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| FOR IMMEDIATE RELEASE Sept. 21, 2003, 9:30 a.m. EDT |
For more information, please contact the ATA at thyroid@thyroid.org. |
Involvement of a New Gene in Thyroid-related Eye Disease
(PALM BEACH, FLA., Sept. 21, 2003) - Gene therapy to decrease levels of
a gene found in the eye socket may be a new option for addressing a difficult-to-treat
inflammatory eye disease that strikes up to half of those with a common
thyroid condition, known as Graves' disease, according to a study being
presented today at the 75th Annual Meeting of the American Thyroid Association.
Graves' disease is a common thyroid disorder that affects women at a higher
rate than men. One in 1000 women are diagnosed with Graves' disease each
year. In addition to hyperthyroidism, 25 percent to 50 percent of individuals
with Graves' disease have an eye disease known as Graves' ophthalmopathy
(GO), also called thyroid-associated ophthalmopathy or TAO. While some
patients with GO experience only mild eye discomfort, 3 percent to 5 percent
of patients suffer from intense pain and inflammation with double vision
or even loss of vision. Currently, GO is not preventable or predictable.
Therapeutic options are limited and, because of side effects, are generally
reserved for patients with severe disease.
Examination of the tissues behind the eyes of patients with GO shows that
the fat tissues are expanded in size, with swelling of the surrounding
connective tissues. This increase in volume of tissues within the eye
socket may result in forward protrusion of the eyeball. In addition, there
may be compression of the optic nerve within the socket, which can lead
to blindness.
For these reasons, researchers at the Mayo Clinic in Rochester, Minn.,
began studying the fat tissue behind the eyes of patients with GO to determine
what causes it to enlarge. This process of growing new fat tissue is called
adipogenesis. They obtain eye tissues from patients who undergo surgery
for severe GO, and then the tissues are examined directly or grown for
a period of time in their laboratory.
In this study, the researchers measured the activity or expression of
a gene called secreted frizzled protein-1 (FRP-1) in eight GO patients'
eye tissues and compared the results with eye tissues from eight people
who had eye surgery for other reasons. They chose this gene because it
"turns off" another gene called Wnt, which when "turned
on" inhibits new fat cell production. Thus, FRP-1 is itself a stimulator
of adipogenesis. Their results showed that FRP-1 expression is 5.5 times
higher in the GO patients' tissues than it is in normal eye tissues.
"Results of this study suggest that lowering levels of the gene FRP-1
within the eye socket might be a way to decrease the harmful growth of
new fat tissue," said Rebecca Bahn, MD, senior author of the study
and a consultant in endocrinology at the Mayo Clinic. "Other approaches
might include blocking the action of FRP-1 on Wnt, or stimulating the
Wnt system directly. New medications with some of these actions are currently
under development and might be useful in the future for treatment of Graves'
ophthalmopathy."
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