Abstract

Gastroesophageal varices are present in approximately 50% of patients with cirrhosis and bleeding from these is the most common lethal complication of cirrhosis [ [1] Garcia-Tsao G. Sanyal A.J. Grace N.D. Carey W. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Hepatology. 2007; 46: 922-938 Crossref PubMed Scopus (1333) Google Scholar ]. Cirrhotic patients without varices can develop them at a rate of 8% per year, and the ones with small varices can develop large varices at a similar rate [ 2 Groszmann R.J. Garcia-Tsao G. Bosch J. et al. Beta-blockers to prevent gastroesophageal varices in patients with cirrhosis. N Engl J Med. 2005; 353: 2254-2261 Crossref PubMed Scopus (712) Google Scholar , 3 Merli M. Nicolini G. Angeloni S. et al. Incidence and natural history of small esophageal varices in cirrhotic patients. J Hepatol. 2003; 38: 266-272 Abstract Full Text Full Text PDF PubMed Scopus (377) Google Scholar ]. Among these, variceal hemorrhage occurs at a yearly rate of 5–15%, with most important risk factors for bleeding being the size of varices, decompensated cirrhosis (Child B/C) and the endoscopic presence of red wale marks [ 1 Garcia-Tsao G. Sanyal A.J. Grace N.D. Carey W. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Hepatology. 2007; 46: 922-938 Crossref PubMed Scopus (1333) Google Scholar , 4 The North Italian Endoscopic Club for the Study and Treatment of Esophageal Varices Prediction of the first variceal hemorrhage in patients with cirrhosis of the liver and esophageal varices. A prospective multicenter study. N Engl J Med. 1988; 319: 983-989 Crossref PubMed Scopus (1060) Google Scholar ]. The current guidelines by the American Association for the Study of Liver Diseases (AASLD) recommend combination of pharmacological therapy (somatostatin or its analogues octreotide and vapreotide; terlipressin) and endoscopic therapy (endoscopic variceal ligation or sclerotherapy) to control active variceal bleeding [ [1] Garcia-Tsao G. Sanyal A.J. Grace N.D. Carey W. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Hepatology. 2007; 46: 922-938 Crossref PubMed Scopus (1333) Google Scholar ]. These recommendations, based on the results of two randomized trials, demonstrate the superiority of combined therapy versus endoscopic variceal ligation alone. Although these advances in the management of bleeding oesophageal varices over the last two decades have led to significant reduction in mortality, mortality rates are still at least 20% at 6 weeks [ [5] Bendtsen F. Krag A. Møller S. Treatment of acute variceal bleeding. Dig Liver Dis. 2008; 40: 328-336 Abstract Full Text Full Text PDF PubMed Scopus (49) Google Scholar ]. The major cause of this mortality is the initial failure to control bleeding or the early rebleeding within the first week of admission [ [1] Garcia-Tsao G. Sanyal A.J. Grace N.D. Carey W. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Hepatology. 2007; 46: 922-938 Crossref PubMed Scopus (1333) Google Scholar ]. Most of these high risk patients are the ones with very high (>20 mmHg) hepatic venous pressure gradient. If no treatment is administered, late rebleeding occurs in approximately 60% of untreated patients, mostly within 1–2 years of the index haemorrhage [ [1] Garcia-Tsao G. Sanyal A.J. Grace N.D. Carey W. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Hepatology. 2007; 46: 922-938 Crossref PubMed Scopus (1333) Google Scholar ]. Hence, can we perform a better therapy which is easy to use, has less rebleeding rates and more importantly decreases mortality compared to the current recommended management?

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