

Although methylprednisolone, the standard treatment, can be of benefit, it has no effect in preventing neurodegeneration or subsequent vision impairment.

Importantly, optic neuritis, which can be a first sign of multiple sclerosis (MS), is considered an ideal model for an acute inflammatory attack on the nervous system and resulting neurodegeneration. Therefore, any treatment that provides neuroprotection for patients with optic neuritis could have potentially exciting broader implications.
 

The TONE trial

Preclinical studies have shown that EPO provides a small, potential degree of neuroprotection. To further evaluate EPO in this setting, Dr. Lagreze and colleagues conducted the TONE trial (Treatment of Optic Neuritis With Erythropoietin) in Germany between 2014 and 2017, in which they enrolled 108 patients with optic neuritis.

Inclusion criteria were having only unilateral optic neuritis as a clinically isolated syndrome that presented within 10 days of the first symptoms and having moderate to severe loss of visual acuity.

Persons with known MS were excluded; however, patients who were diagnosed with MS at the beginning of the study during the workup evaluation were included. Hence, about 20% of patients did have newly diagnosed MS, Dr. Lagreze noted.

The participants were randomly assigned in double-blind 1:1 ratio to receive treatment with either 33,000 IU EPO or placebo intravenously for 3 days as an adjunct to high-dose intravenous methylprednisolone (1,000 mg/day).

The final analysis included 52 patients who received EPO and 51 patients who received placebo. There were no significant differences between the groups in the first primary outcome of retinal nerve fiber layer atrophy, assessed with optic coherence tomography at week 26 (P = .76).

Likewise, no significant difference between groups was observed in the second primary outcome of low-contrast visual acuity at week 26, assessed using the 2.5% Sloan chart score of the affected eye (P = .38).

In addition, there were no significant differences between the groups in the rates of optic neuritis relapse.

In terms of safety measures, one patient in the EPO group developed sinus venous thrombosis, which was treated with anticoagulants and resolved without complications.
 

Reduced conversion to MS?

Interestingly, after 6 months, significantly fewer patients in the EPO arm (36%) had converted from clinically isolated syndrome to MS, compared with 57% in the placebo arm (P = .032). The difference became apparent as early as week 4.

Although those findings suggest that EPO provided some neuroprotection, there are notable caveats, Philippe Albrecht, MD, of the department of neurology at the University Hospital Dusseldorf (Germany), and a coauthor on the study, said.

“The significant separation of EPO and placebo group regarding MS conversion was observed very early on in the course and did not change thereafter,” Dr. Albrecht noted.

“One would expect a true disease-modifying effect of EPO on MS conversion to take longer to develop, and this early separation may very well have been due to an imbalance in the treatment groups, [for example] regarding MRI imaging findings such as gadolinium enhancement at baseline,” he said.

Dr. Lagreze said that it was a surprise to see no benefit from the drug, and a closer look at certain subgroups may still be worthwhile. Factors that could have a bearing on results include a shorter time interval for inclusion, having no concomitant use of steroids, and longer duration of treatment with EPO.

“If I could do the study again, I would do the treatment for longer than 3 days – that was based on experiences in previous EPO trials,” he said. “I would also love to do the trial without the concomitant methylprednisolone, but that is not possible from an ethical point of view.”
 

Trial nevertheless important

Commenting on the study, E. Anne Yeh, MD, of the division of neurology at the Hospital for Sick Children, Toronto, agreed that a challenge in evaluating therapies for optic neuritis is the potential for confounding from existing therapies that patients need to take.

“This agent could not be evaluated alone for its protective effect in comparison to no treatment at all,” she said.

In addition, improved metrics for gauging outcomes are needed to better determine the true effects, she added.

“The development of newer vision-related outcome metrics is important for future studies, and many are hard at work on both structural and functional metrics that may help us to understand the benefits of any protective therapies in a more nuanced manner than we are currently able to,” she said.

However, results of any kind – negative or positive – are valuable in improving understanding, Dr. Yeh underscored.

“Negative results can be disappointing in any trial, especially one in which alternative therapeutic pathways are being sought,” Dr. Yeh said. “I want to emphasize, however, that the fact that we are even considering and completing trials in this area is important.”

