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Molecular pathophysiology of chronic pancreatitis—an update

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Journal of Gastrointestinal Surgery

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Conclusion

The pathogenesis of chronic pancreatitis is still not completely understood. However, recent advances in cellular and molecular biology have revealed complex interactions between in.ammatory cells and pancreatic parenchyma cells, as well as alterations in nerves. Furthermore, as a result of novel technologies, it has become possible to identify key genes in the disease process of chronic pancreatitis. Tryptase,15 CRISP3,16 and COMP17 are three of the candidate genes that may serve as disease markers and therapeutic targets in the future. Further molecular and cell biology studies will increase our knowledge of the pathogenesis and pathophysiology of this disease, hopefully resulting in better diagnostic and therapeutic modalities in the future.

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Authors and Affiliations

  1. Department of General Surgery, University of Heidelberg, Im Neuenheimer Feld 110, 69120, Heidelberg, Germany

    Helmut Friess M.D. (Vice-Chairman)

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  1. Helmut Friess M.D.
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  2. Jörg Kleeff M.D.
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  3. Markus W. Büchler M.D.
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Correspondence to Helmut Friess M.D..

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Friess, H., Kleeff, J. & Büchler, M.W. Molecular pathophysiology of chronic pancreatitis—an update. J Gastrointest Surg 7, 943–945 (2003). https://doi.org/10.1016/j.gassur.2003.10.002

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  • DOI: https://doi.org/10.1016/j.gassur.2003.10.002

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