simple blood test to identify multiple sclerosis

By Live Dr - Sun Oct 10, 4:40 pm

The discovery that there may be two distinct versions of multiple sclerosis has big implications for patients: Their responsiveness to the most popular first-line treatment seems to depend on which version they have.

If larger studies of patients confirm the findings, a simple blood test might someday tell people with multiple sclerosis whether they are likely to respond to the standard therapy, says senior study author Lawrence Steinman, MD, professor of neurology and neurological sciences.

Public health may benefit, too, Steinman says, as the cost savings from predicting which patients will benefit from beta-interferon, a costly bioengineered drug whose global sales come to some $4 billion a year, could be considerable.

In the study, published online March 28 in Nature Medicine, Steinman and his colleagues used an animal model of multiple sclerosis called experimental autoimmune encephalitis, or EAE, which prompts the immune system to inappropriately attack the animals’ own myelin nerve-cell coatings.

Many nerve cells in mammalian brains and peripheral tissues must convey electrochemical impulses over great distances, and quickly. Long, wirelike projections that transmit these cells’ signals to other nerve or muscle cells are coated by myelin, a natural substance whose insulating properties sustain the impulses’ strength and increase their speed.

Multiple sclerosis is triggered when, for reasons that are not clear, immune cells called T cells attack the myelin sheathing, causing symptoms including paralysis and blindness.

As for EAE, researchers can induce it using two specific chemicals that T cells secrete into the blood: gamma-interferon and IL-17.

In the new study, Steinman’s team induced two similar forms of EAE in mice by directing the myelin-attacking T cells to predominantly secrete either gamma-interferon or IL-17. The researchers found that beta-interferon improved the condition of animals whose EAE had been induced by gamma-interferon-secreting T cells, but exacerbated symptoms in those whose EAE had been induced by IL-17-secreting T cells.

Intrigued, the investigators turned to humans. The Stanford group obtained blood samples taken from 26 multiple-sclerosis patients who had been treated with beta-interferon. They measured IL-17 levels in those samples, and a clear pattern emerged. Measurements of a particular variety of IL-17, called IL-17F, clustered at either very high or very low levels in individual patients’ blood. Those with very low detectable blood levels of IL-17F responded well to beta-interferon treatment. But patients with very high IL-17F levels — about one out of three subjects — responded poorly. In fact, says Steinman, there is some evidence that beta-interferon actually worsened these patients’ conditions.

Steinman cautions that the results need to be confirmed in larger patient groups, but adds, “I think this has the potential to transform the way we take care of people with multiple sclerosis.” He says a simple, already available blood test could spare many patients the inconvenience and side effects of a drug that most likely won’t do any good. — Bruce Goldman

Stanford’s Office of Technology Licensing has filed a patent application on the use of the blood test described above. The research was funded by the National Multiple Sclerosis Society.


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