Dr. Yeh noted that she is currently involved in a trial that is evaluating the diabetes drug metformin for its remyelinating potential. “We hope to have some pilot data on MS in a few years,” she said.

Dr. Lagreze, Dr. Albrecht, and Dr. Yeh have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Multiple sclerosis (MS) affects Whites, African Americans, and Hispanics differently, a new study finds, and there are big gaps in how they respond to disease-modifying therapies (DMTs).

“Hispanics and African Americans develop a more severe disease course and accumulate more MS-related disability over time despite similar sociodemographic backgrounds and similar patterns of DMT use throughout their disease, suggesting that socioeconomic status and access to health care may not be the main determinants of health,” said neurologist Carlos Pérez, MD, of the University of Texas Health Science Center, Houston. He spoke at the annual meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis and in a follow-up interview.

“In addition,” Dr. Pérez said, “therapeutic responses to individual DMTs, as well as tolerance and side-effect profiles, are also variable among racial/ethnic groups.”

The researchers tracked 150 patients with MS at the University of Texas Health Science Center – 50 Whites, 50 African American, and 50 Hispanic – who were age and gender matched. The average age of the subjects was 45, and 74% of those in each group were women.

While educational levels between the groups were similar, African Americans had a much higher rate of lost employment because of disability (38%) than Hispanics (19%) and Whites (15%, P = .02). Fifty-seven patients (38%) needed escalation of therapy, and 63% were African American.

About 30% of subjects switched DMTs because of intolerance/adverse events, and 47% of those were African American. Interferons most commonly caused adverse effects in African Americans (61%), and Whites were the most likely to not tolerate glatiramer acetate (39%) than Hispanics (8%) and African Americans (13%).

What might be behind the disparities? “It is possible that genetic factors may play a greater role than previously thought. A recent study reported that Hispanic and African American patients with MS have higher levels of peripheral blood plasmablasts, which may provide indirect evidence for potential biological mechanisms underlying racial and clinical disparities in MS,” Dr. Pérez said. “These mechanisms appear to involve higher degrees of inflammation in the central nervous system. This may explain why African Americans may respond better to higher-efficacy therapies initially, when inflammatory processes predominate MS-related pathology, rather than at later stages of the disease when inflammation plays a less prominent role. Neurologists should consider higher-efficacy DMT as first line. We have begun to do this in our practice.”

Dr. Pérez said the findings offer other lessons. “Neurologists should consider that Caucasian patients tolerate glatiramer acetate less frequently, compared with other racial groups, and potentially consider using alternative DMTs unless the benefits outweigh the risks, such as during pregnancy.”

He also noted that African Americans treated with oral DMTs at baseline were more likely to develop worsening disability over time. “This argues in favor of infusion therapies as first-line treatment,” he said, adding that more Hispanics with MS were not on treatment – or discontinued treatment – compared with Whites and African Americans.
 

Close patient monitoring is key

Atlanta-area neurologist Mitzi Joi Williams, MD, who was asked to comment on the study findings, said in an interview that it “adds to the body of real-world evidence to assist understanding of MS in minority populations.”

She noted that African American patients who started on infusions appeared to be more stable. “There are a great deal of questions surrounding starting patients on injectables versus higher-efficacy therapy initially to prevent disability and this may lend credence to the need for closer examination of initial therapy for these patients. It is important to closely monitor patients and consider a switch in DMT if there is any clinical or radiologic progression, especially for African American and Hispanic patients since there is a great deal of data to suggest they may have more aggressive disease.”

Moving forward, more research like this is needed, she said. “Patients did all have insurance and were largely educated, but there could be other social determinants of health – i.e., transportation, lapses in insurance, or technology barriers – that may have led to worse outcomes.”

No study funding was reported, and Dr. Pérez reported no disclosures. Dr. Williams disclosed research support from EMD Serono, Genentech, and Novartis and advisory committee/consultant relationships with AbbVie, Biogen Idec, Bristol-Myers Squibb, EMD Serono, Genentech, Novartis, and Sanofi Genzyme.

Multiple sclerosis (MS) affects Whites, African Americans, and Hispanics differently, a new study finds, and there are big gaps in how they respond to disease-modifying therapies (DMTs).

