Statistics from Altmetric.com
I wish to raise some questions regarding the paper of Benjaminov et al on portopulmonary hypertension in decompensated cirrhosis with refractory ascites (Gut 2003;52:1355–62).
Although the role of endothelin-1 in portopulmonary hypertension has been suggested by many clinicians and is timely, as well as clinically important, issues remain concerning the limited number of patients (n = 10 portopulmonary patients) presented in this study. Furthermore, it is very difficult to demonstrate or hypothesise a role of endothelin-1 in portopulmonary hypertension without measuring gradients of endothelin-1 over the pulmonary and portal vascular beds. Without these data, how do they know where the increased levels of endothelin-1 came from?
Furthermore, why did the authors not analyse the role of circulating cytokines, such as interleukin 6 and interleukin 1β which are implicated in the pathogenesis of pulmonary hypertension? We found high plasma concentrations of endothelin-1 and in particular interleukin-6 in 15 patients affected by portopulmonary hypertension and in a group of 20 patients with primary pulmonary hypertension (endothelin-1, 5.26 (3.5) v 5.69 (1.4) pg/ml; interleukin 6, 9.1 (3.1) v 6.6 (4.4) pg/ml, respectively) compared with a group of 30 cirrhotics with ascites (endothelin-1, 1.79 (0.8); interleukin 6, 3.43 (2.7)). Our data suggest that endothelin-1 and in particular interleukin 6 show similar plasma concentrations in portopulmonary hypertension and primary pulmonary hypertension and could play a part in the pathogenesis of these diseases.1
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.