new drug information for MS patients:

mrsD · 09-22-2006, 08:47 AM

This article appeared in last weeks Science News...thought you all would
be interested. Also in the biblio, there are links to other articles.

Quote:

Week of Sept. 16, 2006; Vol. 170, No. 12 , p. 179
Weapon against MS: Transplant drug limits nerve damage

Nathan Seppa

A drug originally devised to prevent immune rejection of organ transplants can lessen relapses in patients with multiple sclerosis, a new study finds.

The drug, called fingolimod, inhibits immune cells from destroying the fatty coatings of nerve fibers in the brain and spinal cord. Damage of such myelin sheaths leads to multiple sclerosis (MS) symptoms, which include fatigue, balance problems, and loss of muscle control.

Although preliminary, the study is the second piece of welcome news this year for MS patients. Citing new findings (SN: 3/4/06, p. 131: http://www.sciencenews.org/articles/20060304/fob1.asp) of the effectiveness and safety of the drug natalizumab (Tysabri), the Food and Drug Administration in June reinstated it for some MS patients. The agency had approved the drug in 2004, but sales were halted for safety reasons.

In the latest study, researchers in Europe and Canada gave a daily fingolimod pill to 160 MS patients. Half the recipients got a dose four times as high as the dose that the others received. Another group of 81 patients received inert pills.

All the patients saw a doctor regularly and underwent monthly magnetic resonance imaging (MRI) to detect myelin-sheath damage in the brain or spinal cord. The doctors didn't know which patients were receiving doses of the drug or the placebo.

Over 6 months, patients getting either drug dose were less than half as likely as the placebo patients to relapse, either developing new or stronger MS symptoms, says study coauthor Ludwig Kappos, a neurologist at the University Hospital Basel in Switzerland. MRI scans during that time revealed that patients getting the drug had fewer new sites of myelin damage than the participants receiving the placebo had.

After 6 months, the patients getting the placebo were switched to one of the fingolimod doses. Over 6 more months, most of those people had fewer relapses and fewer sites of new myelin damage than they had while receiving the placebo, the scientists report in the Sept. 14 New England Journal of Medicine (NEJM).

Fingolimod suppresses immunity. People taking the higher dose were more likely than those in the other groups to get upper respiratory infections, the researchers say.

Fingolimod appears to work by snagging newly minted immune cells that target myelin in the central nervous system and sequestering them in lymph nodes, pathologists Steffen Massberg and Ulrich von Andrian of Harvard Medical School in Boston say in the NEJM carrying the new study.

"These data are impressive," says Peter A. Calabresi, a neurologist at Johns Hopkins Medical Institutions in Baltimore. Judging from this study, fingolimod may hold off relapses better than do common MS drugs such as interferon. Only natalizumab, which is injected monthly, has performed better in tests, says Calabresi, who acknowledges that he has consulted for Novartis, the Switzerland-based manufacturer that makes fingolimod and funded the new study.

Effectiveness aside, fingolimod's real advantage might be that it's a pill, Calabresi says. "All the other drugs we have on the market are injectable therapies," he notes.

Two longer-term studies with more participants are under way, Kappos says. One is testing fingolimod against interferon beta-1a injections, and the other is another comparison with a placebo.

If you have a comment on this article that you would like considered for publication in Science News, send it to editors@sciencenews.org. Please include your name and location.

References:

Kappos, L., et al. 2006. Oral fingolimod (FTY720) for relapsing multiple sclerosis. New England Journal of Medicine 355(Sept. 14):1124-1140. Abstract available at http://content.nejm.org/cgi/content/...ct/355/11/1124.

Massberg, S., and U.H. von Andrian. 2006. Fingolimod and sphingosine-1-phosphate—modifiers of lymphocyte migration. New England Journal of Medicine 355(Sept. 14):1088-1091. Extract available at http://content.nejm.org/cgi/content/extract/355/11/1088.

Further Readings:

Matloubian, M., et al. 2004. Lymphocyte egress from thymus and peripheral lymphoid organs is dependent on S1P receptor 1. Nature 427(Jan. 22):355-360. Abstract available at http://dx.doi.org/10.1038/nature02284.

Seppa, N. 2006. Do over: New MS drug may be safe after all. Science News 169(March 4):131. Available at http://www.sciencenews.org/articles/20060304/fob1.asp.

______. 2005. Critical for coating: Protein directs nerve-sheath construction. Science News 168(Sept. 10):163. Available to subscribers at http://www.sciencenews.org/articles/20050910/fob1.asp.

Sospedra, M., and R. Martin. 2005. Immunology of multiple sclerosis. Annual Review of Immunology 23(April):683-747. Abstract available at http://dx.doi.org/10.1146/annurev.im....021704.115707.

For additional information, go to http://www.clinicaltrials.gov/ct/show/NCT00340834, and http://www.fda.gov/cder/drug/infopage/natalizumab/.

Sources:

Peter A. Calabresi
Johns Hopkins Hospital
Department of Neurology
Pathology 627
600 N. Wolfe Street
Baltimore, MD 21287

Ludwig Kappos
Departments of Neurology and Research
University Hospital
Petersgraben 4
4031 Basel
Switzerland

Steffen Massberg
Harvard Medical School
CBR Institute for Biomedical Research
200 Longwood Avenue
Boston, MA 02115

Ulrich H. von Andrian
Harvard Medical School
CBR Institute for Biomedical Research
200 Longwood Avenue
Boston, MA 02115

From Science News, Vol. 170, No. 12, Sept. 16, 2006, p. 179.

http://www.sciencenews.org/articles/20060916/fob1.asp

michael178 · 03-09-2007, 08:07 PM

Hello Mrs Doubtfire. I met you on another forum where you were an expert on all sorts of things. I am glad to find you here. And have a question, if you do not mind. I have had problems with exercise. I was a nationally ranked master swimmer, and my workout regularly consisted of multiple sets totaling 5,000 yards. That is, until one day I could not swim 300 yards without pain. I experimented with repeat swims of 50 yds at a very easy pace. At the end of three swims, or 150 yds, I hung onto the edge of the pool panting, to resupply oxygen to muscles, yet because it was such an easy swim, I had built up no CO2 and accordingly had no feelings of needing oxygen. Months later I happened to come across a bottle of multivitamins and took two. I felt a vague surge, and said to myself, I think I can swim again. Sure enough the next day I jumped into the pool and knocked off 2,000 yds in a straight swim.
I have asked everyone I could think of, what was happening to me...and have found no answers. Something obviously was interrupting my utilization of oxygen. But why the multivitamin effect?
Do you have any clues for me.
I have a rare, genetic white matter disease: an adult onset leukodystrophy (unknown type). Thanks for listening. And I'll hunt for an answer if you happen to read this and post one.

mrsD · 03-14-2007, 07:38 PM

One of the vits in the mixture is B6 which is vital for proper functioning of
muscles. Some muliti formulas have chromium in them, and this mineral helps
with glucose metabolism. If you are zinc deficient, the multi would fix that too.
Most males need zinc more than iron (for females).

However, just popping a couple of mulitis and then seeing such a surge is not
typical. Alot depends on what was in your formula, and how much.

The B-complex is typically energizing for most people, especially in higher doses.

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