title: The functional angiotensin converting enzyme gene I/D polymorphism does not alter susceptibility to chronic pancreatitis.
abstract: BACKGROUND
  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 renin-angiotensin system plays a role in the development of pancreatic fibrosis and ACE inhibitors decrease pancreatic fibrosis in experimental models.
  
  
  OBJECTIVE
  We investigated the frequency of the ACE gene insertion/deletion polymorphism in chronic pancreatitis patients and controls.
  
  
  METHODS
  Subjects with familial pancreatitis (n=51), sporadic chronic pancreatitis (n=104), and healthy controls (n=163) were evaluated.
  
  
  METHODS
  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. patients with ACE-deletion genotype.
  
  
  CONCLUSIONS
  We conclude that the ACE deletion genotype does not make a significant contribution to the pathogenesis and the progression of chronic pancreatitis.
authors.affiliation: Department of Medicine, Division of Gastroenterology, and the Center for Genomic Sciences, University of Pittsburgh. Pittsburgh, PA, USA.
authors.forename: Nevin
authors.initials: N
authors.lastname: Oruc
authors.forename: Janette
authors.initials: J
authors.lastname: Lamb
authors.forename: Onur C
authors.initials: OC
authors.lastname: Kutlu
authors.forename: Michael M
authors.initials: MM
authors.lastname: Barmada
authors.forename: Mary E
authors.initials: ME
authors.lastname: Money
authors.forename: Adam
authors.initials: A
authors.lastname: Slivka
authors.forename: David C
authors.initials: DC
authors.lastname: Whitcomb
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000483:Alleles; D002114:Calcinosis / Q000453:epidemiology / Q000235:genetics; D002908:Chronic Disease; D004252:DNA Mutational Analysis; D018450:Disease Progression; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D016254:Mutagenesis, Insertional; D010182:Pancreatic Diseases / Q000453:epidemiology / Q000235:genetics; D010183:Pancreatic Ducts / Q000002:abnormalities; D010192:Pancreatic Pseudocyst / Q000453:epidemiology / Q000235:genetics; D010195:Pancreatitis / Q000453:epidemiology / Q000235:genetics*; D007703:Peptidyl-Dipeptidase A / Q000235:genetics* / Q000502:physiology; D011110:Polymorphism, Genetic; D012084:Renin-Angiotensin System / Q000502:physiology; D017384:Sequence Deletion
chemical_list: D007703:Peptidyl-Dipeptidase A