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Two different types of MS, one big step toward personalized medicine

Larry Steinman, MD, is so committed to multiple-sclerosis research that every time he Googles something his laptop mysteriously inserts the term “multiple sclerosis” into the search – with sometimes surprising results.

Now Steinman, whose work in the 1980s led to the development of the drug Tysabri, has made another potentially profound discovery: There are apparently not just one but two types of multiple sclerosis, each associated with a distinct inflammatory mechanism.

Patients with one type (about two-thirds of the total MS population) tend to respond very well to the mainstay therapy for this disease, a costly bioengineered version of beta-interferon, a naturally occurring protein. But for the other estimated one-third of patients, beta-interferon doesn’t help. In fact, if anything it may exacerbate the condition.

Finding out which type of MS a patient has requires nothing more than administering a simple blood test to determine that patient’s circulating levels of a substance called IL-17F. No long wait for FDA approval, either: This test is already available in diagnostic labs.

If Steinman’s data (which he says needs to be corroborated in bigger studies and by other investigators) holds up, this finding could be a tough pill for beta-interferon’s three manufacturers to swallow. Beta-interferon, the first-line treatment for MS, is a $4 billion/year drug. Losing one-third of that market is going to be painful for them.

But it’s going to be a boon for patients, who will either be rerouted from the get-go to another drug more likely to be effective or, when put on beta-interferon, at least have the additional fortitude and motivation that come from being told that this regimen – which can cause nasty flu-like symptoms – is really likely to work. That’s an upgrade from beta-interferon’s reputation as a drug with only so-so prospects of success, perhaps due to the previous inability to distinguish patient populations for whom it will work from those for whom it won’t.

And it’s a big step forward for personalized medicine. No complex or pricey whole-genome scans or gene-expression microarrays or statistical analysis required, just a visit to the doc’s office and a cheap stick in the arm. Why genotype when you can phenotype?

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