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Study claims Tysabri improves cognitive impairment(14/07/15)

Researchers in Italy have published findings claiming Tysabri (natalizumab) can improve cognitive impairment in patients with relapsing remitting multiple sclerosis (RRMS) over the course of at least three years.

In the study, Natalizumab Significantly Improves Cognitive Impairment Over Three Years In MS: Pattern Of Disability Progression And Preliminary MRI Findings, researchers at the Spedali Civili of Brescia investigated the impact of Tysabri treatment on cognitive impairment in a cohort of 24 patients with RRMS who were treated for three years. Patients were assessed through neuropsychological tests and in terms of relapse rate and expanded disability status scale (EDSS) score.

Researchers found that after three years of Tysabri treatment, a significant reduction in the number of impaired neuropsychological tests was achieved, along with a considerable decrease in annualized relapse rate and a stable EDSS in comparison to baseline. A particular significant improvement was found in memory, attention and executive function test scores.

The team also analysed brain cortical atrophy in a patient subgroup through magnetic resonance imaging (MRI). Preliminary results showed that after three years of Tysabri treatment there were no alterations in grey matter volume but a significantly greater parahippocampal and prefrontal grey matter density, which correlated with the neuropsychological improvement observed.

The research team concluded that Tysabri therapy can reduce cognitive impairment in RRMS patients in a long-term period of three years. The team suggests that Tysabri most likely has a neuroprotective role concerning cortical grey matter in the brain.

The findings were published in the journal PLoS One.

Source: Multiple Sclerosis News Today © BioNews Services 2015 (14/07/15)

Tags: MS, multiple sclerosis, Cognition, Natalizumab, Tysabri, Research

Tysabri review launched in Europe(11/05/15)

In light of growing evidence, the European Medicines Agency (EMA) has been asked to launch a review of the multiple sclerosis drug Tysabri to assess whether advice on managing known risks for progressive multifocal leukoencephalopathy (PML) should be revised.

PML is a rare brain infection caused by the JC virus (JCV), which has symptoms that may resemble those of an MS attack and may be fatal or result in severe disability. In addition to the presence of anti-JCV antibodies, other risk factors for PML are treatment duration, especially beyond two years, and immunosuppressant use before receiving Tysabri. Patients with all of the above risk factors have a significantly higher risk for PML.

Tysabri was approved in the European Union in June 2006 as a single disease-modifying therapy in highly active relapsing remitting MS (RRMS). It's indicated for patients with high disease activity despite treatment with a β-interferon or glatiramer acetate and in those with rapidly evolving severe RRMS. Tysabri was first approved by the US Food and Drug Administration (FDA) in November 2004.

The review will involve evaluating the data on the risk for PML, with the aim of better defining the risk and identifying further measures to minimize it and will be carried out by the Pharmacovigilance Risk Assessment Committee (PRAC), which will make a set of recommendations. The PRAC recommendations will then be forwarded to the Committee for Medicinal Products for Human Use.

The final stage of the review procedure is the adoption by the European Commission of a legally binding decision applicable to all EU member states.

The EMA has recently been made aware of new information in three key related issues, a statement from the agency notes:

Risk estimates: Tysabri treatment decisions are based on an algorithm in which the estimated PML incidences are calculated in a static way by pooling data from all sources (clinical studies, registries, spontaneous reports). However, interim data from the STRATIFY 2 study for patients with positive anti-JCV antibody status with and without a history of immunosuppressive treatment suggested a higher risk for PML than currently described in the algorithm.

Diagnosis of PML before the development of clinical symptoms: New data seem to suggest that asymptomatic PML cases have a higher survival rate (95.6 per cent) than do symptomatic cases (77.1 per cent). Current recommendations are to perform MRI within 3 months before initiating treatment and then annually. Recent literature suggests that more frequent MRI testing may detect a greater proportion of asymptomatic cases.

Anti-JCV antibodies: It was thought that a negative serologic anti-JCV antibody test suggested a very low probability of PML (about 0.01 per cent), but evidence from the AFFIRM and STRATIFY 1 studies showed nearly 13 per cent of negative patients could become positive during follow-up.

Currently, it's recommended that these patients be retested every six months for antibodies, but a more sensitive second-generation enzyme-linked immunosorbent assay was recently developed. Whether this affects current recommendations for antibody testing needs to be assessed.

