Fighting A Crippler

By J. MADELEINE NASH CHICAGO

Imagine what it must be like to stroll down a street and then suddenly lurch like a drunkard. To see double images of a coffee cup, a friend's face, a newspaper. To feel dizzy because rooms seem to spin like merry-go-rounds. The onset of such symptoms 10 years ago sent Chicago sales representative Suzanne Arens, now 39, stumbling to a neurologist. The diagnosis: multiple sclerosis. "It was devastating," she recalls. "The disease progressed to where I would have an attack every six months. I was hospitalized three times." For the past five years, however, Arens has managed to remain symptom-free, the result, she is convinced, of regular treatments with a promising, if still experimental drug, beta interferon. "I used to see a wheelchair at the end of the tunnel," says Arens. "Now I see a life."

In reality, Arens doesn't know for sure whether the injections she has been giving herself every other day contain beta interferon. As one of 372 participants in a clinical trial overseen by 11 medical centers in the U.S. and Canada, Arens realizes she may have been randomly assigned to a control group and given a harmless placebo, in this case saline solution. But some telltale side effects -- chills and inflammation at the injection site -- suggest, to Arens at least, that she has been receiving the genuine article.

Last week a Food and Drug Administration panel reviewed soon-to-be-published results from the clinical trial in which Arens has been participating. The study showed that patients receiving a recombinant form of beta interferon did better than those getting the placebo. The difference was quite dramatic for those patients who received high dosages of the drug, which is manufactured by Chiron Corp. and Berlex Laboratories. Compared with the control group, high- dose patients suffered 50% fewer serious attacks of the disease, and those attacks were of shorter duration. Moreover, brain scans revealed that this group of patients incurred fewer central nervous system lesions, suggesting that the therapy may be more than purely palliative. It may in fact be the first effective weapon to slow the progress of the disease, which afflicts as many as 350,000 Americans.

The panel was sufficiently impressed to recommend -- by a vote of 7 to 2 -- that the FDA approve the drug for the 30% of MS patients who, like Arens, have a mild or moderate form of the disease, characterized by months of quiescence interrupted by terrifying relapses.

Multiple sclerosis is considered an autoimmune disease, caused by the biological equivalent of friendly fire. For reasons that remain vague, cells of the immune system turn their potent chemical weapons against the myelin sheath that protects nerve fibers in the spinal cord and brain. While the severity of the disease varies widely, the resulting nerve damage can cause progressive disablement that, after two decades, leaves 30% of patients in wheelchairs.

The path that led medical researchers to beta interferon was hardly straightforward. Initially, some scientists believed attacks characteristic of multiple sclerosis might be triggered by chronic viral infections. So in 1984 they began testing gamma interferon, one of the body's own antiviral weapons, in MS patients. To their horror, patients became dramatically worse. The false step proved instructive however. "It told us that gamma interferon was a major player in this disease," explains neurologist Dr. Kenneth Johnson of the University of Maryland at Baltimore.

Researchers later learned that the level of gamma interferon present in the cerebrospinal fluid of MS patients skyrocketed just before and during acute attacks. Attention therefore shifted to a cousin molecule, beta interferon, which appears to play the role of inhibiting gamma. At the University of Chicago, Dr. Avertano Noronha and his colleagues demonstrated that beta interferon markedly decreased the activity of white blood cells obtained from multiple sclerosis patients. Beta interferon, they found, not only restrained the proliferation of these cells, it also shut down their production of myelin-destroying compounds.

No one, it should be stressed, believes beta interferon is a cure for multiple sclerosis. Some patients receiving the drug have continued to deteriorate, while others who appear to have benefited probably would have improved anyway (the disease is often punctuated by remissions). Moreover, the utility of beta interferon for steadily progressive forms of multiple sclerosis -- an unfortunate minority of cases -- has yet to be shown.

Still, the appearance of any compound that can positively alter the course of this relentless disease is cause for cautious celebration. "Half a loaf," observes University of Chicago neurologist Dr. Barry Arnason, whose research helped stimulate interest in beta interferon, "is a lot better than no bread." If the FDA goes along with the panel's recommendation and approves the drug, says Stephen Reingold, chief of research for the National Multiple Sclerosis Society, "I predict it will be used widely -- and it should be."

With reporting by Dick Thompson/Washington