It is well known that alcohol abstinence is related to maintenance or even reductions of selleck chemicals HVPG values in patients receiving or not receiving drug therapy,9, 20 whereas alcohol consumption clearly worsens portal hypertension both in the short21 and long term.9 Lastly, it is worth remarking that, in contrast to the study by Villanueva et al.,9 the loss of long-term response in our responders could not be attributed to a reduction of drug doses during follow-up due to intolerance or noncompliance. Only five patients (12.5%) in our cohort had their doses reduced, three of whom maintained the initial response. The present study was designed to evaluate the hemodynamic

evolution and outcomes of responders. Consequently, the comparison between the outcomes of initial responders and nonresponders is not suitable, because there are relevant differences between those groups in terms of baseline

risks, treatments received, and follow-up times. Nonetheless, two secondary observations derived from the analysis of the whole study cohort deserve consideration. First, the prognosis of those patients who rebled before the second HVPG was dismal (seven deaths and five transplants of 13 patients), which confirms data from previous studies. Second, the protection from rebleeding of nonresponders, which were kept from PF 01367338 the beginning with endoscopic ligation combined with drug therapy, was excellent. The low rebleeding rate of initial nonresponders (12%) could be related at least in part to a shorter follow-up (26 months) or a higher incidence of competing events in this subcohort, although the competing risk analysis suggested otherwise. However, from our results and from that of recent observations,22 we clearly feel that adding ligation to drug therapy in nonresponders (instead of switching them to ligation alone, as in the majority of previous studies) could be an effective approach, which should be nevertheless evaluated in a randomized controlled trial. The potential practical implications of the present study are straightforward. Our results suggest that, in an HVPG-guided

prophylactic regimen, responders could be safely treated with drug therapy alone during the 上海皓元 first 1-2 years, but whether this strategy remains effective in the long term is unknown. Consequently, it would be reasonable to reassess HVPG regularly in patients with viral cirrhosis and/or active alcohol consumption and to protect patients who have lost their response. Early rebleeders (those who rebleed before the second HVPG) may be regarded as candidates for more aggressive therapies (such as early TIPS)23 or liver transplantation, and initial or long-term nonresponders may be considered to have ligation added to drugs. All these potential implications should be ideally tested in randomized controlled trials. Before these results could be transferred to patient care, several limitations related to the design of our study should be taken into account.