“Hispanics and African Americans develop a more severe disease course and accumulate more MS-related disability over time despite similar sociodemographic backgrounds and similar patterns of DMT use throughout their disease, suggesting that socioeconomic status and access to health care may not be the main determinants of health,” said neurologist Carlos Pérez, MD, of the University of Texas Health Science Center, Houston. He spoke at the annual meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis and in a follow-up interview.

“In addition,” Dr. Pérez said, “therapeutic responses to individual DMTs, as well as tolerance and side-effect profiles, are also variable among racial/ethnic groups.”

The researchers tracked 150 patients with MS at the University of Texas Health Science Center – 50 Whites, 50 African American, and 50 Hispanic – who were age and gender matched. The average age of the subjects was 45, and 74% of those in each group were women.

While educational levels between the groups were similar, African Americans had a much higher rate of lost employment because of disability (38%) than Hispanics (19%) and Whites (15%, P = .02). Fifty-seven patients (38%) needed escalation of therapy, and 63% were African American.

About 30% of subjects switched DMTs because of intolerance/adverse events, and 47% of those were African American. Interferons most commonly caused adverse effects in African Americans (61%), and Whites were the most likely to not tolerate glatiramer acetate (39%) than Hispanics (8%) and African Americans (13%).

What might be behind the disparities? “It is possible that genetic factors may play a greater role than previously thought. A recent study reported that Hispanic and African American patients with MS have higher levels of peripheral blood plasmablasts, which may provide indirect evidence for potential biological mechanisms underlying racial and clinical disparities in MS,” Dr. Pérez said. “These mechanisms appear to involve higher degrees of inflammation in the central nervous system. This may explain why African Americans may respond better to higher-efficacy therapies initially, when inflammatory processes predominate MS-related pathology, rather than at later stages of the disease when inflammation plays a less prominent role. Neurologists should consider higher-efficacy DMT as first line. We have begun to do this in our practice.”

Dr. Pérez said the findings offer other lessons. “Neurologists should consider that Caucasian patients tolerate glatiramer acetate less frequently, compared with other racial groups, and potentially consider using alternative DMTs unless the benefits outweigh the risks, such as during pregnancy.”

He also noted that African Americans treated with oral DMTs at baseline were more likely to develop worsening disability over time. “This argues in favor of infusion therapies as first-line treatment,” he said, adding that more Hispanics with MS were not on treatment – or discontinued treatment – compared with Whites and African Americans.
 

Close patient monitoring is key

Atlanta-area neurologist Mitzi Joi Williams, MD, who was asked to comment on the study findings, said in an interview that it “adds to the body of real-world evidence to assist understanding of MS in minority populations.”

She noted that African American patients who started on infusions appeared to be more stable. “There are a great deal of questions surrounding starting patients on injectables versus higher-efficacy therapy initially to prevent disability and this may lend credence to the need for closer examination of initial therapy for these patients. It is important to closely monitor patients and consider a switch in DMT if there is any clinical or radiologic progression, especially for African American and Hispanic patients since there is a great deal of data to suggest they may have more aggressive disease.”

Moving forward, more research like this is needed, she said. “Patients did all have insurance and were largely educated, but there could be other social determinants of health – i.e., transportation, lapses in insurance, or technology barriers – that may have led to worse outcomes.”

No study funding was reported, and Dr. Pérez reported no disclosures. Dr. Williams disclosed research support from EMD Serono, Genentech, and Novartis and advisory committee/consultant relationships with AbbVie, Biogen Idec, Bristol-Myers Squibb, EMD Serono, Genentech, Novartis, and Sanofi Genzyme.

Multiple sclerosis (MS) affects Whites, African Americans, and Hispanics differently, a new study finds, and there are big gaps in how they respond to disease-modifying therapies (DMTs).

“Hispanics and African Americans develop a more severe disease course and accumulate more MS-related disability over time despite similar sociodemographic backgrounds and similar patterns of DMT use throughout their disease, suggesting that socioeconomic status and access to health care may not be the main determinants of health,” said neurologist Carlos Pérez, MD, of the University of Texas Health Science Center, Houston. He spoke at the annual meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis and in a follow-up interview.

“In addition,” Dr. Pérez said, “therapeutic responses to individual DMTs, as well as tolerance and side-effect profiles, are also variable among racial/ethnic groups.”

