Diabetes may worsen liver encephalopathy
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In patients with cirrhosis of the liver due to infection with hepatitis C virus (HCV), the presence of diabetes is associated with earlier onset and greater severity of liver or “hepatic” encephalopathy, according to results of a prospective study.
Hepatic encephalopathy is a complication of cirrhosis of the liver. Toxic substances like ammonia that accumulate in the blood and impair the function of brain cells are believed to be contributing factors.
Dr. Samuel H. Sigal and colleagues theorize that diabetes predisposes a cirrhotic patient to hepatic encephalopathy and its exacerbation by increasing ammonia levels as a result of delayed emptying of contents of the stomach and slowed intestinal motility contributing to bacterial overgrowth. Constipation often precedes the development of hepatic encephalopathy.
Sigal, from the New York Weill Cornell Medical Center, and colleagues at the Mount Sinai School of Medicine in New York, tested their theory in 65 patients from a liver transplant program, who had HCV-related cirrhosis.
Eleven (17 percent) had no evidence of hepatic encephalopathy, 33 had mild hepatic encephalopathy, and 21 had severe hepatic encephalopathy.
Twenty patients had diabetes, including one (5 percent) who had no hepatic encephalopathy, seven (35 percent) who had mild hepatic encephalopathy, and 12 (60 percent) who had severe hepatic encephalopathy.
Sigal and colleagues found that diabetics had significantly more severe hepatic encephalopathy, at earlier stages of liver dysfunction, compared with nondiabetic subjects. However, the investigators discerned no relationship between cirrhosis severity and hepatic encephalopathy.
These findings “emphasize the importance of optimizing diabetic control,” Sigal’s group writes in the American Journal of Gastroenterology.
They caution that their study included only cirrhotic patients with HCV and so it “should not be interpreted to imply that the presence of diabetes is invariably associated with hepatic encephalopathy.”
SOURCE: American Journal of Gastroenterology July 2006.
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