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Gastroenterology Research and Practice
Volume 2017, Article ID 9505460, 7 pages
Review Article

The Differential Role of Human Cationic Trypsinogen (PRSS1) p.R122H Mutation in Hereditary and Nonhereditary Chronic Pancreatitis: A Systematic Review and Meta-Analysis

1Department of Integrated Traditional Chinese and Western Medicine, West China Medical School/West China Hospital, Sichuan, China
2Division of Gastroenterology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA
3Department of Pediatric Gastroenterology, Children’s Hospital of Pittsburgh of UPMC and School of Medicine, University of Pittsburgh, Pittsburgh, PA, USA

Correspondence should be addressed to Li Wen; moc.liamg@7007ilnew, Stephen J. Pandol; gro.shsc@lodnap.nehpets, and Qing Xia; nc.moc.liamdem@gniqaix

Received 3 May 2017; Revised 22 August 2017; Accepted 7 September 2017; Published 8 October 2017

Academic Editor: Niccola Funel

Copyright © 2017 Cheng Hu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. Environmental factors and genetic mutations have been increasingly recognized as risk factors for chronic pancreatitis (CP). The PRSS1 p.R122H mutation was the first discovered to affect hereditary CP, with 80% penetrance. We performed here a systematic review and meta-analysis to evaluate the associations of PRSS1 p.R122H mutation with CP of diverse etiology. Methods. The PubMed, EMBASE, and MEDLINE database were reviewed. The pooled odds ratio (OR) with 95% confidence intervals was used to evaluate the association of p.R122H mutation with CP. Initial analysis was conducted with all etiologies of CP, followed by a subgroup analysis for hereditary and nonhereditary CP, including alcoholic or idiopathic CP. Results. A total of eight case-control studies (1733 cases and 2415 controls) were identified and included. Overall, PRSS1 p.R122H mutation was significantly associated with an increased risk of CP (OR = 4.78[1.13–20.20]). Further analysis showed p.R122H mutation strongly associated with the increased risk of hereditary CP (OR = 65.52[9.09–472.48]) but not with nonhereditary CP, both alcoholic and idiopathic CP. Conclusions. Our study showing the differential role of p.R122H mutation in various etiologies of CP indicates that this complex disorder is likely influenced by multiple genetic factors as well as environmental factors.