Washington, D.C., June 10 -- Researchers at the University of Pittsburgh Medical Center (UPMC) have successfully controlled incontinence in an animal model of diabetes using a modified herpes virus to shuttle a therapeutic gene into damaged bladder nerves. The results, which demonstrate the feasibility of this approach in humans, could eventually benefit the more than half of all diabetics who suffer nerve damage that renders them permanently unable to urinate normally. The findings are being presented June 10 at the annual meeting of the American Society of Gene Therapy in Washington, D.C.
"This study provides the first evidence that we can repair visceral nerves and improve bladder function," said William Goins, Ph.D., assistant professor of molecular genetics and biochemistry at the University of Pittsburgh School of Medicine.
Diabetes causes a number of complications, including damage to sensory nerves that supply various tissues. Lacking sensory nerve input to the bladder, someone with diabetes cannot sense when it's time to urinate. As a result, urine backs up, causing the bladder to enlarge. The swollen bladder, which often becomes infected, is untreatable except with catheterization.
Because patients with diabetes do not have a sufficient amount of a substance called nerve growth factor (NGF), which heals injured nerve cells, the UPMC researchers surmised that delivery of the gene for NGF could provide a potential treatment for this form of incontinence.
"We are encouraged that our study may soon translate into real clinical benefit for diabetic patients," said Michael B. Chancellor, M.D., associate professor of urologic surgery at the University of Pittsburgh School of Medicine.
The UPMC team capitalized on herpes' natural ability to infect nerve cells.
They placed the gene for NGF inside a herpes vector modified to be harmless.
Then the team injected the NGF gene-bearing herpes vector into the bladders of
rats with experime
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Contact: Lauren Ward
wardle@msx.upmc.edu
412-624-2607
University of Pittsburgh Medical Center
10-Jun-1999