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Cathepsin B gene polymorphism Val26 is not associated with idiopathic chronic pancreatitis in European patients
  1. F U Weiss1,
  2. C-O Behn1,
  3. P Simon1,
  4. M Ruthenbürger1,
  5. W Halangk2,
  6. M M Lerch3
  1. 1Department of Medicine A, Ernst-Moritz-Arndt Universität, Friedrich-Loefflerstr 23A, 17475 Greifswald, Germany
  2. 2Department of Experimental Surgery, Otto-von-Guericke Universität, 39120 Magdeburg, Germany
  3. 3Department of Medicine A, Ernst-Moritz-Arndt Universität, Friedrich-Loefflerstr 23A, 17475 Greifswald, Germany
  1. Correspondence to:
    F U Weiss
    Department of Medicine A, Ernst-Moritz-Arndt Universität, Friedrich-Loefflerstr 23A, 17475 Greifswald, Germany; ulrich.weiss{at}uni-greifswald.de

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Pancreatitis is thought to be a disease of autodigestion triggered by premature and intracellular activation of digestive proteases.1 We and others have shown that lysosomal cathepsin B can activate trypsinogen intracellularly2 and that a large proportion of pancreatic cathepsin B is physiologically sorted into the secretory compartment.3 Further support for a role of cathepsin B in pancreatitis came from a recent study published by Mahurkar and coworkers in Gut4 in which the authors reported that a leucine to valine mutation at position 26 of cathepsin B (L26V) is associated with tropical calcifying pancreatitis (odds ratio ∼2.2) in patients from southern India. Tropical calcifying pancreatitis is also associated (in up to 50% of cases) with mutations in the SPINK1 gene5—with N34S being the most common mutation. In the study by Mahurkar et al the cathepsin B L26V …

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