E J Duell1, E Lucenteforte2, S H Olson3, P M Bracci4, D Li5, H A Risch6, D T Silverman7, B T Ji7, S Gallinger8, E A Holly4, E H Fontham9, P Maisonneuve10, H B Bueno-de-Mesquita11, P Ghadirian12, R C Kurtz13, E Ludwig13, H Yu14, A B Lowenfels15, D Seminara16, G M Petersen17, C La Vecchia18, P Boffetta19. 1. Unit of Nutrition, Environment and Cancer, Cancer Epidemiology Research Program, Catalan Institute of Oncology (ICO-IDIBELL), Barcelona, Spain. Electronic address: eduell@iconcologia.net. 2. Department of Epidemiology, Institute for Pharmacological Research 'Mario Negri', Milan; Department of Preclinical and Clinical Pharmacology 'Mario Aiazzi Mancini', University of Florence, Florence, Italy. 3. Department of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer Center, New York. 4. Department of Epidemiology and Biostatistics, School of Medicine, University of California, San Francisco. 5. Department of Gastrointestinal Medical Oncology, the University of Texas MD Anderson Cancer Center, Houston. 6. Department of Epidemiology and Public Health, School of Public Health, School of Medicine, Yale University, New Haven. 7. Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, USA. 8. Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada. 9. School of Public Health, Louisiana State University, New Orleans, USA. 10. Division of Epidemiology and Biostatistics, European Institute of Oncology, Milan, Italy. 11. National Institute for Public Health and the Environment, Bilthoven; Department of Gastroenterology and Hepatology, University Medical Centre, Utrecht, The Netherlands. 12. Epidemiology Research Unit, Research Centre of the University of Montreal Hospital Centre (CRCHUM), Montreal, Canada. 13. Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York. 14. Department of Epidemiology and Public Health, School of Public Health, School of Medicine, Yale University, New Haven; Cancer Epidemiology Program, Cancer Research Center of Hawaii, University of Hawaii, Honolulu. 15. Department of Surgery, New York Medical College, Valhalla. 16. Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda. 17. Departments of Health Science Research, Gastroenterology, and Medical Genetics, Mayo Clinic College of Medicine, Rochester, USA. 18. Department of Epidemiology, Institute for Pharmacological Research 'Mario Negri', Milan; Department of Occupational Health, University of Milan, Milan, Italy. 19. The Tisch Cancer Institute and Institute for Translational Epidemiology, Mt Sinai School of Medicine, New York, USA.
Abstract
BACKGROUND: Pancreatitis is a known risk factor for pancreatic cancer; however, an unknown fraction of the disease is thought to be a consequence of tumor-related duct obstruction. PATIENTS AND METHODS: A pooled analysis of a history of pancreatitis and risk of pancreatic cancer was carried out considering the time interval between diagnoses and potential modification by covariates. Adjusted pooled odds ratios (ORs) and 95% confidence intervals (CIs) were estimated from 10 case-control studies (5048 cases of ductal pancreatic adenocarcinoma and 10,947 controls) taking part in the International Pancreatic Cancer Case-Control Consortium (PanC4). RESULTS: The association between pancreatitis and pancreatic cancer was nearly three-fold at intervals of >2 years between diagnoses (OR: 2.71, 95% CI: 1.96-3.74) and much stronger at intervals of ≤2 years (OR: 13.56, 95% CI: 8.72-21.90) probably reflecting a combination of reverse causation and antecedent misdiagnosis of pancreas cancer as pancreatitis. The younger (<65 years) pancreatic cancer cases showed stronger associations with previous (>2 years) pancreatitis (OR: 3.91, 95% CI: 2.53-6.04) than the older (≥65 years) cases (OR: 1.68, 95% CI: 1.02-2.76; P value for interaction: 0.006). CONCLUSIONS: Despite a moderately strong association between pancreatitis (diagnosed before >2 years) and pancreatic cancer, the population attributable fraction was estimated at 1.34% (95% CI: 0.612-2.07%), suggesting that a relatively small proportion of pancreatic cancer might be avoided if pancreatitis could be prevented.
BACKGROUND:Pancreatitis is a known risk factor for pancreatic cancer; however, an unknown fraction of the disease is thought to be a consequence of tumor-related duct obstruction. PATIENTS AND METHODS: A pooled analysis of a history of pancreatitis and risk of pancreatic cancer was carried out considering the time interval between diagnoses and potential modification by covariates. Adjusted pooled odds ratios (ORs) and 95% confidence intervals (CIs) were estimated from 10 case-control studies (5048 cases of ductal pancreatic adenocarcinoma and 10,947 controls) taking part in the International Pancreatic Cancer Case-Control Consortium (PanC4). RESULTS: The association between pancreatitis and pancreatic cancer was nearly three-fold at intervals of >2 years between diagnoses (OR: 2.71, 95% CI: 1.96-3.74) and much stronger at intervals of ≤2 years (OR: 13.56, 95% CI: 8.72-21.90) probably reflecting a combination of reverse causation and antecedent misdiagnosis of pancreas cancer as pancreatitis. The younger (<65 years) pancreatic cancer cases showed stronger associations with previous (>2 years) pancreatitis (OR: 3.91, 95% CI: 2.53-6.04) than the older (≥65 years) cases (OR: 1.68, 95% CI: 1.02-2.76; P value for interaction: 0.006). CONCLUSIONS: Despite a moderately strong association between pancreatitis (diagnosed before >2 years) and pancreatic cancer, the population attributable fraction was estimated at 1.34% (95% CI: 0.612-2.07%), suggesting that a relatively small proportion of pancreatic cancer might be avoided if pancreatitis could be prevented.
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