Sanofi Genzyme‘s Lemtrada (alemtuzumab) and Biogen‘s Tysabri (natalizumab) are more effective in preventing conversion to secondary progressive multiple sclerosis (SPMS) compared to older injectable drugs, researchers from the University of Cambridge in the U.K. reported at the 7th Joint ECTRIMS-ACTRIMS Meeting Oct. 25-28 in Paris.
The findings indicate that SPMS is, in part, a result of earlier inflammation, and that disease-modifying drugs can offset the risk of people with relapsing-remitting (RR) disease progressing to SPMS.
The study, “The effect of disease-modifying treatments on conversion to secondary progressive multiple sclerosis,” was presented by Will Brown, and examined outcomes of MS patients followed in the MSBase international registry.
According to Brown, there is “conflicting previous data about whether injectable therapies delay SPMS.”
The goal of this study was to “determine whether immunomodulatory drugs influence conversion to SPMS; determine whether the potency of disease-modifying drugs influences conversion to SPMS; and determine whether the timing of immunosuppression influences conversion to SPMS,” Brown said.
Patients in the study were treated for at least four years with a single disease-modifying treatment: injectables — a group composed of interferons and Copaxone (glatiramer acetate) — along with Gilenya (fingolimod), Lemtrada, or Tysabri.
The analysis included only patients treated with injectables before 2006, when more effective treatments became available, to reduce the risk that this group included people with milder disease.
To explore the impact of treatment in progression to SPMS, researchers compared these patients to 622 untreated patients who had been followed for an average of 9.2 years in an earlier study. To make comparisons more valid, they matched patients according to sex, baseline age, annualized-relapse rate, disability level, and disease duration.
Analyses showed that each treatment group lowered the risk of progression to SPMS to various degrees.
However, “a smaller proportion of patients converted to SPMS following treatment with fingolimod [Gilenya], natalizumab [Tysabri] or alemtuzumab [Lemtrada] compared to injectable therapies,” Brown said.
The risk (assessed as hazard ratios) to convert to SPMS among patients treated with injectables was 0.31 (follow-up of 7.9 years), 0.23 with Gilenya (follow-up 4.6 years), 0.50 with Tysabri (follow-up 4.9 years), and 0.60 with Lemtrada (follow-up 7.2 years), compared to matched untreated patients. The higher the hazard ratio, the lesser the risk.
When comparing Tysabri and Lemtrada, however, researchers noted no difference in risk of progression. Therefore, the team combined these two treatments as being “high-efficacy therapies” and compared all patients receiving them to those treated with injectables.
The analysis demonstrated that people on Tysabri or Lemtrada had a lower risk of developing SPMS compared to patients treated with injectables, over a follow-up period of 5.7 years.
The data supports the hypothesis that early inflammation drives progression to SPMS — an idea that has not been widely explored in earlier studies. It also underscores that the risk of progression can be altered by disease-modifying treatments.
“The risk of conversion from RRMS to SPMS is modifiable over 5 years with existing DMTs [disease-modifying therapies], more so with high-efficacy therapies, [Lemtrada] and [Tysabri],” the team concluded.
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