This Is MS - Lessons from Campath: Early Protection of CNS Critical

Campath-1H is a experimental treatment for MS currently in clinical trials. While this new report touches upon the promising efficacy of the treatment, its main focus is on the difference between the effectiveness of therapeutic intervention at the relapsing-remitting stage of Multiple Sclerosis versus the secondary progressive stage. The ultimate conclusion is that early and potent treatment can significantly improve the patient's health, whereas attempting to do the same when the disease has already progressed lacks impact. In a very important point, this is even true when the MRI scans show no further disease progression-- reiterating what we have learned about secondary progressive MS not being an inflammatory condition, but rather one of neuronal/axonal loss and/or degradation.

Now this study does not mean that people who are secondary progressive are beyond therapeutic hope-- what it implies is that secondary progressive patients will not benefit from this specific type of treatment targeting the reduction of inflammatory cells (e.g., likewise with Tysabri), presumably because the disease is no longer an inflammatory condition by that point. This is a positive finding, as it helps narrow the scope of treatment rather than blindly trying various poweful therapies in the hopes one will work. As bystanders to the research, it becomes quite clear that treating MS effectively will require tailored therapies-- if not to the individual then to the individual's disease stage. While we already see this in the current therapies, reinforcement breeds familiarity.

"From 1991-2002, we treated 58 patients with multiple sclerosis (MS) using the humanised monoclonal antibody, Campath- 1H, which causes prolonged T lymphocyte depletion. Clinical and surrogate markers of inflammation were suppressed. In both the relapsing- remitting (RR) and secondary progressive (SP) stages of the illness, Campath-1H reduced the annual relapse rate (from 2.2 to 0.19 and from 0.7 to 0.001 respectively; both p < 0.001). Remarkably, MRI scans of patients with SP disease, treated with Campath-1H 7 years previously, showed no new lesion formation. However, despite these effects on inflammation, disability was differently affected depending on the phase of the disease."

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Full Abstract

J Neurol. 2005 Jul 27;

The window of therapeutic opportunity in multiple sclerosis: Evidence from monoclonal antibody therapy.

Coles AJ, Cox A, Le Page E, Jones J, Trip SA, Deans J, Seaman S, Miller DH, Hale G, Waldmann H, Compston DA.

Department of Clinical Neurosciences, Box 165, Addenbrooke's Hospital, Cambridge CB2 2QQ, UK, ajc1020@medschl.cam.ac.uk.

From 1991-2002, we treated 58 patients with multiple sclerosis (MS) using the humanised monoclonal antibody, Campath- 1H, which causes prolonged T lymphocyte depletion. Clinical and surrogate markers of inflammation were suppressed. In both the relapsing- remitting (RR) and secondary progressive (SP) stages of the illness, Campath-1H reduced the annual relapse rate (from 2.2 to 0.19 and from 0.7 to 0.001 respectively; both p < 0.001). Remarkably, MRI scans of patients with SP disease, treated with Campath-1H 7 years previously, showed no new lesion formation. However, despite these effects on inflammation, disability was differently affected depending on the phase of the disease. Patients with SPMS showed sustained accumulation of disability due to uncontrolled progression marked by unrelenting cerebral atrophy, attributable to ongoing axonal loss. The rate of cerebral atrophy was greatest in patients with established cerebral atrophy and highest inflammatory lesion burden before treatment (2.3 versus 0.7 ml/year; p = 0.04). In contrast, patients with RR disease showed an impressive reduction in disability at 6 months after Campath-1H (by a mean of 1.2 EDSS points) perhaps owing to a suppression of on-going inflammation in these patients with unusually active disease. In addition, there was a further significant, albeit smaller, mean improvement in disability up to 36 months after treatment.We speculate that this represents the beneficial effects of early rescue of neurons and axons from a toxic inflammatory environment, and that prevention of demyelination will prevent long-term axonal degeneration. These concepts are currently being tested in a controlled trial comparing Campath-1H and IFN-beta in the treatment of drug-naive patients with early, active RR MS.

PMID: 16044212 [PubMed - as supplied by publisher] Copyrights to respective holders.