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Pancreas Divisum Is Not a Cause of Pancreatitis by Itself But Acts as a Partner of Genetic Mutations

Bertin, Caroline PhD1; Pelletier, Anne-Laure PhD2; Vullierme, Marie Pierre PhD1; Bienvenu, Thierry PhD3; Rebours, Vinciane PhD2; Hentic, Olivia PhD2; Maire, Frédérique PhD2; Hammel, Pascal PhD2; Vilgrain, Valérie PhD1; Ruszniewski, Philippe PhD2; Lévy, Philippe PhD2

American Journal of Gastroenterology: February 2012 - Volume 107 - Issue 2 - p 311–317
doi: 10.1038/ajg.2011.424
Pancreas and Biliary Tract

OBJECTIVES: 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, orCFTRgene 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, andPRSS1-,SPINK1-, andCFTR-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 withCFTRgene-associated pancreatitis as compared with those with idiopathic and alcoholic pancreatitis (P<0.0001) and with those withSPINK1andPRSS1gene-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 withCFTRmutations or polymorphisms, suggesting a cumulative effect of these two cofactors.

1 Pôle Biologie Imagerie Pathologie Pharmacie, Service de Radiologie générale, Hôpital Beaujon, AP-HP, Université Paris VII-Denis Diderot, Clichy, France

2 Pôle des Maladies de l'Appareil Digestif, Service de Gastroentérologie–Pancréatologie, Hôpital Beaujon, AP-HP, Université Paris VII-Denis Diderot, Clichy, France

3 Laboratoire de Biochimie et Génétique Moléculaires, Hôpital Cochin, AP-HP, Paris, France

Correspondence: Philippe Lévy, PhD, Pôle des Maladies de l'Appareil Digestif, Service de Gastroentérologie-Pancréatologie, APHP, Hôpital Beaujon, 92118 Clichy Cedex, France. E-mail:

Received 26 April 2011; accepted 25 August 2011

published online 13 December 2011

© The American College of Gastroenterology 2012. All Rights Reserved.
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