The researchers tracked 150 patients with MS at the University of Texas Health Science Center – 50 Whites, 50 African American, and 50 Hispanic – who were age and gender matched. The average age of the subjects was 45, and 74% of those in each group were women.

While educational levels between the groups were similar, African Americans had a much higher rate of lost employment because of disability (38%) than Hispanics (19%) and Whites (15%, P = .02). Fifty-seven patients (38%) needed escalation of therapy, and 63% were African American.

About 30% of subjects switched DMTs because of intolerance/adverse events, and 47% of those were African American. Interferons most commonly caused adverse effects in African Americans (61%), and Whites were the most likely to not tolerate glatiramer acetate (39%) than Hispanics (8%) and African Americans (13%).

What might be behind the disparities? “It is possible that genetic factors may play a greater role than previously thought. A recent study reported that Hispanic and African American patients with MS have higher levels of peripheral blood plasmablasts, which may provide indirect evidence for potential biological mechanisms underlying racial and clinical disparities in MS,” Dr. Pérez said. “These mechanisms appear to involve higher degrees of inflammation in the central nervous system. This may explain why African Americans may respond better to higher-efficacy therapies initially, when inflammatory processes predominate MS-related pathology, rather than at later stages of the disease when inflammation plays a less prominent role. Neurologists should consider higher-efficacy DMT as first line. We have begun to do this in our practice.”

Dr. Pérez said the findings offer other lessons. “Neurologists should consider that Caucasian patients tolerate glatiramer acetate less frequently, compared with other racial groups, and potentially consider using alternative DMTs unless the benefits outweigh the risks, such as during pregnancy.”

He also noted that African Americans treated with oral DMTs at baseline were more likely to develop worsening disability over time. “This argues in favor of infusion therapies as first-line treatment,” he said, adding that more Hispanics with MS were not on treatment – or discontinued treatment – compared with Whites and African Americans.
 

Close patient monitoring is key

Atlanta-area neurologist Mitzi Joi Williams, MD, who was asked to comment on the study findings, said in an interview that it “adds to the body of real-world evidence to assist understanding of MS in minority populations.”

She noted that African American patients who started on infusions appeared to be more stable. “There are a great deal of questions surrounding starting patients on injectables versus higher-efficacy therapy initially to prevent disability and this may lend credence to the need for closer examination of initial therapy for these patients. It is important to closely monitor patients and consider a switch in DMT if there is any clinical or radiologic progression, especially for African American and Hispanic patients since there is a great deal of data to suggest they may have more aggressive disease.”

Moving forward, more research like this is needed, she said. “Patients did all have insurance and were largely educated, but there could be other social determinants of health – i.e., transportation, lapses in insurance, or technology barriers – that may have led to worse outcomes.”

No study funding was reported, and Dr. Pérez reported no disclosures. Dr. Williams disclosed research support from EMD Serono, Genentech, and Novartis and advisory committee/consultant relationships with AbbVie, Biogen Idec, Bristol-Myers Squibb, EMD Serono, Genentech, Novartis, and Sanofi Genzyme.

While they’re extraordinarily expensive, a trio of newly approved medications is providing a variety of effective treatment options for patients with neuromyelitis optica spectrum disorder (NMOSD), a neurologist told colleagues.

“Patients have a choice of different options with different types of action. It’s good news,” said Sean J. Pittock, MD, of the Mayo Clinic in Rochester, Minn. “If you don’t stop the clinical attacks, patients can become very disabled very quickly. These medications have a significant impact in reducing the likelihood of having a clinical relapse. If you can stop the relapses, you certainly can eventually stop most – if not all – of the disability accrual.”

Dr. Pittock spoke at the annual meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis and answered follow-up questions in an interview.
 

Treatment advances for NMOSD

NMOSD, also known as NMO, is a relapsing autoimmune inflammatory disorder that causes recurrent optic neuritis and myelitis. It’s a rare disease, affecting 0.5-10 people per 100,000, mostly women.

Several recent trials have supported the use of the drugs eculizumab (Soliris), satralizumab (Enspryng) and inebilizumab (Uplizna) in NMOSD, Dr. Pittock said, and all have received Food and Drug Administration approval to treat the condition over the past 2 years. Dr. Pittock led the PREVENT trial of eculizumab, which showed a 94% reduction of relapse risk versus placebo.

