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Alcohol-dependent effect of PRSS1-PRSS2 haplotype in chronic pancreatitis
  1. Eszter Hegyi1,2,3,
  2. Anna Zsófia Tóth1,
  3. Áron Vincze4,
  4. Andrea Szentesi2,5,
  5. Péter Hegyi2,3,
  6. Miklós Sahin-Tóth1,6
  1. 1Center for Exocrine Disorders, Department of Molecular and Cell Biology, Boston University Henry M Goldman School of Dental Medicine, Boston, Massachusetts, USA
  2. 2Institute for Translational Medicine, University of Pécs Medical School, Pécs, Hungary
  3. 3Szentágothai Research Centre, University of Pécs Medical School, Pécs, Hungary
  4. 4First Department of Medicine, University of Pécs Medical School, Pécs, Hungary
  5. 5First Department of Medicine, University of Szeged, Szeged, Hungary
  6. 6Department of Surgery, UCLA, Los Angeles, California, USA
  1. Correspondence to Dr Miklós Sahin-Tóth, 675 Charles E Young Drive South, MRL 2220, Los Angeles, CA 90095, USA; msahintoth{at}mednet.ucla.edu

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We read with great interest the studies by Derikx et al,1 Boulling et al2 and Masson et al,3 in which the authors report that a commonly occurring haplotype spanning the PRSS1-PRSS2 locus (encoding human cationic and anionic trypsinogen) is associated with chronic pancreatitis with an allelic OR of 0.7 in European cohorts (figure 1). Tagged by the c.-408C>T variant (rs10273639), this haplotype was first identified in a GWAS by the Whitcomb laboratory.4 The small but significant protective effect is likely due to the c.-204C>A promoter variant (rs4726576) in PRSS1, which decreases trypsinogen expression and thereby reduces the risk of premature trypsin activation in the pancreas.2 Curiously, Derikx et al1 found a clear association of the PRSS1-PRSS2 haplotype with alcoholic pancreatitis only, whereas no association was evident with non-alcoholic disease. Whitcomb et al also noted that the effect of the haplotype seemed to be amplified by alcohol.4 The French study did not specify disease aetiology.2 …

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