Researchers Find MS Drug Fingolimod Decreases Gd-enhancing Lesions
Fingolimod 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.
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.