The newly approved drugs are stunningly expensive. According to Dr. Pittock, eculizumab costs $710,000 a year, while inebilizumab runs $393,000 the first year, then $262,000 a year. Satralizumab is $219,000 the first year, then $190,000 a year. Assistance programs are available, Dr. Pittock said, “and we’ve not had any major problems in terms of initiation.”

The cost of rituximab (Rituxan), which has a history of use as an off-label treatment option, is $18,000 a year and dropping, according to Dr. Pittock. There’s also new research on rituximab: In 2020, a small Japanese trial (n = 38) reported prevention of relapses compared with placebo, but Dr. Pittock cautioned that “the placebo patients seem to have a more benign course or more benign phenotypes” than the intervention group.

“There’s no doubt that rituximab works, but does it work as well as the other medications that have been through more of a robust trial process?” he asked. Keep in mind, he added, that perhaps 20%-50% of patients will relapse on rituximab.

Dr. Pittock advised colleagues to consider factors like patient schedules and compliance when choosing a drug. Satralizumab is self-administered monthly, while inebilizumab and rituximab are infused every 6 months.
 

Progress in anti-MOG disease

The trials in NMOSD should spur studies of the drugs in anti–myelin oligodendrocyte glycoprotein (MOG) disease, he said. “I think we’ll see a more rapid move toward phase 3 trials because of the experience with NMO. We will just have to wait and see which medications enter trial.”

Anti-MOG disease, also known as MOG antibody disease (MOGAD) and anti-MOG–associated encephalomyelitis, is caused by anti-MOG antibodies. Optic neuritis is very common, and transverse myelitis can occur.

The condition “actually responds to different drugs than MS and has a different immune pathophysiology,” Dr. Pittock said.

He cautioned colleagues to be aware that “the ability of the antibody to tell you whether or not the patient has the disease is less clear for MOGAD than it is for other diseases. If your patient has a low titer of MOG antibody, and their phenotype really doesn’t look like [MOGAD], you really need to interpret that with significant caution.”

He also highlighted a 2018 report that offers guidance about diagnosis and when MOG-IgC antibody tests are appropriate in CNS demyelinating disease.

Dr. Pittock reported numerous disclosures plus patents issued or pending.

While they’re extraordinarily expensive, a trio of newly approved medications is providing a variety of effective treatment options for patients with neuromyelitis optica spectrum disorder (NMOSD), a neurologist told colleagues.

“Patients have a choice of different options with different types of action. It’s good news,” said Sean J. Pittock, MD, of the Mayo Clinic in Rochester, Minn. “If you don’t stop the clinical attacks, patients can become very disabled very quickly. These medications have a significant impact in reducing the likelihood of having a clinical relapse. If you can stop the relapses, you certainly can eventually stop most – if not all – of the disability accrual.”

Dr. Pittock spoke at the annual meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis and answered follow-up questions in an interview.
 

Treatment advances for NMOSD

NMOSD, also known as NMO, is a relapsing autoimmune inflammatory disorder that causes recurrent optic neuritis and myelitis. It’s a rare disease, affecting 0.5-10 people per 100,000, mostly women.

Several recent trials have supported the use of the drugs eculizumab (Soliris), satralizumab (Enspryng) and inebilizumab (Uplizna) in NMOSD, Dr. Pittock said, and all have received Food and Drug Administration approval to treat the condition over the past 2 years. Dr. Pittock led the PREVENT trial of eculizumab, which showed a 94% reduction of relapse risk versus placebo.

The newly approved drugs are stunningly expensive. According to Dr. Pittock, eculizumab costs $710,000 a year, while inebilizumab runs $393,000 the first year, then $262,000 a year. Satralizumab is $219,000 the first year, then $190,000 a year. Assistance programs are available, Dr. Pittock said, “and we’ve not had any major problems in terms of initiation.”

The cost of rituximab (Rituxan), which has a history of use as an off-label treatment option, is $18,000 a year and dropping, according to Dr. Pittock. There’s also new research on rituximab: In 2020, a small Japanese trial (n = 38) reported prevention of relapses compared with placebo, but Dr. Pittock cautioned that “the placebo patients seem to have a more benign course or more benign phenotypes” than the intervention group.

