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WEDNESDAY, Sept. 9 (HealthDay News) -- Scientists may have discovered part of the reason why Tysabri, a drug used to treat multiple sclerosis, may lead to the development of a rare but potentially deadly brain disease in some patients.
The drug seems to rouse the typically dormant JC virus from its slumber, allowing it to cross into the brain.
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Although this finding may lead to a way of predicting who is at risk for the brain infection -- called progressive multifocal leukoencephalopathy (PML) -- at this point, the implications are still unclear.
"We don't know what this means until we find out over time whether or not people actually do get PML," said Patricia O'Looney, vice president of biomedical research at the National Multiple Sclerosis Society in New York City. "But it certainly is exploring a key question."
The study authors also warned against coming to premature conclusions.
"We don't advocate a change in management [of the disease] at this point because the clinical relevance of these findings is still unknown," said Dr. Igor J. Koralnik, senior author of a paper appearing in the Sept. 10 issue of the New England Journal of Medicine. "But it should spur further research."
Natalizumab (Tysabri) first received U.S. Food and Drug Administration approval in November 2004, only to be pulled from the market three months later after several patients in clinical trials developed the rare but deadly viral infection.
According to the study authors, as of July 24, 2009, 13 patients with multiple sclerosis taking Tysabri are known to have developed PML, along with one patient with Crohn's disease (Tysabri was approved to treat Crohn's in early 2008).
The JC virus is present yet dormant in about 90 percent of people. It can reactivate in people with AIDS or otherwise compromised immune systems.
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