By Emma Ross
Associated Press
LONDON — Preliminary research suggests that a new drug could stop the progression of type I diabetes by halting the destruction of insulin-producing cells.
Experts say that as well as stopping deterioration in people in the early stages of the disease, the drug eventually could also be given to pre-diabetics to prevent the illness, an incurable autoimmune disease which afflicts about 15 million people worldwide.
"Right now this is probably the most exciting thing we have in front of us," said Dr. Jerry Palmer, a professor of medicine at the University of Washington who was not connected to the study. He called the results "tantalizing."
In type I diabetes, the immune system goes awry and kills insulin-producing beta cells in the pancreas. It occurs mostly in children and adolescents, but is increasingly being seen in adults. In type II diabetes, which accounts for 90 percent of diabetes and is not an autoimmune condition, the beta cells are intact but the body doesn’t use insulin properly.
Scientists believe that type I diabetes may be triggered by an infection or other irritant that puts the insulin-producing cells under stress.
The cells secrete a stress chemical, attracting immune system cells patrolling the body. The immune cells mistake the stressed beta cells as foreign invaders and release a poison to kill them.
The experimental drug, developed by Israeli pharmaceutical company Peptor Ltd., contains a substance that prompts the immune cells to release a harmless anti-inflammatory chemical meant to calm inflamed tissue instead of a deadly poison meant for an unwelcome stranger.
Similar approaches are being pursued for other autoimmune diseases, such as rheumatoid arthritis.
"This is the first study to show that you can stop beta cell destruction by outside immunization," said one of the investigators, Dr. Itamar Raz, head of the Hadassah Center for Diabetes at Hadassah-Hebrew University Medical School in Jerusalem. "We do know today for the first time that by giving a small amount of antigen we can change the whole characteristic of the immune system and stop that attack."
The study, published this week in The Lancet medical journal, involved 31 men who had been diagnosed with type I diabetes within the previous six months.
They all got the insulin injections they needed, but in addition, 15 got the drug, DiaPep277, and 16 got a fake injection. The injections were given on the first day of the study, after one month and after six months. They were followed for four more months.
"At the beginning of the study, we think that they had 3 to 7 percent of their beta cells left," Raz said. "At the end of the study, those on placebo had less than 1 percent of their beta cells left. Those on the drug had the same — 3 to 7 percent."
By the end, those who were on the drug hardly needed outside insulin, while those on placebo needed an increasing amount as the time passed, the study found.
Dr. Zihai Li, an immunologist at the University of Connecticut School of Medicine in Farmington, Conn., said that while the results were encouraging, it’s too early to say whether it’s going to be a viable option.
If the drug proves itself in further studies, it could be used to make pancreatic cell transplants more successful, Li said.
Experts estimate that when they become diabetic, patients have about 40 percent of their beta cells left.
"There is some hope to stabilize the disease very early, when there are still beta cells and it is easier to prevent later complications," said Volker Burkart, a professor of immunology and cellular biology at the German Diabetes Research Institute in Dusseldorf. "We are not sure if it can completely arrest beta cell loss, but we think it can be refined. This is just a first trial to show if there was any effect at all."
Copyright ©2001 Associated Press. All rights reserved. This material may not be published, broadcast, rewritten, or redistributed.
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