“There’s no doubt that rituximab works, but does it work as well as the other medications that have been through more of a robust trial process?” he asked. Keep in mind, he added, that perhaps 20%-50% of patients will relapse on rituximab.

Dr. Pittock advised colleagues to consider factors like patient schedules and compliance when choosing a drug. Satralizumab is self-administered monthly, while inebilizumab and rituximab are infused every 6 months.
 

Progress in anti-MOG disease

The trials in NMOSD should spur studies of the drugs in anti–myelin oligodendrocyte glycoprotein (MOG) disease, he said. “I think we’ll see a more rapid move toward phase 3 trials because of the experience with NMO. We will just have to wait and see which medications enter trial.”

Anti-MOG disease, also known as MOG antibody disease (MOGAD) and anti-MOG–associated encephalomyelitis, is caused by anti-MOG antibodies. Optic neuritis is very common, and transverse myelitis can occur.

The condition “actually responds to different drugs than MS and has a different immune pathophysiology,” Dr. Pittock said.

He cautioned colleagues to be aware that “the ability of the antibody to tell you whether or not the patient has the disease is less clear for MOGAD than it is for other diseases. If your patient has a low titer of MOG antibody, and their phenotype really doesn’t look like [MOGAD], you really need to interpret that with significant caution.”

He also highlighted a 2018 report that offers guidance about diagnosis and when MOG-IgC antibody tests are appropriate in CNS demyelinating disease.

Dr. Pittock reported numerous disclosures plus patents issued or pending.

While they’re extraordinarily expensive, a trio of newly approved medications is providing a variety of effective treatment options for patients with neuromyelitis optica spectrum disorder (NMOSD), a neurologist told colleagues.

“Patients have a choice of different options with different types of action. It’s good news,” said Sean J. Pittock, MD, of the Mayo Clinic in Rochester, Minn. “If you don’t stop the clinical attacks, patients can become very disabled very quickly. These medications have a significant impact in reducing the likelihood of having a clinical relapse. If you can stop the relapses, you certainly can eventually stop most – if not all – of the disability accrual.”

Dr. Pittock spoke at the annual meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis and answered follow-up questions in an interview.
 

Treatment advances for NMOSD

NMOSD, also known as NMO, is a relapsing autoimmune inflammatory disorder that causes recurrent optic neuritis and myelitis. It’s a rare disease, affecting 0.5-10 people per 100,000, mostly women.

Several recent trials have supported the use of the drugs eculizumab (Soliris), satralizumab (Enspryng) and inebilizumab (Uplizna) in NMOSD, Dr. Pittock said, and all have received Food and Drug Administration approval to treat the condition over the past 2 years. Dr. Pittock led the PREVENT trial of eculizumab, which showed a 94% reduction of relapse risk versus placebo.

The newly approved drugs are stunningly expensive. According to Dr. Pittock, eculizumab costs $710,000 a year, while inebilizumab runs $393,000 the first year, then $262,000 a year. Satralizumab is $219,000 the first year, then $190,000 a year. Assistance programs are available, Dr. Pittock said, “and we’ve not had any major problems in terms of initiation.”

The cost of rituximab (Rituxan), which has a history of use as an off-label treatment option, is $18,000 a year and dropping, according to Dr. Pittock. There’s also new research on rituximab: In 2020, a small Japanese trial (n = 38) reported prevention of relapses compared with placebo, but Dr. Pittock cautioned that “the placebo patients seem to have a more benign course or more benign phenotypes” than the intervention group.

“There’s no doubt that rituximab works, but does it work as well as the other medications that have been through more of a robust trial process?” he asked. Keep in mind, he added, that perhaps 20%-50% of patients will relapse on rituximab.

Dr. Pittock advised colleagues to consider factors like patient schedules and compliance when choosing a drug. Satralizumab is self-administered monthly, while inebilizumab and rituximab are infused every 6 months.
 

Progress in anti-MOG disease

The trials in NMOSD should spur studies of the drugs in anti–myelin oligodendrocyte glycoprotein (MOG) disease, he said. “I think we’ll see a more rapid move toward phase 3 trials because of the experience with NMO. We will just have to wait and see which medications enter trial.”

