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Urotensin II Levels Are an Important Marker for the Severity of Portal Hypertension in Children

Pawar, Reshma*; Kemp, William; Roberts, Stuart; Krum, Henry; Yandle, Tim§; Hardikar, Winita*

Journal of Pediatric Gastroenterology & Nutrition: July 2011 - Volume 53 - Issue 1 - p 88–92
doi: 10.1097/MPG.0b013e3182153900
Original Articles: Hepatology and Nutrition

Background and Aim: Urotensin II (U-II), a somatostatin-like cyclic peptide, was recently identified as the most potent human vasoconstrictor peptide; however, the contribution of U-II–mediated alterations in peripheral vascular tone in disease states such as chronic liver disease and portal hypertension is poorly characterised. There are no data examining U-II in chronic liver disease in children. In this study, we aimed to determine whether U-II levels in healthy children are ontogenically regulated and we explored the effect of chronic liver disease on peripheral circulating U-II levels.

Materials and Methods: U-II levels from healthy controls (n = 129) were compared with a healthy adult population (n = 80) in addition to a well-characterised cohort of children with chronic liver disease (n = 20). U-II was measured by radioimmunoassay.

Results: There was no correlation between U-II and age in healthy children (r2 = 0, P = 0.8). U-II levels were similar between the paediatric and the adult control populations (1.35 ± 0.96 vs 1.25 ± 0.78, P = 0.8). U-II was significantly elevated in children with liver disease compared with controls (1.35 ± 0.96 pmol/L vs 3.56 ± 2.21 pmol/L; P < 0.001). In addition, U-II levels positively correlated with severity of liver disease as determined by Child-Pugh score (P < 0.05) and paediatric end-stage liver disease score (P < 0.001). Levels of U-II also correlated with long-term clinical outcome.

Conclusions: These data suggest that U-II is an important marker of severity of portal hypertension in children. It is independent of age and may be a potential therapeutic target in the chronic liver disease population.

*Department of Paediatrics, University of Melbourne, Australia

Department of Gastroenterology, Alfred Hospital, Prahran, Australia

Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia

§University of Otago, Dunedin, New Zealand.

Received 3 November, 2010

Accepted 19 January, 2011

Address correspondence and reprint requests to Winita Hardikar, MBBS, FRACP, PhD, Head of Hepatology, Department of Gastroenterology, Royal Children's Hospital, Flemington Rd, Parkville VIC 3051, Australia (e-mail: winita.hardikar@rch.org.au).

The authors report no conflicts of interest.

Copyright 2011 by ESPGHAN and NASPGHAN