Angiotensin-converting enzyme gene insertion/deletion polymorphism in patients with chronic pancreatitis and pancreatic cancer

• Published in: Digestive surgery Vol. 28; no. 4; p. 258
• Main Authors: Lukic, Snezana, Nikolic, Aleksandra, Alempijevic, Tamara, Popovic, Dragan, Sokic Milutinovic, Aleksandra, Ugljesic, Milenko, Knezevic, Srbislav, Milicic, Biljana, Dinic, Dragica, Radojkovic, Dragica
• Format: Journal Article
• Language: English
• Published: Switzerland 01-01-2011
• Subjects: Adult; Age Factors; Aged; Female; Gene Frequency; Genotype; Humans; Logistic Models; Male; Middle Aged; Odds Ratio; Pancreatic Neoplasms - genetics; Pancreatitis, Chronic - genetics; Peptidyl-Dipeptidase A - genetics; Polymorphism, Genetic; Sex Factors; Smoking
• DOI: 10.1159/000328666
• EISSN: 1421-9883

The purpose of this study was to determine the frequency of angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and to investigate its role as a potential risk factor in patients with chronic pancreatitis and pancreatic cancer. Deletion polymorphism of the 287-bp fragment of intron 16 of the ACE gene results in higher levels of circulating enzyme and therefore may represent a risk factor for disease development. The study included 55 patients with chronic pancreatitis, 45 patients with pancreatic cancer and 128 healthy subjects. The presence of I and D variants in the ACE gene was analyzed by a polymerase chain reaction (PCR) method. Distribution of ACE ID genotypes was analyzed by means of logistic regression. When chronic pancreatitis and pancreatic cancer groups were compared in the univariate analysis, the following factors were identified as statistically significant predictors of pancreatic disease: age, gender, smoking, fat intake, ACE II genotype and ACE DD genotype. However, in the multivariate analysis, only age, gender and smoking were singled out as predictors for the occurrence of pancreatic disease. Our findings indicate that the ACE I/D polymorphism could play a role in the development of chronic pancreatitis and pancreatic cancer through interaction with other genetic and environmental factors.