European Congress on the Treatment and Research in Multiple Sclerosis (ECTRIMS) June 6-9 2000. Toulouse, France. Treatment with Betaferon significantly reduces damage to people with Secondary Progressive Multiple Sclerosis (SPMS) and health related quality of life in addition to reducing the development of "black holes" and further confirms the importance of Betaferon in reducing disease progression and an increase in time to becoming wheelchair bound.(1)
The results on thinking and memory cognition were presented by Dr Dawn Langdon, from Royal Holloway and Institute of Neurology, London UK. Commenting, she said: "These results showing a positive effect of Interferon beta 1-b are an important step forward and confirm hints from other less comprehensive studies that the known effects of SPMS can be mitigated. Over time, patients receiving Betaferon were significantly less likely to be cognitively impaired than those receiving placebo. It has been previously documented that loss of cognitive function is associated with:
Loss of cognitive function in SPMS is a submarine dementia, it may run silent but it runs deep and is a source of destruction in people's lives." Methodological restrictions on the original trial design and the problems of comparing two populations, treated and untreated over a fraction of the disease course, led to a pre-planned secondary analysis of the data. If patients showed well below normal scores in three of five cognitive tests, they were designated 'cognitively impaired'. A significant difference was obtained between Betaferon treated and placebo patients, at 36 months (p < 0.05) when healthy volunteer learning characteristics were taken into account.
Concluding, Dr Langdon said: "There are many emotional and social factors that contribute to the impact of cognitive loss on an individual, but people with multiple sclerosis may want to take these results into account when considering proven disease modifying treatment with their doctor."
Results from the European Study Group have already demonstrated a highly significant reduction in physician related disability in people with SPMS. The study also examined health related quality of life from the patient's perspective, from a range of measures including the Sickness Impact Profile (SIP), a self-report questionnaire validated for use in MS specifically for this trial.
The results indicated a statistically significant (p<0.05) effect of Betaferon when compared to placebo at both six and twelve months and at last visit. There was also a correlation between physician and patient reported measures of change.
Discussing the results, Dr Michael Hutchinson of the Department of Neurology, St Vincent Hospital Dublin, said: "Health related quality of life is of increasing importance both to patients and health authorities. This study shows that Interferon beta 1-b slows down deterioration in patient's quality of life, it still occurs, but at a much slower rate. Significant differences were seen at various points in the study, including at the last visit.
All studies in this area have used physician measures such as disability and MRI but this is the first time that the patient's view of the effects of treatment were taken into account. What patients had to say about treatment is in accordance with physician assessment about disease activity. All measures of improvement compared to placebo treatment are relevant to treatment choices."
The study on the development of "black holes"(2) was performed in five centers, using a subgroup of 95 people with SPMS, participating in a placebo-controlled trial of Betaferon at 8 million international units (MIU) on alternate days. Six monthly unenhanced T1-weighted spin-echo magnetic resonance imaging (MRI) images were acquired over 36 months. Hypointense lesions were marked and quantified by blinded observers.
Dr Barkhof of the Vrije University Hospital, Amsterdam, said: "Our study showed that by using Interferon beta-1b (IFBN-1b) in SPMS, it is possible to reduce the formation of black holes by 45 percent over three years and a treatment effect was seen as soon as six months. The burden of disease in multiple sclerosis (MS) builds over decades rather than months or years. Reducing damage to axons and preserving the network of connections in the brain therefore may offer long-term prevention of functional damage. These results, together with other recent findings, support the idea that treating early in the development of multiple sclerosis can delay irreversible pathological changes like axonal loss, which is followed by nerve cell death. This study reinforces main clinical findings from the European trial indicating that IFNB-1b slowed disease progression in people with SPMS considerably, which is in line with our results."
The European Study of IFNB-1b in 718 people with SPMS published two years ago in The Lancet, showed a highly significant delay in the time to disease progression and time to becoming wheelchair bound in people with SPMS who received Betaferon.
In a further analysis, Professor Ludwig Kappos of Basle University, Switzerland, showed that once the trial against placebo was stopped and placebo patients could choose to take Betaferon, or not, those who chose to take Betaferon for the first time began to loose function slower than before, but that those who had been treated earlier and continued on Betaferon retained an advantage.
Professor Kappos said: "These additional analyses confirmed the robustness of the original study results and in the open label extension, there was a confirmed and sustained effect right up to 54 months. There was no one prognostic indicator of treatment response and no remarkable side effects were observed."
1) All results from the European Study Group on IFBN in SPMS. Kappos et al.
(2) 'Black holes' are destructive brain lesions, which are also known as hypointense T1 lesions. These holes destroy axons, critical nerve cells, which pass messages to the brain.
Statistical information cited within this release is provided by the European Study Group on Interferon Beta 1-b in Secondary Progressive Multiple Sclerosis.