Tysabri is a monoclonal antibody, administered through intravenous injection, that is designed to recognize and attach to a protein on the surface of leucocytes. By blocking this protein, the drug prevents leukocytes from going from the blood to the brain, thereby reducing inflammation and nerve damage caused by MS.

Source: Medscape Multispeciality Copyright © 1994-2015 by WebMD LLC (11/05/15)

Increasing Tysabri dosing interval may cut PML risk(23/04/15)

Freedom from relapse was maintained in multiple sclerosis patients on Tysabri who received the infusion drug less frequently than the recommended 4-week interval, with lower risk of progressive multifocal leukoencephalopathy (PML), preliminary results from an ongoing analysis have indicated.

Among 886 patients treated with "extended" dosing at 10 American MS centers, the mean annualized relapse rate was the same at 0.1 per year as in 1,078 patients receiving Tysabri at the standard 4-week interval, according to Lana Zhovtis-Ryerson, MD, of NYU Langone Medical Center in New York City. MRI lesions counts were also similar.

Although patients testing positive for the JC virus - the pathogen whose reactivation triggers PML, a sometimes fatal brain inflammation - comprised 59 per cent of the extended dosing group, none have so far developed PML, she reported to the American Academy of Neurology's annual meeting.

With a total of 1,023 patient-years of exposure to Tysabri in this JC-positive subgroup, published risk algorithms show an expected incidence of 2.5 cases, Zhovtis-Ryerson and colleagues calculated.

At this point the finding of zero cases with extended dosing is not statistically significant, the researchers cautioned - but if the exposure reaches 1,248 patient-years with still no cases, it will be significant.

Meanwhile, two PML cases have developed in the standard-dosing group, among whom 41 per cent are JC-positive and who have received a mean of 30 Tysabri doses (SD 22).

Brian Weinshenker, MD, of the Mayo Clinic, who was not involved with the study, told MedPage Today the approach deserves more study but urged caution in adopting it clinically.

He noted if just one patient in the extended dosing group developed PML, "it would have completely negated any trend to reduced risk."

PML has been the primary concern with Tysabri almost since it was introduced in 2004. When several cases turned up shortly after its approval, the drug was withdrawn for some months, then relaunched with a restricted distribution program that included clinician and patient education on the risk.

The question of how to reduce PML risk with Tysabri, which exceeds one per cent in patients positive for JC virus and who have two other risk factors (treatment duration and history of immunosuppressant therapy), has occupied MS neurologists since the relaunch. Most studies have shown patients who discontinue the drug or take long "holidays" experience a spike in relapse risk. Switching to another drug has not prevented such spikes because a months-long washout period after Tysabri discontinuation is needed before starting a different agent.

Some clinicians have been experimenting instead with longer dosing intervals, in the belief that the four-week schedule keeps the drug's target - alpha4beta1 integrin, an adhesion molecule involved in immune cell trafficking - so saturated that JC virus immune surveillance is eliminated. Extending the interval may relax the immune suppression just enough to keep latent JC virus under control while still maintaining the anti-relapse effect.

In the current study, Zhovtis-Ryerson and colleagues sought to capture this empirical experience by canvassing centers that have adopted the strategy with some patients.

They defined extended dosing as any interval from 31 days up to 61 days. They further subdivided the extended dosing patients into those with early extended dosing and late extended dosing. Another 309 patients had dosing that varied and could not be classified into either of those groups.

Patients in the extended dosing groups were at somewhat higher risk for PML than those treated at the recommended interval, with a higher proportion testing positive for JC virus, more patients with a history of immunosuppressant therapy (18 per cent versus 11 per cent), and more total Tysabri doses (mean 39 versus 30). Patient age, disease duration, and gender balance did not differ markedly between standard and extended dosing groups, however.

Among extended dosing patients, the mean duration of that schedule was 23 months overall. These varied only modestly between the early, late, and variable dosing regimens.

Treatment efficacy (Tysabri 's forte) was excellent irrespective of dosing interval. Some 65 per cent of standard and 65 per cent of extended dosing groups showed no evidence of disease activity (NEDA). That is, no active MRI lesions and no clinical activity. The variable extended dosing group suffered a little bit in this respect, with 55 per cent meeting the NEDA standard compared with about 70 per cent for both early and late dosing.

