Researchers Find MS Drug Fingolimod Decreases Gd-enhancing Lesions

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fingolimod and RRMS

fingolimod and RRMSFingolimod is a disease modifying therapy (DMT) used to treat relapsing remitting multiple sclerosis (RRMS) patients as well as patients who continue to present with relapses despite treatment with beta interferon drugs, and is the first oral medication to be approved by the U.S. Food and Drug Administration (FDA) to modify disease activity in multiple sclerosis.

Fingolimod’s mechanisms of action are thought to include impairment of potential cytotoxic T cells from leaving the lymph nodes, thus preventing them from inducing disease progression in the central nervous system.

It is still not known whether fingolimod directly helps or protects the cells in a person’s CNS, but evidence suggests that it may have a direct effect on nerve cell damage, enhancing the repair of myelin and holding neuroprotective properties with direct implications for patients with progressive MS.

Despite all the positive outcomes, fingolimod can also be responsible for some toxic side effects, such as temporary bradycardia (decrease in heart rate) and atrioventricular block (a type of heart rhythm disorder).

Clinical trials are currently analyzing fingolimod as a potential treatment for primary progressive MS, and the two largest clinical studies involving fingolimod have been the focus of review in a recent Multiple Sclerosis News Today article.

Fingolimod is comparable to natalizumab, a monoclonal antibody against the cell adhesion molecule α4-integrin, in preventing MS relapses, however, this correlation has not been investigated in clinical trials and natalizumab is usually preferred in the clinic since experience with this drug is more extended.

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A team of researchers from Maastricht University in The Netherlands recently studied a 31-year old woman with RRMS, who experienced severe side effects on natalizumab.

The study, entitled “Fingolimod in active multiple sclerosis: an impressive decrease in Gd-enhancing lesions and published in the BMC Neurology journal, demonstrated that after the patient had been voluntarily untreated for 4 months, she suffered a severe relapse. Treatment for the relapse included prednisone and plasmapheresis, with fingolimod administration initiated thereafter.

The researchers observed that in the following months, magnetic resonance imaging (MRI) signs significantly improved, suggesting that fingolimod can be a viable alternative for natalizumab especially for RRMS patients, with highly active and advanced disease, when natalizumab treatment is interrupted due to side effects or after a severe relapse.

Future research should be developed to understand the true potential and eventual risks of fingolimod, however, the current results are an important piece of the puzzle, with potential implications for patients suffering from RRMS.

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One comment

  1. ROBERT MORGAN says:

    Same thing happened to me. I took 17 Tysabri treatments with no mri evidence of disease progression; however, side effects were devastating with qol greatly diminished. I insisted on stopping treatment with MY plan being to participate in the phase 3 trial of BG-12. I experienced tremendous improvement in qol while off of treatment, but after 3 months suffered Tysabri withdrawal syndrone which at the time was not warned against. I suffered a bad relapse and was extremely ill until I began treatment in the active wing of the BG-12 trial. I knew that I was taking the test drug as I am sensitive to most drugs and BG-12 has easily identifiable side effects. It stabilized my condition, but after several months, the side effects became intolerable even at half dose. I quit the trial at the 18 month mark due to those side effects and soon fell ill again waiting for Gilenya’s approval by the FDA.I became so ill by the time Gilenya became available, that I did not know if I would be able to go to the monitoring site to get the first dose. I made it and after a week started to see improvements. I was the first patient in NC to receive the drug and had the experience of having been on Tysbri previously. My research and experience with both drugs instructed me of their similar but different methods of action. I hoped that Gilenya would not cause my drug sensitivity issue to prevent it’s future use. I began Gilenya Dec.of 2010 and while confident and grateful that I needed it, the side effects of fatigue and pain became extremely problematic and I read where you could try every other day dosing with a better outcome. I have been waiting to begin Lemtrada with the idea that I still have neuronal reserve that may allow myelin repair and that 2 yearly treatments may eliminate or at least reduce the drug sensitivity issues associated with other drugs that require regular ongoing dosing.

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