UB Study Shows that Early Drug Treatment Can Delay Symptoms of Multiple Sclerosis in High-Risk Patients

BUFFALO, N.Y. -- A study in this week's New England Journal of Medicine led by Lawrence Jacobs, Irvin and Rosemary Smith Professor of Neurology at the University at Buffalo, has shown that early treatment with one of the drugs used to control multiple sclerosis (MS) can significantly reduce the rate at which people at high risk develop full-blown symptoms of the disease.

"The results of this study demonstrated that treatment with interferon beta-1a reduced the rate of development of clinically definite MS for these high-risk individuals by 44 percent versus treatment with placebo," Jacobs said.

The study involved 50 medical centers in the United States and Canada, and was halted early because the results were so strong. Researchers believe the results could help thousands of patients who currently don't get treatment until they have substantial brain or nerve damage.

"To date, there are no accepted guidelines for treating patients who have experienced a single MS-like attack, but who have not yet developed clinically definite MS," Jacobs said. "This study is important because it indicated that initiating therapy with interferon beta-1a at the first indication that a patient may have MS can significantly delay development of the disease."

Jacobs and colleagues urged physicians to use MRI scans to identify patients at high risk of MS so that this early treatment can be considered as an option to avoid further nerve damage. Jacobs heads the Department of Neurology at Kaleida Health's Buffalo General Hospital and is chief of the Baird Multiple Sclerosis Research Center at Kaleida's Millard Fillmore Hospital.

MS is a chronic disease of the central nervous system that affects approximately 350,000 Americans and about 1 million people worldwide. It strikes primarily young women between the ages of 20 and 40 years. Symptoms include vision problems, loss of balance, numbness, weakness, difficulty walking and paralysis.

The condition is thought to be caused by an immune attack on myelin, the fatty tissue that surrounds and protects central-nervous-system nerve fibers and facilitates the flow of nerve impulses to and from the brain. The loss of myelin disrupts this flow and produces the symptoms of MS.

The current trial sought to determine the effect of treatment with interferon beta-1a in individuals who had experienced the first symptoms of nerve damage, such as visual loss in one eye, and whose MRI scans showed brain abnormalities indicating they were at high risk for the second clinical attack or the diagnosis of clinically definitive MS. Current guidelines for diagnosis of clinically definitive MS stipulate there must be at least two separate clinical attacks at least one month apart and more than one area of central-nervous-system myelin damage, Jacobs said.

The study involved 383 patients determined to have a high probability of developing MS based on symptoms associated with the disease and brain changes seen on MRI scans. Participants received weekly muscular injections of either the active drug or placebo. Results showed:

• The rate of development of clinically diagnosed MS was 44 percent lower in the drug treated group than in the placebo group

• The volume of brain lesions was 91 percent lower in the treated patients than in the non-treated patients

• Brain MRIs can identify persons at risk and should be taken at the earliest symptoms of potential MS.

Jacobs was the first American researcher, beginning in the 1970s, to test a form of beta interferon, a naturally occurring substance in the body, in the treatment of MS. Since that time, he has lead several MS studies using interferon beta-1a, a genetically engineered form of beta interferon. His prior research has shown that the drug, approved by the Federal Drug Administration in 1996, slows the accumulation of physical disability and decreases the frequency of clinical flare-ups in patients with relapsing forms of MS.