More MS news articles for May 2002

Drug stops progression of type 1 diabetes in study

2002-05-29 17:00:30 -0400
By Amy Norton
Reuters Health

A drug that modulates the immune system's attack on the body's insulin-producing cells may slow or halt the course of newly diagnosed type 1 diabetes, preliminary research suggests.

The small study showed that in a majority of type 1 diabetics, a short course of treatment with a new monoclonal antibody preserved what remained of their insulin production and reduced their need for shots of synthetic insulin. The findings are published in the May 30th issue of The New England Journal of Medicine.

The antibody, which takes aim at a protein on immune system cells called CD3, is believed to specifically target the immune-system T cells that attack insulin-producing cells in the pancreas. It is this misguided assault on the body's own tissue that leads to type 1 diabetes. Because the body needs insulin to move sugar from the blood and into cells to be used for energy, type 1 diabetics depend on daily shots of synthetic insulin to live.

Researchers have tried before to use existing immune-modulating drugs to treat type 1 diabetes, but the problems of such long-term, "broad-spectrum" immune suppression--such as the risk of infection or cancer--have been major obstacles.

But compared with these previous attempts, "this drug, we believe, is more specific in its action," the study's lead author, Dr. Kevan C. Herold of Columbia University in New York, told Reuters Health.

In their study, Herold and his colleagues found that just 2 weeks of treatment with the antibody maintained insulin production over one year in 9 of 12 patients. This allowed them better control of their blood sugar, while reducing their need for insulin injections and causing no major side effects, according to the report.

In contrast, 10 of 12 untreated study patients saw a further decline in their ability to secrete insulin. Although the exact mechanism is unclear, the study authors speculate that the antibody therapy alters the immune response that causes type 1 diabetes.

Herold noted that if the antibody can interfere with the "natural history" of type 1 diabetes--in which patients completely lose the ability to produce insulin--this would be "no small thing." Research has shown that patients who retain some insulin production have better blood-sugar control. Better control of diabetes, in turn, reduces the risk of long-term complications of the disease, which include heart disease, kidney failure and eye damage.

All of the treated study patients, who ranged in age from 7 to 27 years, were given the antibody within 6 weeks of being diagnosed with type 1 diabetes. Herold said one of the goals of future research will be to see whether starting treatment later also works.

A larger, phase 2 study of the antibody is now under way. Exactly how long the treatment can maintain patients' insulin production is unknown; Herold said his team hopes to find it can do so "indefinitely."

In addition, the researchers want to look into whether the antibody can prevent type 1 diabetes in people considered to be at high risk. But another report in the same journal issue indicates that one preventive tactic--long-term, low-dose insulin therapy--does not work for these individuals.

The study found that daily insulin injections, plus annual infusions of the hormone, did not cut the risk of type 1 diabetes among 339 close relatives of patients with the disease. The study participants were believed to have a 50% chance of developing diabetes over the next 5 years, based on genetic screening, immune system markers and metabolic functioning.

Despite the discouraging findings, the study authors speculate that intervening earlier, or with higher doses of insulin, could still work.

In an editorial accompanying both reports, Dr. Edwin A.M. Gale of the University of Bristol in the UK calls the antibody study "encouraging."

"However," Gale adds, "the study was too small and too short to do more than whet the appetite for more."

SOURCE: The New England Journal of Medicine 2002;346:1685-1691, 1692-1698, 1740-1741.

Copyright © 2002 Reuters Limited