A new study using an “experimental mice model” has linked the use of non-steroidal anti-inflammatory drugs (NSAIDs) to liver damage in patients with a certain genetic deficiency. A team of researchers at Washington University in St. Louis published their findings in the October issue of Hepatology.

In the study, researchers administered the NSAID indomethacin (Indocin) in nontoxic doses to mice that carried a mutated form of a human gene associated with alpha-1-AT deficiency. They found that the NSAID “significantly increased liver damage” in the mice.

“These data demonstrate that environmental factors such as drug administration can affect the development of liver injury in this animal model,” says lead author David Rudnick. “And they raise the possibility that NSAIDs could have similar effects on gene and protein expression and perhaps on liver injury in people with alpha-1-AT deficiency.”

Only one in 2,000 people suffer from alpha-1-AT deficiency, but these individuals should be cautious when it comes to taking NSAIDs, a category of medication that includes popular over-the-counter options such as ibuprofen and naproxen.

“…I tell my patients with any form of chronic liver injury they should avoid NSAIDs,” Rudnick says. “The drugs have an established potential hepatotoxicity. I would say alpha-1-AT deficiency liver disease is another example where these drugs should be avoided.”

People with alpha-1-AT deficiency are susceptible to a buildup of an abnormal protein called alpha-1-ATZ in the liver. Although they’re not sure why, researchers have found that the accumulation of this protein in the liver can often lead to liver damage and even liver cancer. The administration of the NSAID in the experimental mice exacerbated this buildup, which, according to Rudnick, is a clear sign of liver injury.

This entry was posted on Monday, November 20th, 2006 at 11:04 am and is filed under Legal News.