Anti-MOG disease, also known as MOG antibody disease (MOGAD) and anti-MOG–associated encephalomyelitis, is caused by anti-MOG antibodies. Optic neuritis is very common, and transverse myelitis can occur.

The condition “actually responds to different drugs than MS and has a different immune pathophysiology,” Dr. Pittock said.

He cautioned colleagues to be aware that “the ability of the antibody to tell you whether or not the patient has the disease is less clear for MOGAD than it is for other diseases. If your patient has a low titer of MOG antibody, and their phenotype really doesn’t look like [MOGAD], you really need to interpret that with significant caution.”

He also highlighted a 2018 report that offers guidance about diagnosis and when MOG-IgC antibody tests are appropriate in CNS demyelinating disease.

Dr. Pittock reported numerous disclosures plus patents issued or pending.

Each year, roughly 1 in 60 adult patients with multiple sclerosis (MS) aged 65 years and under is hospitalized with urinary or kidney infections, a new study suggests. That’s more than quadruple the rate in a control cohort. Other types of infections affected patients with MS at a higher rate too.

“The relative risk of all types of inpatient infections and most types of outpatient infections was significantly elevated among the patients with MS. While we expected there to be increased relative risk of urinary or kidney and respiratory infections, we also found higher relative risk of viral, fungal, skin, and opportunistic infections,” said study lead author Riley Bove, MD, an assistant professor at the Weill Institute for Neurosciences at the University of California, San Francisco, who presented the findings at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis. She answered follow-up questions in an interview.

A common and treatable condition

“Bladder dysfunction may be present in over 80% of persons in MS and can be a significant source of decreased function and quality of life in addition to increased health care costs and morbidity,” neurologist Barbara Giesser, MD, of the University of California, Los Angeles, said in an interview. “It is common among persons with MS to have bladders that do not empty urine completely. This can predispose them to bladder and kidney infections. Also, some patients may try to self-manage bladder symptoms by restricting fluids, and this can predispose them to infection as well.”

Dr. Giesser, who was asked to comment on the present research, advised neurologists to bring up urinary disorders themselves instead of waiting for patients to mention them. “Patients are often embarrassed to start a discussion about genitourinary dysfunction with their neurologists but will be very appreciative of the opportunity for it to be investigated and treated,” she said. “Neurologists should make sure that this area of neurologic function is addressed in the routine management of their patients with MS because bladder dysfunction, morbidity, and complications associated with it are treatable and preventable.”

For her part, Dr. Bove recommended “early and effective identification of risk, appropriate referral to first-line interventions such as pelvic floor physical therapy and patient education, and early referral to urologists skilled in treating neurogenic bladder. Further, it is important to monitor side effects of medications to ensure there are no unrecognized immune deficits.”

She also cautioned that “common symptoms of [urinary tract infections] in people with MS include symptoms that are also prevalent in neurogenic bladder: urgency, incontinence, and frequency. It is possible that having baseline lower urinary tract symptoms could mask the recognition of a urinary infection, resulting in delayed recognition and treatment of the infections.”

EMD Serono funded the study. Dr. Bove is funded by the National MS Society’s Harry Weaver Award. She has received research support from Biogen and Roche Genentech and consulting/advisory board fees from Alexion, Biogen, EMD Serono, Roche Genentech, Sanofi Genzyme, and Novartis. Dr. Giesser reported no disclosures.

Each year, roughly 1 in 60 adult patients with multiple sclerosis (MS) aged 65 years and under is hospitalized with urinary or kidney infections, a new study suggests. That’s more than quadruple the rate in a control cohort. Other types of infections affected patients with MS at a higher rate too.

“The relative risk of all types of inpatient infections and most types of outpatient infections was significantly elevated among the patients with MS. While we expected there to be increased relative risk of urinary or kidney and respiratory infections, we also found higher relative risk of viral, fungal, skin, and opportunistic infections,” said study lead author Riley Bove, MD, an assistant professor at the Weill Institute for Neurosciences at the University of California, San Francisco, who presented the findings at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis. She answered follow-up questions in an interview.

