Abstract
Objectives: Chronic pancreatitis (CP) may be difficult to diagnose in early stages. We aimed to measure pancreatic juice (PJ) prostaglandin E2 (PGE2) concentrations to determine whether they are elevated in CP and improve diagnosis of early disease. Methods: We measured PJ PGE2 in 10 patients with established CP, 25 patients who met criteria for "minimal change" chronic pancreatitis (MCCP), and 10 normal control participants. Results: Median PJ PGE2 was elevated in CP (307 pg/ml, IQR (249-362)) and MCCP (568 pg/ml, (418-854)) compared with normal controls (104 pg/ml, (68-206)) (P ≤ 0.001). Area under receiving operator curve (AUROC) for diagnosis of CP and MCCP was 0.9 and 0.62, respectively, for PJ bicarbonate concentration alone; AUROC was 1.0 and 0.94 for the combination of PJ bicarbonate and PGE2 concentrations. Conclusions: PJ PGE2 appears to be a biomarker for CP and is elevated in both established and "minimal change" chronic pancreatitis.
Original language | English |
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Article number | e72 |
Journal | Clinical and Translational Gastroenterology |
Volume | 6 |
Issue number | 1 |
DOIs | |
State | Published - Jan 1 2015 |
Bibliographical note
Publisher Copyright:© 2015 the American College of Gastroenterology All rights reserved.
Funding
Guarantor of the article: Mark Topazian, MD. Specific author contributions: BK Abu Dayyeh: conception and design, data analysis, drafting of the manuscript. Darwin Conwell: data collection and analysis, critical revision of the manuscript. NS Buttar: data collection and analysis, critical revision of the manuscript. PA Hart, BL Bick, ST Chari, JE Clain, FC Gleeson, MJ Levy, RK Pearson, BT Petersen, S Suleiman, PA Banks, E Rajan, SS Vege: critical revision of the manuscript. V Kadilaya: data collection. LS Lee: data collection. S Chowdhary: data collection. M Topazian: conception and design, data collection, data analysis, critical revision of the manuscript, overall study supervision. All authors: approved the final version of the manuscript. Financial support: Division of Gastroenterology and Hepatology, Department of Internal Medicine, Mayo Clinic, Rochester, MN; Harvard Digestive Diseases Center (DC, NIH 5 P30 DK034854-24); and NIH NIDDK (DC, 1R21 DK081703-01A2), Burrill Family Research Grant. These entities did not participate in the conception or design of the study, the analysis or interpretation of data, the writing of the manuscript, or approval of the final manuscript. Potential competing interests: None.
Funders | Funder number |
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Division of Gastroenterology and Hepatology, Department of Internal Medicine, Mayo Clinic | |
Harvard Digestive Diseases Center | |
NIH NIDDK | 1R21 DK081703-01A2 |
National Institutes of Health (NIH) | 5 P30 DK034854-24 |
ASJC Scopus subject areas
- Gastroenterology