Weinshenker commented that selection of patients for extended dosing, which was not random, might have involved "biases against committing more aggressive MS patients on the extended interval program, which might reduce the ability of the investigators to detect reduction in efficacy."

Nevertheless, he said, extended dosing "is a promising and sensible approach that might turn out to be effective."

Zhovtis-Ryerson and colleagues have established a registry called EXTEND to which other clinicians may contribute, at www.msbase.org. They are also planning a prospective study to examine effects of the different regimens on disability progression over time.

The study had no external funding and authors declared they had no financial interests relevant to the work.

Source: Medpage Today © Medpage Today 2015 (23/04/15)

Extending natalizumab up to eight weeks ‘safe and effective’(21/04/15)

In a study of 1,964 patients with multiple sclerosis, researchers at the NYU Langone Multiple Sclerosis Comprehensive Care Center found that extending the dose of natalizumab from four weeks up to eight weeks was shown to be well-tolerated and effective in patients, and resulted in no cases of the potentially fatal side effect progressive multifocal leukoencephalopathy (PML).

The drug showed similar efficacy in treating disease activity among patients, according to the study led by Lana Zhovtis-Ryerson, MD, an assistant professor of neurology at the NYU Langone Multiple Sclerosis Comprehensive Care Center.

Natalizumab is an infusion drug known as a monoclonal antibody that is used to prevent MS symptoms and flare-ups and slow worsening disability.

However, taking the medication for longer than two years may increase risk for a rare but potentially fatal side effect called PML, an untreatable brain infection that occurs in up to 1.3 percent of patients taking natalizumab.

The medication is typically prescribed in 300-milligram infusions every four weeks.

"There remains much unknown about whether the drug will lose effectiveness if dosing is extended," explains Dr. Zhovtis-Ryerson. "Our study showed treatment with natalizumab was safe for patients with similar efficacy reported as the standard dosing, potentially enabling patients to stay on effective MS medication at a reduced frequency of infusions and with lower risk of PML. "

Zhotvis-Ryerson and colleagues at 10 American MS. Centers sought to compare the safety and efficacy of an extended dose of natalizumab to the standard dose. They retrospectively compared 1,078 patients taking a standard 4-week dose to 886 taking an extended dose between 4 weeks, 3 days and 8 weeks, 5 days.

The researchers found extending the dosing schedule of natalizumab to between 5 and 8 weeks does not affect the drug's efficacy profile with 65 per cent of participants in each group not showing clinical MS activity, and comparable rates of new lesions reported on imaging. Zero cases of PML were reported in the extended dosing group, while two cases were reported in the standard dose group, though the researchers said statistical significance has not been reached yet. No other major adverse events were reported.

"While the findings are encouraging, more research is needed to determine whether extending natalizumab dosing may reduce disability progression," says Dr. Zhovtis-Ryerson.

Natalizumab is manufactured by Biogen and Elan, and sold under the name Tysabri.

Source: MedicalXpress © Medical Xpress 2011-2015, Science X network (21/04/15)

Possible biomarker for Tysabri response in MS(18/03/15)


Hematopoietic mobilization: Potential biomarker of response to natalizumab in multiple sclerosis.

Mattoscio et al.

OBJECTIVE: To ascertain the mobilization from the bone marrow and the functional relevance of the increased number of circulating hematopoietic stem and progenitor cells (HSPC) induced by the anti-α-4 integrin antibody natalizumab in MSers.

METHODS: We evaluated CD45lowCD34+ HSPC frequency by flow cytometry in blood from 45 natalizumab-treated MSers (12 of whom were prospectively followed during the first year of treatment as part of a pilot cohort and 16 prospectively followed for validation), 10 untreated MSers with MS, and 24 healthy donors. In the natalizumab-treated group, we also assessed sorted HSPC cell cycle status, T- and B-lymphocyte subpopulation frequencies (n = 29), and HSPC differentiation potential (n = 10).

RESULTS: Natalizumab-induced circulating HSPC were predominantly quiescent, suggesting recent mobilization from the bone marrow, and were capable of differentiating ex vivo. Circulating HSPC numbers were significantly increased during natalizumab, but heterogeneously, allowing the stratification of mobilizer and non-mobilizer subgroups. Non-mobilizer status was associated with persistence of disease activity during treatment. The frequency of B cells and CD103+CD8+ regulatory T cells persistently increased, more significantly in mobilizer MSers, who also showed a specific naive/memory B-cell profile.

