title: Angiotensin-converting enzyme insertion/deletion polymorphism in patients with acute and chronic pancreatitis.
abstract: BACKGROUND
  Reduction in angiotensin-converting enzyme (ACE) activity has been shown to attenuate pancreatic stellate cell activation and pancreatic fibrosis and suggested as a potential treatment for chronic pancreatitis. The ACE gene insertion/deletion (I/D) polymorphism in intron 16 accounts for nearly half the variation in serum ACE levels. This study determined the frequency of the I/D polymorphism in patients with acute and chronic pancreatitis.
  
  
  METHODS
  In total, 887 patients (346 with alcoholic, 443 with nonalcoholic, and 98 with acute pancreatitis) were enrolled, and were compared with 1294 healthy controls. Genotyping of the I/D polymorphism was performed by PCR or melting curve analyses.
  
  
  RESULTS
  No significant differences were found in the prevalence of the ACE-deletion genotype frequencies when patients with alcoholic (27.5%), nonalcoholic (26.4%), and acute pancreatitis (32.7%) were compared with controls (26.9%). Likewise, allele frequencies of the ACE deletion polymorphism were not significantly different in patients with alcoholic (53.8%), nonalcoholic (50.6%), and acute pancreatitis (54.1%) and controls (52.7%).
  
  
  CONCLUSIONS
  The I/D polymorphism of the ACE gene was not found to be associated with acute and chronic pancreatitis.
authors.affiliation: Department of Medicine II (Gastroenterology, Hepatology and Infectious Diseases), University of Heidelberg, Mannheim D-68167, Germany.
authors.forename: Tomas
authors.initials: T
authors.lastname: Hucl
authors.forename: Marja-Leena
authors.initials: ML
authors.lastname: Kylanpää
authors.forename: Beat
authors.initials: B
authors.lastname: Künzli
authors.forename: Heiko
authors.initials: H
authors.lastname: Witt
authors.forename: Marko
authors.initials: M
authors.lastname: Lempinen
authors.forename: Alexander
authors.initials: A
authors.lastname: Schneider
authors.forename: Esko
authors.initials: E
authors.lastname: Kemppainen
authors.forename: Matthias
authors.initials: M
authors.lastname: Löhr
authors.forename: Stephan L
authors.initials: SL
authors.lastname: Haas
authors.forename: Helmut
authors.initials: H
authors.lastname: Friess
authors.forename: Johann
authors.initials: J
authors.lastname: Ockenga
authors.forename: Jonas
authors.initials: J
authors.lastname: Rosendahl
authors.forename: Hans-Ulrich
authors.initials: HU
authors.lastname: Schulz
authors.forename: Thomas
authors.initials: T
authors.lastname: Gress
authors.forename: Manfred V
authors.initials: MV
authors.lastname: Singer
authors.forename: Roland H
authors.initials: RH
authors.lastname: Pfützer
mesh_terms: D000208:Acute Disease; D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002648:Child; D002675:Child, Preschool; D004198:Disease Susceptibility; D005260:Female; D005387:Finland; D017353:Gene Deletion; D005838:Genotype; D005858:Germany; D006801:Humans; D008297:Male; D008875:Middle Aged; D016254:Mutagenesis, Insertional / Q000235:genetics*; D010195:Pancreatitis / Q000235:genetics* / Q000378:metabolism; D050500:Pancreatitis, Chronic / Q000235:genetics* / Q000378:metabolism; D007703:Peptidyl-Dipeptidase A / Q000235:genetics* / Q000378:metabolism; D011110:Polymorphism, Genetic; D055815:Young Adult
chemical_list: D007703:Peptidyl-Dipeptidase A