A common and treatable condition

“Bladder dysfunction may be present in over 80% of persons in MS and can be a significant source of decreased function and quality of life in addition to increased health care costs and morbidity,” neurologist Barbara Giesser, MD, of the University of California, Los Angeles, said in an interview. “It is common among persons with MS to have bladders that do not empty urine completely. This can predispose them to bladder and kidney infections. Also, some patients may try to self-manage bladder symptoms by restricting fluids, and this can predispose them to infection as well.”

Dr. Giesser, who was asked to comment on the present research, advised neurologists to bring up urinary disorders themselves instead of waiting for patients to mention them. “Patients are often embarrassed to start a discussion about genitourinary dysfunction with their neurologists but will be very appreciative of the opportunity for it to be investigated and treated,” she said. “Neurologists should make sure that this area of neurologic function is addressed in the routine management of their patients with MS because bladder dysfunction, morbidity, and complications associated with it are treatable and preventable.”

For her part, Dr. Bove recommended “early and effective identification of risk, appropriate referral to first-line interventions such as pelvic floor physical therapy and patient education, and early referral to urologists skilled in treating neurogenic bladder. Further, it is important to monitor side effects of medications to ensure there are no unrecognized immune deficits.”

She also cautioned that “common symptoms of [urinary tract infections] in people with MS include symptoms that are also prevalent in neurogenic bladder: urgency, incontinence, and frequency. It is possible that having baseline lower urinary tract symptoms could mask the recognition of a urinary infection, resulting in delayed recognition and treatment of the infections.”

EMD Serono funded the study. Dr. Bove is funded by the National MS Society’s Harry Weaver Award. She has received research support from Biogen and Roche Genentech and consulting/advisory board fees from Alexion, Biogen, EMD Serono, Roche Genentech, Sanofi Genzyme, and Novartis. Dr. Giesser reported no disclosures.

Each year, roughly 1 in 60 adult patients with multiple sclerosis (MS) aged 65 years and under is hospitalized with urinary or kidney infections, a new study suggests. That’s more than quadruple the rate in a control cohort. Other types of infections affected patients with MS at a higher rate too.

“The relative risk of all types of inpatient infections and most types of outpatient infections was significantly elevated among the patients with MS. While we expected there to be increased relative risk of urinary or kidney and respiratory infections, we also found higher relative risk of viral, fungal, skin, and opportunistic infections,” said study lead author Riley Bove, MD, an assistant professor at the Weill Institute for Neurosciences at the University of California, San Francisco, who presented the findings at the meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis. She answered follow-up questions in an interview.

A common and treatable condition

“Bladder dysfunction may be present in over 80% of persons in MS and can be a significant source of decreased function and quality of life in addition to increased health care costs and morbidity,” neurologist Barbara Giesser, MD, of the University of California, Los Angeles, said in an interview. “It is common among persons with MS to have bladders that do not empty urine completely. This can predispose them to bladder and kidney infections. Also, some patients may try to self-manage bladder symptoms by restricting fluids, and this can predispose them to infection as well.”

Dr. Giesser, who was asked to comment on the present research, advised neurologists to bring up urinary disorders themselves instead of waiting for patients to mention them. “Patients are often embarrassed to start a discussion about genitourinary dysfunction with their neurologists but will be very appreciative of the opportunity for it to be investigated and treated,” she said. “Neurologists should make sure that this area of neurologic function is addressed in the routine management of their patients with MS because bladder dysfunction, morbidity, and complications associated with it are treatable and preventable.”

For her part, Dr. Bove recommended “early and effective identification of risk, appropriate referral to first-line interventions such as pelvic floor physical therapy and patient education, and early referral to urologists skilled in treating neurogenic bladder. Further, it is important to monitor side effects of medications to ensure there are no unrecognized immune deficits.”

She also cautioned that “common symptoms of [urinary tract infections] in people with MS include symptoms that are also prevalent in neurogenic bladder: urgency, incontinence, and frequency. It is possible that having baseline lower urinary tract symptoms could mask the recognition of a urinary infection, resulting in delayed recognition and treatment of the infections.”

EMD Serono funded the study. Dr. Bove is funded by the National MS Society’s Harry Weaver Award. She has received research support from Biogen and Roche Genentech and consulting/advisory board fees from Alexion, Biogen, EMD Serono, Roche Genentech, Sanofi Genzyme, and Novartis. Dr. Giesser reported no disclosures.