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Reuters Health Information (2006-03-30): Long-term prophylaxis can prevent variceal bleeding in cirrhotic patients

Clinical

Long-term prophylaxis can prevent variceal bleeding in cirrhotic patients

Last Updated: 2006-03-30 15:05:42 -0400 (Reuters Health)

NEW YORK (Reuters Health) - In cirrhotic patients with esophageal varices, pharmacologic reduction in hepatic venous pressure gradient (HVPG) to 12 mm Hg or below, or more than 20% of baseline, is associated with a dramatic and sustained decrease in the risk of first variceal bleeding, a new study shows.

"Pharmacologic therapy did not delay but effectively prevented first variceal bleeding during its long-term use," investigators point out in the American Journal of Gastroenterology for March. "These findings support the recommendation that patients with cirrhosis and esophageal varices should receive lifelong pharmacologic therapy to prevent first variceal bleeding."

Nonselective beta-blockers are the first-line therapy. Published reports indicate that the risk of first bleeding is nearly halved by continued propranolol or nadolol therapy over a median follow-up of 2 years.

The current study shows that the protective effects of continued beta-blocker therapy extend to 8 years. The cohort consisted of 71 cirrhotic patients with esophageal varices who received propranolol (20 mg twice daily) alone or with isosorbide mononitrate (up to 40 mg twice daily).

Twenty-five patients (35%) responded to therapy. The remaining 46 patients (65%) did not respond to treatment.

According to Dr. Juan Turnes and colleagues from the University of Barcelona, Spain, the 8-year cumulative probability of being free of first variceal bleeding was 90% in responders versus 45% in nonresponders. The lack of hemodynamic response was an independent predictor of first variceal bleeding.

Moreover, reduction in HVPG also lowered the long-term risk of spontaneous bacterial peritonitis and bacteremia.

"These findings emphasize the validity of measuring the HVPG response as a surrogate marker of the clinical response to the pharmacological treatment of portal hypertension," Dr. Turnes and colleagues conclude.

Am J Gastroenterol 2006;101:506-512.

 
 
 
 
                 
 
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