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FRIDAY, July 11 (HealthDayNews) -- Scientists have long known that people suffering from Graves' disease have certain molecules that mistakenly attack their bodies, sending their thyroids into overdrive.

But for 40 years, no one has been able to identify these elusive molecules, known as autoantibodies. Now, in the July 12 issue of The Lancet, British researchers report they have finally managed to isolate the human monoclonal autoantibody that causes the thyroid to overproduce.

Although the molecule was isolated in only one patient, a 19-year-old man with Graves' disease, it could hold significant promise for the future diagnosis and treatment of the disease.

"Monoclonal" means that the antibodies come from one line of cells. "It's thought to be one rogue cell that then multiplies itself," says Donald Bergman, president of the American Association of Clinical Endocrinologists. "It means a single clone of cells that's gone awry is producing this antibody that's causing all this damage. It's a very, very exciting discovery."

Because only one cell line appears to be involved, researchers may be able to find extremely targeted treatments for the disease.

"The identification of this antibody and its availability to medical scientists represents a major step forward. Further studies will likely lead to a better understanding of Graves' disease," says Dr. Kenneth Hupart, chief of endocrinology, metabolism and diabetes at Nassau University Medical Center in East Meadow, N.Y. "More importantly, this report offers the promise of new therapies that may benefit patients with Graves' disease, the disfiguring eye problems that they can develop and can give rise to new approaches to caring for patients with thyroid cancer."

But Hupart also has a caveat. "These potential benefits will not be realized today or tomorrow, but they may help doctors lessen the burden of these thyroid diseases for patients in future years," he says.

The leading cause of hyperthyroidism, Graves' disease represents a basic defect in the immune system, causing production of antibodies that stimulate and attack the thyroid gland, causing growth of the gland and overproduction of thyroid hormone, according to the National Graves' Disease Foundation.

The disease comes about through a complicated process of reactions and counter-reactions. First, plasma cells in the body produce autoantibodies that attack the TSH (thyroid-stimulating hormone) receptor on the thyroid gland. In response, mirror-image antibodies are produced which stimulate the TSH receptor to neutralize the original autoantibodies. This causes the thyroid gland to overproduce thyroid hormone.

Graves' disease is unusual in this respect. "Most autoimmune processes are destructive. Either an antibody or an immune cell is programmed to destroy something," Bergman explains. "In Graves', that antibody is being produced to stimulate. It's mighty unusual."

But, if this is going to happen, it's just as well that it involves a monoclonal antibody, or just one cell line. This means that not all of the immune cells are being programmed to interfere with the thyroid gland, which in turn is good news when it comes to treatment possibilities.

"You certainly don't want to destroy the whole immune system," Bergman says. With this finding, it may be possible to devise an extremely targeted treatment which would affect only that one cell line and not the whole immune system.

Right now, treatment options for Graves' disease involve incapacitating or removing the thyroid gland. According to the National Graves' Disease Foundation, there are three standard methods of treatment. A patient might take drugs to inhibit the production of active thyroid hormone; he or she might take radioactive iodine to destroy part or all of the gland; or most of the gland could be surgically removed.

"Roughly half who take these drugs are cured," Bergman says. "Otherwise you have to destroy the thyroid or take it out. People who take synthetics [hormones] feel OK, but they don't feel quite like they did before because they lose the ability to make second-to-second adjustments. It's better than nothing."

More information

For more on Graves' disease, visit the National Graves' Disease Foundation or the American Thyroid Association.