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Acute pancreatitis: Molecular biology update |
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| Authors: | David?C.?Whitcomb author-information" > author-information__contact u-icon-before" > mailto:whitcomb@pitt.edu" title=" whitcomb@pitt.edu" itemprop=" email" data-track=" click" data-track-action=" Email author" data-track-label=" " >Email author |
| Affiliation: | (1) Cell Biology & Physiology, and Human Genetics, University of Pittsburgh and Pittsburgh VA Health Care System, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania;(2) Division of Gastroenterology, Hepatology, and Nutrition, University of Pittsburgh and Pittsburgh VA Health Care System, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania;(3) Division of Gastroenterology, Hepatology, and Nutrition, Mezzanine Level, C Wing, UPMC Presbyterian Hospital, 200 Lothrop St., 15213 Pittsburgh, PA |
| Abstract: | Conclusion Molecular genetic studies provide critical information that points to trypsin as the central molecule in initiating acute pancreatitis. Susceptibility to acute pancreatitis appears to be related to the body’s ability to protect itself from trypsin activation. Once acute pancreatitis is initiated, the extent, severity, and complications are largely controlled by other factors, such as the immune response. Knowledge of these concepts will likely become more and more important as risk and pathways are better de.ned and early interventions developed. |
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