Scientists Learn How Cancer Drugs Cause Hypertension
WEDNESDAY, Aug. 5 (HealthDay News) -- A new study reveals why high blood pressure develops in up to one-third of cancer patients who take drugs to block the formation of blood vessels that feed tumors.
"Anti-angiogenesis drugs like Avastin, Sutent or Nexavar inhibit an important substance called vascular endothelial growth factor [VEGF] that stimulates the creation of new vessels that support malignant growth," senior study author Dr. Thomas Coffman, a professor of medicine, cell biology and immunology at Duke University Medical Center in Durham, N.C., said in a school news release. "Our studies in mice show that blocking VEGF causes hypertension because it disrupts an important biological system -- the nitric oxide pathway that regulates blood vessel health."
The researchers used an antibody to block an important VEGF receptor called VEGFR2. After about a week, the mice that received a high dose of the antibody showed a "rapid and sustained" increase in blood pressure.
"The higher doses of anti-angiogenesis drugs that patients need to keep their cancers from growing translate into a significant increase in risk for hypertension and, by extension, for cardiovascular complications," Coffman said.
The study appears online Aug. 3 in the journal Hypertension.
Cancer patients are living longer, Coffman noted. This means that hypertension and other side effects that might once have seemed less important must now be taken more seriously.
"Long-term hypertension can have serious consequences," Coffman said.
For many cancer patients taking anti-angiogenesis drugs, hypertension is controlled with traditional blood pressure medications, said Dr. Herbert Hurwitz, a medical oncologist at Duke.
"However, these new findings are important since they point to specific ways to better protect against the risks of long-term hypertension. They also suggest ways to protect patients against other serious but uncommon side effects, like stroke or heart attack," Hurwitz said in the news release.
-- Robert Preidt
SOURCE: Duke University Medical Center, news release, Aug. 3, 2009
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