CONCLUSIONS: The data suggest that natalizumab-induced circulating HSPC increase is the result of true mobilization from the bone marrow and has clinical and immunologic relevance. HSPC mobilization, associated with clinical remission and increased proportion of circulating B and regulatory T cells, may contribute to the treatment's mode of action; thus, HSPC blood counts could represent an early biomarker of responsiveness to natalizumab.

Source: Neurology. 2015 Mar 11. © 2015 American Academy of Neurology.(18/03/15)

Anti-NMDA may explain some MS mental deficits(11/11/14)

Prematurely severe cognitive impairment in multiple sclerosis patients could be an effect of autoantibodies against the N-methyl-D-aspartate (NMDA) receptor complex, with natalizumab (Tysabri) withdrawal a potential contributor, a case report from Germany suggested.

In an MS patient who had to be confined to a nursing home at age 39 because of cognitive deficits amounting to dementia, immunoglobulin G-type antibodies to the NMDA receptor's NR1 subunit were found in cerebrospinal fluid samples, according to Klemens Ruprecht, MD, of Charité-Universitätsmedizin Berlin, and colleagues.

These autoantibodies are "the characteristic laboratory finding of anti-NMDA receptor encephalitis," they wrote online in JAMA Neurology.

When severe cognitive deficits appear at young ages, Ruprecht and colleagues concluded, they could "be related to a superimposed antibody-mediated autoimmune encephalitis."

Cognitive deficits are common in MS patients but the mechanisms underlying them are not well understood, the researchers noted. Normally these come on gradually and at later ages. However, as in the current case, occasionally such deficits appear early and progress rapidly. In such cases, clinicians should consider causes outside the MS disease process, Ruprecht and colleagues suggested.

"The diagnosis of those patients will require a high degree of clinical suspicion as cognitive symptoms are rather frequent in MS and may mask or be confounded with features of antibody-mediated encephalitides," they wrote. "Nevertheless, testing for antineuronal antibodies appears warranted in patients with MS with unusual neuropsychiatric symptoms."

Also, in the patient who was the subject of the case report, the anti-NMDA antibody pathology may have had some relation to treatment with natalizumab.

Case Details

The woman was first diagnosed with MS at age 33. Her disease course was unremarkable until age 37 when she gave birth, and then rapidly developed cognitive deficits marked primarily by memory loss. She was treated aggressively with MS therapies including natalizumab, cyclophosphamide, and mitoxantrone, with no impact on the progression of cognitive decline.

At age 43, during her fourth year of nursing home residency, she underwent a complete re-evaluation that included analysis of current and stored serum and CSF samples. At that point, anti-NMDA antibodies were discovered in the CSF samples, including those taken shortly after the cognitive symptoms appeared.

The natalizumab was withdrawn 2 years after the patient started on it, out of concern for the risk of progressive multifocal leukoencephalopathy since she had also been on immunosuppressive therapy.

Five months later, she developed a "fulminant" MS relapse, the researchers indicated, which was accompanied by a spike in anti-NMDA antibody titers -- a sign that the latter may have had some connection to the natalizumab withdrawal.

Ruprecht and colleagues noted that the drug suppresses CD138-positive plasma cells. "Therefore, it seems plausible that natalizumab withdrawal facilitated entry of NMDA receptor antibody-producing plasma cells to the central nervous system," they wrote.

The patient died of urosepsis last December, almost 8 years after the onset of cognitive symptoms.

She represented only the second known case of anti-NMDA encephalitis in an MS patient, the researchers indicated, and the first in whom the antibodies targeted the receptor complex's NR1 subunit (NR2B was the target in the previous case).

But they suggested the comorbid conditions may occur more frequently than these case reports might suggest, because cognitive impairments are common in MS and clinicians may not think to look for other causes.

The study was funded by the German government. Authors reported relationships with Bayer Healthcare, Merck Serono, Biogen Idec, Novartis, Ovamed, Teva, Diamed, Genzyme, and Sanofi.

Primary source: JAMA Neurology
Source reference: Fleischmann R, et al "Severe cognitive impairment associated with intrathecal antibodies to the NR1 subunit of the N-methyl-D-aspartate receptor in a patient with multiple sclerosis" JAMA Neurology 2014; DOI: 10.1001/jamaneurol.2014.1817.

