Background: In liver cirrhosis, the renin-angiotensin-aldosterone system is involved in the pathogenesis of portal hypertension. Its effector, angiotensin II, is generated by angiotensin-converting enzyme (ACE). Serum ACE levels are affected by I/D polymorphism of its gene, with alleles I and D being associated, respectively, with lesser and greater activity of the enzyme. In cirrhotic patients carrying the ACE I allele, an increased risk for gastro-oesophageal varices was observed. Aim: The aim of our study was to evaluate whether ACE I/D polymorphism influenced portal pressure. Methods: Fifty-one consecutive cirrhotic patients were divided based on ACE genotype (DD, ID, and II). Kidney and liver function tests, upper endoscopy, and hepatic venous pressure gradient measurement (HVPG) were performed in all patients. Results: The presence of the ACE I allele was associated with a higher HVPG value (18.7 ± 6.4 vs 10.3 ± 6.3 mmHg; P < .001), higher frequency of large gastrooesophageal varices (59.3% vs 25.0%; P < .05), and higher frequency of variceal bleeding (63.0% vs 29.2%; P < .05). No significant differences were found between patients with and those without the ACE I allele regarding Child-Pugh score, MELD score, ascites, and hepatic encephalopathy. Conclusion: ACE I/D polymorphism seems to influence the severity of portal hypertension and the risk of variceal bleeding in liver cirrhosis, regardless of the severity of liver disease.
- ACE polymorphism
- Gastro-esophageal varices
- Hepatic venous pressure gradient