Darwin L Conwell1,2, Peter A Banks3, Bimaljit S Sandhu4, Stuart Sherman5, Samer Al-Kaade6, Timothy B Gardner7, Michelle A Anderson8, C Mel Wilcox9, Michele D Lewis10, Thiruvengadam Muniraj11, Christopher E Forsmark12, Gregory A Cote5, Nalini M Guda13, Ye Tian14, Joseph Romagnuolo15, Stephen R Wisniewski14, Randall Brand16, Andres Gelrud17, Adam Slivka16, David C Whitcomb16, Dhiraj Yadav16. 1. Brigham and Women's Hospital, Boston, MA, USA. darwin.conwell@osumc.edu. 2. Division of Gastroenterology, Hepatology and Nutrition, Ohio State University Wexner Medical Center, Columbus, OH, 43210, USA. darwin.conwell@osumc.edu. 3. Brigham and Women's Hospital, Boston, MA, USA. 4. Virginia Commonwealth University School of Medicine, Richmond, VA, USA. 5. Indiana University School of Medicine, Indianapolis, IN, USA. 6. Saint Louis University School of Medicine, St. Louis, MO, USA. 7. Dartmouth-Hitchcock Medical Center, Lebanon, NH, USA. 8. University of Michigan School of Medicine, Ann Arbor, MI, USA. 9. University of Alabama at Birmingham Hospital, Birmingham, AL, USA. 10. Mayo Clinic, Jacksonville, FL, USA. 11. Griffin Hospital, Derby, CT, USA. 12. University of Florida College of Medicine, Gainesville, FL, USA. 13. University of Wisconsin School of Medicine, Milwaukee, WI, USA. 14. Department of Epidemiology, University of Pittsburg Graduate School of Public Health, Pittsburgh, PA, USA. 15. Medical University of South Carolina, Charleston, SC, USA. 16. University of Pittsburgh Medical Center, Pittsburgh, PA, USA. 17. University of Chicago School of Medicine, Chicago, IL, USA.
Abstract
BACKGROUND/ OBJECTIVES: Our aim was to validate recent epidemiologic trends and describe the distribution of TIGAR-O risk factors in chronic pancreatitis (CP) patients. METHODS: The NAPS-2 Continuation and Validation (NAPS2-CV) study prospectively enrolled 521 CP patients from 13 US centers from 2008 to 2012. CP was defined by definitive changes in imaging, endoscopy, or histology. Data were analyzed after stratification by demographic factors, physician-defined etiology, participating center, and TIGAR-O risk factors. RESULTS: Demographics and physician-defined etiology in the NAPS2-CV study were similar to the original NAPS2 study. Mean age was 53 years (IQR 43, 62) with 55% males and 87% white. Overall, alcohol was the single most common etiology (46%) followed by idiopathic etiology (24%). Alcohol etiology was significantly more common in males, middle-aged (35-65 years), and non-whites. Females and elderly (≥65 years) were more likely to have idiopathic etiology, while younger patients (<35 years) to have genetic etiology. Variability in etiology was noted by participating centers (e.g., alcohol etiology ranged from 27 to 67% among centers enrolling ≥25 patients). Smoking was the most commonly identified (59%) risk factor followed by alcohol (53%), idiopathic (30%), obstructive (19%), and hyperlipidemia (13%). The presence of multiple TIGAR-O risk factors was common, with 1, 2, ≥3 risk factors observed in 27.6, 47.6, and 23.6% of the cohort, respectively. CONCLUSION: Our data validate the current epidemiologic trends in CP. Alcohol remains the most common physician-defined etiology, while smoking was the most commonly identified TIGAR-O risk factor. Identification of multiple risk factors suggests CP to be a complex disease.
BACKGROUND/ OBJECTIVES: Our aim was to validate recent epidemiologic trends and describe the distribution of TIGAR-O risk factors in chronic pancreatitis (CP) patients. METHODS: The NAPS-2 Continuation and Validation (NAPS2-CV) study prospectively enrolled 521 CP patients from 13 US centers from 2008 to 2012. CP was defined by definitive changes in imaging, endoscopy, or histology. Data were analyzed after stratification by demographic factors, physician-defined etiology, participating center, and TIGAR-O risk factors. RESULTS: Demographics and physician-defined etiology in the NAPS2-CV study were similar to the original NAPS2 study. Mean age was 53 years (IQR 43, 62) with 55% males and 87% white. Overall, alcohol was the single most common etiology (46%) followed by idiopathic etiology (24%). Alcohol etiology was significantly more common in males, middle-aged (35-65 years), and non-whites. Females and elderly (≥65 years) were more likely to have idiopathic etiology, while younger patients (<35 years) to have genetic etiology. Variability in etiology was noted by participating centers (e.g., alcohol etiology ranged from 27 to 67% among centers enrolling ≥25 patients). Smoking was the most commonly identified (59%) risk factor followed by alcohol (53%), idiopathic (30%), obstructive (19%), and hyperlipidemia (13%). The presence of multiple TIGAR-O risk factors was common, with 1, 2, ≥3 risk factors observed in 27.6, 47.6, and 23.6% of the cohort, respectively. CONCLUSION: Our data validate the current epidemiologic trends in CP. Alcohol remains the most common physician-defined etiology, while smoking was the most commonly identified TIGAR-O risk factor. Identification of multiple risk factors suggests CP to be a complex disease.
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