Source: Medpage Today © 2014 MedPage Today, LLC (11/11/14)

Natalizumab neutralizing antibodies in MS appear inreased by smoking(06/10/14)

Smoking appears to increase the likelihood of developing neutralizing antibodies to natalizumab (Tysabri, Biogen Idec), which cause the drug to have little, if any, therapeutic effect in multiple sclerosis (MS), a new study suggests.

The study was presented by Tomas Olsson, MD, Karolinska Hospital, Stockholm, Sweden, at the recent MS Boston 2014, the 2014 Joint Americas and European Committees for Treatment and Research in Multiple Sclerosis (ACTRIMS/ECTRIMS) meeting.

"The lung seems to be an important immunoreactive organ where irritation such as smoking may increase risk not only for inflammatory diseases, but also neutralizing antibodies to biologicals like interferon β and monoclonal antibodies such as natalizumab," he concluded.

"While smoking should not prohibit use of natalizumab, the percentage of patients developing antibodies, neutralizing the effect of the treatment, is not negligible," Dr Olsson commented to Medscape Medical News. "Therefore patients should be advised about our findings. This comes on top of an increased risk for MS with smoking, and probably a worse disease course."

In his presentation, Dr Olsson explained that smoking is thought to contribute to the induction of neutralizing antibodies to interferon β-1a, so he and his colleagues aimed to investigate the influence of smoking on the risk of developing antibodies to natalizumab, another biological drug in the treatment of MS.

The study was based on 1338 natalizumab-treated patients with MS included in either of two Swedish case-control studies in which information on smoking habits was collected. Treatment-related information was obtained from the Swedish national MS registry and antibody status from the Swedish Nab lab. Enzyme-linked immunosorbent assay was applied before therapy start and after 6, 12 and 24 months. Through use of logistic regression, patients with different smoking habits were compared regarding risk of developing anti-natalizumab antibodies.

Results showed that compared with nonsmokers, the odds ratio (OR) of developing anti-natalizumab antibodies was 2.4 (95% confidence interval [CI], 1.2 - 4.4) for patients who smoked at the time of screening, and a significant trend showed higher risk of developing antibodies with higher intensity of smoking.

The increased risk remained when smoking within 2 years prior to screening was considered (OR, 2.7; 95% CI, 1.5 - 5.1).

Still Try Natalizumab in Smokers

Commenting on the study for Medscape Medical News, Heinz Wiendl, MD, University of Münster, Germany, called this an "interesting observation," but he said the findings would not discourage him from using natalizumab in smokers.

"The prevalence of neutralizing antibodies to natalizumab is quite low — maybe affecting around 5% to 9% of patients. We can easily identify the patients who develop these antibodies because they don't respond to the drug."

He continued: "If a patient has neutralizing antibodies the drug effect will be zero. Natalizumab is a strong drug and there should be an obvious reduction of relapses and MRI lesions when a patient starts on it. If this does not happen, I think we can assume there are neutralizing antibodies present and then we would switch to a differemt treatment."

Dr Olsson has received nonrestricted MS research grants and/or compensations for lectures and advisory boards from Biogen Idec, Genzyme, Novartis, TEVA, and Merck. Dr Wiendl reports honoraria and consultation fees from Bayer HealthCare, Biogen Idec, Fresenius Medical Care, GlaxoSmithKline, GW Pharmaceuticals, Merck Serono, Novartis, Sanofi-Genzyme BioVentures, and Teva Pharmaceutical Industries.

MS Boston 2014: 2014 Joint Americas and European Committees for Treatment and Research in Multiple Sclerosis (ACTRIMS/ECTRIMS). Abstract PS5.4. Presented September 11, 2014.

Source: Medscape Multispeciality © 1994-2014 by WebMD LLC (06/10/14)

PML risk with Natalizumab in MS identified with new test(30/09/14)

A new test seems to be able to stratify patients at risk for progressive multifocal leukoencephalopathy (PML) while receiving the multiple sclerosis (MS) drug natalizumab more effectively than anything available at present.

The test is based on observations that patients who develop PML appear to have very low levels of L-selectin (CD62L) on CD4+ T cells in the months or years before they develop the condition.

"We believe that very low levels of L-selectin is a predictive test for the future risk of PML on natalizumab," stated Dr. Heinz Wiendl, University of Münster, Germany.

