Nevin Oruc, Janette Lamb, Adam Slivka, David C Whitcomb, M Michael Barmada, Onur Cagri Kutlu, Mary E Money
Context :Alterations of the renin-angiotensin system have been implicated in the pathogenesis of various diseases. The angiotensin converting enzyme is a key enzyme in the renin-angiotensin system. A deletion polymorphism of a 287-bp fragment of intron 16 of the angiotensin converting enzyme gene allele results in higher levels of circulating enzyme. ACE deletion genotype has been linked to heart diseases, sarcoidosis and liver fibrosis. The pancreatic reninangiotensin system plays a role in the development of pancreatic fibrosis and ACE inhibitors decrease pancreatic fibrosis in experimental models. Objectives :We investigated the frequency of the ACE gene insertion/deletion polymorphism in chronic pancreatitis patients and controls. Patients Subjects with familial pancreatit is (n=51), sporadic chronic pancreatitis (n=104), and healthy controls (n=163) were evaluated. Main outcome measure :The presence of ACE insertion/deletion polymorphism. Results :The frequency of the ACE gene deletion allele was similar in familial pancreatitis (49.0%) sporadic pancreatitis (51.0%) and controls (55.8%). Furthermore, there was no significant difference in clinical features between patients with ACE-insertion or insertion/deletion genotypes vs. patientswith ACE-deletion genotype. Conclusion :We conclude that the ACE deletion genotype does not make a significant contribution to the pathogenesis and the progression of chronic pancreatitis.
