title: Pancreas divisum is not a cause of pancreatitis by itself but acts as a partner of genetic mutations.
abstract: OBJECTIVE
  The role of pancreas divisum (PD) as a cause of acute recurrent or chronic pancreatitis (AR/CP) is still a matter of debate.
  
  
  METHODS
  The aims of this study were to evaluate the frequency of PD diagnosed using magnetic resonance cholangiopancreatography (MRCP) in patients with AR/CP of unknown origin (n=40) after careful exclusion of all known causes and to test the hypothesis of an interaction between anatomical (PD) and functional genetic anomalies (SPINK1, PRSS1, or CFTR gene mutations or polymorphisms (n=19, 25, and 30, respectively)) that could result in AR/CP. Patients with alcohol-induced pancreatitis (n=29) and subjects who had MRCP for a nonpancreatic disease (n=45) served as controls.
  
  
  RESULTS
  PD frequency was 7% in subjects without pancreatic disease, 7% in patients with alcohol-induced pancreatitis, and 5, 16, 16, and 47% in those with idiopathic, and PRSS1-, SPINK1-, and CFTR-associated pancreatitis, respectively (P<0.0001). There was no significant difference between idiopathic pancreatitis and the two control groups. The frequency of PD was higher in patients with CFTR gene-associated pancreatitis as compared with those with idiopathic and alcoholic pancreatitis (P<0.0001) and with those with SPINK1 and PRSS1 gene-associated pancreatitis (P<0.02).
  
  
  CONCLUSIONS
  The frequency of PD was not different in patients with idiopathic pancreatitis as compared with controls, demonstrating that PD by itself is not a cause of pancreatitis. PD frequency was higher in patients with genetic pancreatitis, especially in those with CFTR mutations or polymorphisms, suggesting a cumulative effect of these two cofactors.
authors.affiliation: Pôle Biologie Imagerie Pathologie Pharmacie, Service de Radiologie générale, Hôpital Beaujon, AP-HP, Université Paris VII-Denis Diderot, Clichy, France.
authors.forename: Caroline
authors.initials: C
authors.lastname: Bertin
authors.forename: Anne-Laure
authors.initials: AL
authors.lastname: Pelletier
authors.forename: Marie Pierre
authors.initials: MP
authors.lastname: Vullierme
authors.forename: Thierry
authors.initials: T
authors.lastname: Bienvenu
authors.forename: Vinciane
authors.initials: V
authors.lastname: Rebours
authors.forename: Olivia
authors.initials: O
authors.lastname: Hentic
authors.forename: Frédérique
authors.initials: F
authors.lastname: Maire
authors.forename: Pascal
authors.initials: P
authors.lastname: Hammel
authors.forename: Valérie
authors.initials: V
authors.lastname: Vilgrain
authors.forename: Philippe
authors.initials: P
authors.lastname: Ruszniewski
authors.forename: Philippe
authors.initials: P
authors.lastname: Lévy
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D002352:Carrier Proteins / Q000235:genetics*; D049448:Cholangiopancreatography, Magnetic Resonance; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000235:genetics*; D005260:Female; D056726:Genetic Association Studies; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D008875:Middle Aged; D009154:Mutation; D010179:Pancreas / Q000002:abnormalities*; D010195:Pancreatitis / Q000209:etiology* / Q000235:genetics; D014357:Trypsin / Q000235:genetics*; D014359:Trypsin Inhibitor, Kazal Pancreatic
chemical_list: D002352:Carrier Proteins; C486642:SPINK1 protein, human; D019005:Cystic Fibrosis Transmembrane Conductance Regulator; D014359:Trypsin Inhibitor, Kazal Pancreatic; C489303:PRSS1 protein, human; D014357:Trypsin