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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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