Wednesday, 6 August 2008

Liver Damage In Hepatitis C Patients Could Be Treated With Warfarin, Says Study

�The drug warfarin may help keep liver failure in thousands of citizenry with Hepatitis C, according to new research.





In a study published in the Journal of Thrombosis and Haemostasis, researchers show that warfarin reduces the scarring on the liver caused by Hepatitis C. This scarring, or fibrosis, replaces normal liver cells and can lede to cirrhosis of the liver of the liver and ultimately liver failure.





Following the new findings in mouse models, the Imperial College London researchers are now embarking on a clinical trial of warfarin as a treatment for people with Hepatitis C, funded by the Medical Research Council (MRC).





There are an estimated 300,000 people in the UK with chronic Hepatitis C. The disease progresses much more than quickly in some patients than in others and around one in quintet of those infected will develop cirrhosis.





Treatment to net the infection is presently effective in only round 50 pct of patients and behind have considerable unpleasant side effects such as fatigue duty, nausea and depression. If this treatment fails, in that respect are no currently in effect therapies to slow the progression of fibrosis.





The new research looks at how warfarin affects the patterned advance of fibrosis in mice with inveterate liver injury. Warfarin is already victimized to forbid and treat blood clots in citizenry with artificial heart valves, deep nervure thrombosis, and a legion of other conditions.





A previous study by the same researchers demonstrated that in Hepatitis C, scarring of the liver accelerates in those patients who are prone to form blood clots. This led the researchers to believe that warfarin's anti-clotting properties power enable the drug to fight the disease.





The young study showed that treatment with coumadin significantly reduces the patterned advance of fibrosis in normal mice with chronic liver injury. It also shows that coumadin reduces the progression of fibrosis in mice with chronic liver injury and a genetic mutation known as Factor V Leiden (FVL), which causes fibrosis to progress at a much quicker rate than usual because it amplifies the body's clotting mechanisms.





Professor Mark Thursz, one of the authors of the study from the Division of Medicine at Imperial College London, said: "At the moment there are a dandy many the great unwashed with Hepatitis C world Health Organization have no treatment options left and it would transform their lives if we could prevent them from development liver failure. We ar looking ahead to seeing the results of our upcoming trial run in human race now that we've had such promising results in the trial in mice."





Dr Quentin Anstee, an MRC Clinical Research Fellow and the corresponding author of the subject from Imperial College London, added: "If we have positive results from the new