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Beta blockers not effective in preventing gastroesophageal complications from cirrhosis

Yale University : 13 December, 2005  (New Product)
Beta blockers are not effective in preventing development of varices, veins in the esophagus that can rupture and bleed, as a consequence of cirrhosis, according to a recent study by Yale School of Medicine researchers in the New England Journal of Medicine.
Beta blockers are not effective in preventing development of varices, veins in the esophagus that can rupture and bleed, as a consequence of cirrhosis, according to a recent study by Yale School of Medicine researchers in the New England Journal of Medicine.

Cirrhosis of the liver is the seventh leading cause of death in persons between the ages of 25-65. One of the main consequences of cirrhosis is the development and rupture of varices, which account in large part for the mortality associated with cirrhosis.

One of the lead authors of the study, Roberto Groszmann, M.D, professor in the Department of Internal Medicine, Section of Digestive Diseases, said beta blockers are routinely prescribed to prevent rupture of the varices, but some practitioners also prescribe beta blockers to all patients with cirrhosis, whether or not they have varices. This study examined the effects of beta blockers in the latter situation.

The study enrolled 213 patients of which 108 received the beta blocker timolol and 105 received a placebo. The patients were followed for five years. Forty percent of the patients developed varices, but there were no differences between the beta blocker and the placebo groups.

'Additionally, patients that received the beta blocker had more side effects, many of which were serious,' Groszmann said. 'The findings of this study clearly do not support the use of beta blockers in patients who have cirrhosis without varices since the risks far outweigh the benefits.'

He said another important finding of the study was that the development of varices depended on how high the portal vein pressure was at the beginning of the study and how much it could be lowered. The portal vein takes blood to the liver. The pressure is elevated in cirrhosis and leads to the development of varices.

Groszmann said it is unfortunate that the monitoring of this hepatic venous pressure gradient is rarely used outside of clinical research, although it now should be considered by physicians in treating patients with cirrhosis.
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