We have read the article by Tripathi et al.1 We found the study highly interesting, and the outcomes of the study encourage us to use carvedilol in cases with portal hypertension. Tripathi et al. compared the outcomes of carvedilol and endoscopic band ligation as primary prophylaxis for esophageal varices and concluded that the carvedilol-treated group had lower upper gastrointestinal bleeding risks. However, we have several comments about the methods of the study.
As we know, endoscopic band ligation is the preferred method in the management of bleeding esophageal varices or for secondary prophylaxis of varices. However, pharmacological treatment rather than endoscopic management is usually preferred for primary prophylaxis. Exceptions include patients who have severe liver dysfunction, large varices, or red signs on varices.2 As we have understood from the text, Tripathi et al. enrolled the cases with grade II varices in the band ligation group. A majority of the cases (45 individuals, 87%) in the band ligation group had grade II esophageal varices, whereas only seven (13%) patients had grade III varices. Additionally only two patients had red signs on esophageal varices. A total of nine (14%) patients seem to have a real indication of endoscopic variceal eradication. Hence, the authors performed unnecessary endoscopic band ligation to the majority of patients. Obviously that would increase the bleeding rate of the band ligation group and affects overall outcomes presented in this study.
Secondly, the endoscopic variceal eradication rate was too low in this study. Eradication could be achieved in 58% (43 cases) of the patients who underwent endoscopic band ligation. Moreover, more than 50% (23 cases) of eradicated varices recurred. Recurrence rate was much higher than in previous reports. We think that it would be more realistic to perform comparisons between the carvedilol-treated group and patients in whom varices had been successfully eradicated by endoscopic band ligation.
Finally, there are conflicting results in the literature regarding the development of gastric varices and portal hypertensive gastropathy following endoscopic variceal eradication. Recently, we have reported that esophageal variceal eradication with either band ligation or sclerotherapy increased both the incidence and the severity of portal hypertensive gastropathy and gastric varice formation.3 We wonder about the number of patients who developed gastric varices and portal hypertensive gastropathy in each group in the study performed by Tripathi et al. This will help us to have some information whether gastric varix formation and development of portal hypertensive gastropathy occur as complications of endoscopic variceal treatment or as a natural course of the underlying portal hypertension and cirrhosis.