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Rodent of the Week: Aspirin may prevent liver damage

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Liver damage can occur in a number of ways, such as side effects of drugs, alcohol abuse and obesity-related disease. But a study in mice shows it may be possible to prevent some types of liver damage with aspirin.

The discovery was made when researchers explored, on a detailed molecular level, what happens when the liver is damaged. For example, acetaminophen, or Tylenol, overdoses cause many cases of liver damage. But the drug’s direct effect on the liver is only part of the problem. After the injury occurs, the body’s immune system kicks into high gear, triggering inflammatory cells that release toxic substances and cause even more destruction. ‘Whenever the body gets injured (hammer hitting a thumb) there is the initial injury, and then a secondary inflammation (redness, warmth, pain),’ said Dr. Wajahat Mehal, an associate professor of digestive diseases at the Yale School of Medicine researcher and the lead author of the study, in an e-mail to The Times.

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Mehal found, however, that this second wave of damage was preventable by giving aspirin. He gave mice aspirin and then delivered a toxic dose of acetaminophen to the animals. The aspirin significantly protected the mice against liver damage. The study was published this week in the Journal of Clinical Investigation.

More research is needed, but aspirin may be a tool to prevent some types of liver damage. Acetaminophen poisoning is the most common cause of death due to liver failure in the developed world, Mehal said. Adding aspirin to acetaminophen may reduce toxicity from these accidents. Human studies are now needed to assess the dose of aspirin needed and the timing of aspirin therapy.

‘This offers the exciting possibility of reducing a lot of pain and suffering in patients with liver diseases using a new and very practical approach,’ he said. ‘Unlike a lot of discoveries where it will take years to get the medication to market, this could be applied very quickly and also at relatively little expense.’

-- Shari Roan

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