He presented the data at the recent MS Boston 2014, the 2014 Joint Americas and European Committees for Treatment and Research in Multiple Sclerosis (ACTRIMS/ECTRIMS) meeting.

Dr. Wiendl explained that he and his colleagues noticed that some patients receiving long-term natalizumab had reductions in levels of L-selectin. "In particular patients who developed PML tended to have very low levels of L-selectin, so we thought it might be a good biomarker," he said.

They therefore went back and analyzed blood samples from a larger group of natalizumab recipients. "We now have data on 1000 patients treated with the drug, of whom 15 have developed PML," he reported.

"Of these 15 patients, 14 showed very low levels of L-selectin (less than 21.6) in samples of peripheral blood taken months or years before PML developed."

Asked for comment on these findings, Robert J. Fox, MD, Mellen Center for Multiple Sclerosis at Cleveland Clinic in Ohio, said he thought this was one of the "most exciting developments" presented during the meeting.

Dr. Wiendl told Medscape Medical News that he is now testing all patients after 18 months of natalizumab and then every 6 months thereafter. "If one value is low then the patient is at significant risk of PML and we stop the drug."

Dr. Wiendl believes that L-selectin is far more selective than JC virus V (JCV) antibodies for identifying patients at risk for PML.

"About half of patients test positive for JCV antibodies, but only about 10% of patients have low levels of L-selectin," he noted. "JCV positivity puts patients at a risk of about 1 in 100 of developing PML, but with low L-selectin levels the risk is more like 1 in 10," he estimated.

The L-selectin test is also more reliable in patients who have had previous immunosuppression, he added.

Synergistic With JCV Antibody Status

Dr. Wiendl is not advocating that L-selectin replace the JCV antibody test but rather that they be used together. "I see it as a combined effort, as the 2 markers appear to be synergistic," he said.

The problem, however, is that the L-selectin test is not easy to perform. It involves purifying and isolating mononuclear cells and then performing multicolor flow cytometry. "At the moment our L-selectin test is just at the transition from academic to clinical," he noted. It is now undergoing validation in different cohorts in France and Spain.

Dr. Wiendl's team is offering the test to centers in Germany, Austria, Switzerland, and Benelux (Belgium, the Netherlands, and Luxembourg) at present and is open to the idea of expanding the service to other countries. However, there is a logistical issue in that the blood has to be processed within 24 to 36 hours so the mononuclear cells are still viable, which limits long travel distances to the laboratory. Dr. Wiendl is looking at ways to commercialize the test to enable more widespread use.

Dr. Fox emphasized the importance of risk stratification for complications such as PML. "With these complications what we try to do is risk-stratify and risk-mitigate," he told Medscape Medical News. "We want to stratify patients to understand their risk, and then mitigate that risk as best we can. This test promises to help us do just that."

He said the sensitivity and specificity of the L-selectin test were reported to be about 90%, "which is very encouraging."

"I would be eager to have the test available for general clinical use so that we can use that to help guide patients regarding their risk, and not just predicting the risk but also perhaps identifying those that are in the early stages of having developed PML," he added.

Dr. Wiendl reports honoraria and consultation fees from Bayer HealthCare, Biogen Idec, Fresenius Medical Care, GlaxoSmithKline, GW Pharmaceuticals, Merck Serono, Novartis, Sanofi-Genzyme BioVentures, and Teva Pharmaceutical Industries; grants and contracts with Bayer HealthCare, Biogen Idec, the German Ministry for Education and Research, Deutsche Forschungsgesellschaft, the Else Kröner Fresenius Foundation, the Fresenius Foundation, the Hertie Foundation, Merck Serono, Novartis, the NRW Ministry of Education and Research, the Interdisciplinary Center for Clinical Studies in Münster, Germany, the RE Children's Foundation, sanofi-aventis/Genzyme, and Teva Pharmaceutical Industries. Dr. Fox reports he has received personal consulting fees from Novartis, Biogen Idec, GlaxoSmithKline, MedDay, Questcor, Teva, and XenoPort; has served on advisory committees for Biogen Idec and Novartis; and received research grant funding from Novartis.

MS Boston 2014: 2014 Joint Americas and European Committees for Treatment and Research in Multiple Sclerosis (ACTRIMS/ECTRIMS). Abstract PS6.5. Presented September 11, 2014.

Source: Medscape Multispeciality © 1994-2014 by WebMD LLC (30/09/14)