More MS news articles for April 2002

A Year's Advances Bring Convenience, Little More

A Year's Progress Against Multiple Sclerosis Leaves One Patient Unmoved

http://www.washingtonpost.com/wp-dyn/articles/A16221-2002Apr8.html

Tuesday, April 9, 2002
By Jennifer L. Huget
Special to The Washington Post

In the 12 months and one week since I learned I had multiple sclerosis, I've kept a folder marked "MS" in my file cabinet, filling it with news clippings about advances in MS research. It's a pretty thick file, and well it should be: The National MS Society alone spends $30 million a year on about 300 ongoing research projects, while the National Institutes of Health spends more than twice that amount annually on MS research.

Sticking stuff in the file feels like progress. But progress is relative: For all those hundreds of projects involving thousands of people and millions of dollars, we're really no closer today to curing MS than we were a year ago. In fact, as Stephen Reingold, vice president of research programs for the National MS Society, puts it, we're still at the most primitive levels of understanding the disease, which turns out to be almost infinitely complex, involving complicated interactions among some of the body's most mysterious systems.

MS is commonly known as an autoimmune disease, meaning that in people who have it, the immune system attacks things in the body (in MS, that thing is the protective myelin that coats the nerves in the brain and spinal column) as if they were foreign intruders. But researchers are still teasing out the interrelationships -- involving the immune system, the central nervous system, genes, gender and hormones -- that may contribute to the disease.

These complexities make nearly every aspect of one's life suspect. A study last year showed that teachers, for reasons unknown, develop MS at a higher rate than the general population. Another seemed to confirm the long-standing suspicion that the Epstein-Barr virus, best known as the cause of mononucleosis, may be an MS trigger. We've learned that hormones associated with pregnancy may temporarily suppress MS symptoms. Despite a dearth of scientific evidence, a lot of people maintain that mercury-amalgam fillings cause MS. But nobody has a clue how all of these pieces fit together, or indeed whether they are even part of the puzzle.

Race for the Treatment
 

MS's complexity makes it hard for researchers to figure out how to stop or prevent it. So while talk of a cure is muted these days, research tends to focus on therapy -- drugs and other treatments that might slow or alter the disease's progress in the 250,000 to 350,000 Americans estimated to have it. As a sign of just how important drug therapy is in the MS universe, one of the biggest developments of the past year was the introduction of new diagnostic criteria designed to identify the disease in its earliest stages, using high-tech tools such as magnetic resonance imaging (MRI) and lumbar puncture (spinal tap) to detect the disease rather than waiting around for definitive symptoms to show up. The rationale behind this consensus opinion is that MS is, since the introduction of the interferon drug Betaseron nearly 20 years ago, treatable, and that drug therapies administered early can actually slow its progression.

I benefited from this new policy when I was diagnosed last April; my neurologist caught my disease early and put me right on a course of daily injections of Copaxone, one of four disease-modifying MS drugs now available in the United States for treating the most common form of MS, called relapsing/remitting MS. I'm grateful for the swift action, and doubly grateful that, either because of the daily shots or the unknowable natural course of my disease, I'm really no worse off now than I was a year ago. A recent MRI image showed no evidence of new lesions on my brain, and while my toes tingle all the time and I'm incessantly tired, I'm still walking, seeing and writing.

But who knows if my luck will hold? Reingold calls the current drug therapies -- the interferons Avonex, Betaseron and Rebif (the last of which was approved for use in the United States in March) and Copaxone (the brand name for glatiramer acetate) -- only modestly effective, even though Copaxone and Avonex have been recently proven to prevent accumulation of "black holes," or areas of severe damage, in the brain.

Okay, so the best treatments we have are only modestly effective. Great. What's next?

All eyes are on the new drug Antegren, a monoclonal antibody that approaches MS in a whole different way. While the four other drugs try to intercept damage-causing immune cells before they reach the myelin but after they've entered the central nervous system, Antegren -- in animal studies, anyway -- stops errant immune cells from passing from the blood to the brain in the first place. Large-scale human trials are underway. Watch this space for jubilant celebration if the stuff ends up working. (Antegren is also being tested as a treatment for Crohn's disease, an autoimmune disease affecting the bowel, and it may prove useful in treating other autoimmune diseases.)

In the meantime, many researchers have come to believe that no single drug will be the magic bullet; for them, combination therapies -- pairings of two or more drugs in hopes of maximizing benefits -- offer the greatest hope. Reingold calls this "an evolution in thinking" about treating the disease. Trials testing the safety and efficacy of Avonex and Antegren administered together started in December at sites throughout the country, including George Washington University Medical Center, and a small study pairing Avonex and Copaxone last year showed the combination was safe and a larger trial was warranted.

The MS Horizon
 

Some people are putting a lot of stock in things like gene therapy and stem cell research as eventual keys to solving the MS riddle, but that's looking pretty far down the road. Likewise, a team at Yale this year experimented with taking myelin-producing cells from an MS patient's ankle and sticking them in her brain, to see whether they could produce myelin there. That work is ongoing, and its implications won't be fully understood for years.

I've got all this stuff in my MS file. But more tantalizing to me are articles like the one about a study in which Viagra seemed to help restore nerve function in the brains of rats in whom stroke-like damage -- comparable to that caused by MS -- had been induced. You go, rats! But it is the unwise patient -- not to mention the imprudent journalist -- who puts too much stock in rat studies, which might never translate into benefits for humans.

So I like to stick to concrete, real-time advances. Like, for instance, the fact that, while a pill version of Copaxone failed its trials last year, the drug will soon be available in pre-filled syringes. Doesn't sound like much, but it'll save me a good hour every week that I'd otherwise spend mixing my own. Maybe I'll finally finish reading "The Corrections."

Truth told, the development that likely has had the most payoff for me came not in the field of MS studies but in the realm of breast cancer. Researchers last year determined that participation in a support group, for all its probable social, psychological and practical benefits, didn't translate to higher survival rates for breast cancer patients. For people like me who have opted out of the support group movement, this news came as comfort: Instead of feeling guilty that by staying home I'm not taking enough responsibility for my own healing, I'm happy to know that at least I'm not digging my own grave by doing so.

Mankind has come up with cures for lots of diseases, and you never know when one of those great "Eureka!" moments might happen with MS. So for the foreseeable future, I guess I'll be clipping my articles, stuffing my file and squirting my daily 1.1 ml of Copaxone into one of seven well-bruised injection sites on my body. (Imagine how I look forward to bathing suit season.)

And I'll continue to be optimistic. Things are better now than they were before, and they'll continue to improve, if even in small ways. I'm convinced that a good attitude helps. Plus, it makes it easier for others to put up with me.

So I guess you can say I'm hopeful but not getting my hopes up. Given the past 12 months, it looks like I'm in it for the long haul.

Jennifer Huget is a regular contributor to the Health section.
 

© 2002 The Washington Post Company