Review finds no connection between drugs that block tumor necrosis factor and malignancies
TUESDAY, Oct. 28 (HealthDay News) -- TNF-antagonists, drugs widely used to treat rheumatoid arthritis (RA), don't appear to cause cancer, say Spanish researchers who analyzed data on more than 4,000 RA patients treated with the biologics.
These drugs, which have been used since 1998 and given to more than 600,000 people worldwide, interfere with biologic substances that cause or worsen inflammation in RA patients. But it's been unclear whether blocking TNF (tumor necrosis factor) increases the risk of cancer, according to background information in an American College of Rheumatology (ACR) news release about the study.
Some studies have suggested an association between RA and certain types of cancer, including lung and blood cancers, but the reasons for this increased risk are uncertain.
The data in this new study came from a drug registry called BIOBADASER, established in 2001 for long-term follow up of the safety of biological therapies in RA patients. The 4,529 RA patients treated with TNF-antagonists were compared with RA patients who didn't receive the drugs.
After they adjusted for age, sex, and RA duration/activity, the researchers found that the rate of cancer in the TNF group was very close to that of the non-TNF group (0.92 percent). Based on this, they concluded that TNF use isn't associated with an increased risk of developing cancer.
"Despite foreseen fears, blocking the tumor necrosis factor does not make patients more prone to develop cancer. All on the contrary, blocking the inflammation cascade may help diminish the overall risk of cancer in these patients," Dr. Loreto Carmona, director of the research unit at the Spanish Foundation of Rheumatology, said in the news release.
The study was presented Monday at the ACR annual meeting, in San Francisco.
The U.S. Agency for Healthcare Research and Quality has more about medicines for rheumatoid arthritis.
-- Robert Preidt
SOURCE: American College of Rheumatology, news release, Oct. 25, 2008
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