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      Vitamin K Therapy Slows Spread of Liver Cancer: Presented at DDW

      By Roberta Friedman

      SAN FRANCISCO, CA -- May 29, 2002 -- Portal vein invasion (PVI), seen frequently in patients with hepatocellular carcinoma, can be prevented in half treated with vitamin K, researchers say.

      They presented their results here at the 103rd annual meeting of the American Gastroenterological Association and Digestive Disease Week (DDW), held May 19-23.

      Diagnosis of PVI is a frequent event after diagnosis of liver cancer. Dr. Yukihiro Koike, of the department of gastroenterology, University of Tokyo, Japan, and colleagues previously showed a close association between levels of des-g-carboxy-prothrombin (DCP) in serum and development of portal invasion in patients with hepatocellular carcinoma.

      In Dr. Koike's study, 120 patients were treated with ablation, embolization, or both between February 1999 and November 2001at the University of Tokyo or its affiliated hospitals. All patients enrolled had low serum levels of DCP (60 IU/L or more). Half of patients were randomized to receive oral vitamin K-II at a dose of 45 mg/day.

      Dr. Koike said that 50 of the treated patients had hepatitis C, as did 52 of the controls. The groups were well matched on other criteria as well.

      Average follow up was 12 months. Patients had computed tomography scans every six months, ultrasound at three-month intervals, and DCP levels measured every month.

      Results show that 59 percent of patients treated with vitamin K-II were alive at two years compared to 29 percent of those who were not given vitamin K-II (p=0.14). Invasion of the cancer into the portal vein occurred in 2 percent of the vitamin K-II treated group at one year and in 13 percent at two years, compared to 21 and 55 percent of controls, respectively.

      Dr. Koike said that vitamin K-III, which was not available in Japan at the time of the study, might be an even more effective treatment for prevention of PVI. Vitamin K-III has been shown to interfere with the electron transport chain in mitochondria and thereby slow cell growth and cancer spread, he said.



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