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2nd Edition of International Conference on Gastroenterology

September 24-26, 2026, London,UK

September 24 -26, 2026 | London, UK
Gastro 2026

Cause-specific mortality after acute pancreatitis differs by etiology: A nationwide matched cohort study from SwePan

Speaker at GI Conferences - Daniel Selin
Center for Clinical Research Sormland, Sweden
Title : Cause-specific mortality after acute pancreatitis differs by etiology: A nationwide matched cohort study from SwePan

Abstract:

Introduction: Acute pancreatitis has gallstone and non-gallstone etiologies with distinct risk profiles, yet long-term outcomes are often assessed as a single exposure. Whether cause-specific mortality differs by etiology is unclear.

Aims & Methods: To compare cancer, cardiovascular, and other-cause mortality after acute pancreatitis by etiology. Using the Swedish Pancreatitis Cohort, we identified adults with incident acute pancreatitis (2000–2019) and matched up to three population controls on age, sex, and region. Cause of death was obtained from national registers. Adjusted subdistribution hazard ratios (sHRs) with 95% confidence intervals (CIs) were estimated using Fine–Gray models across follow-up intervals (0–<2, 2–<5, ≥5 years). Models were adjusted for the matching variables, calendar period, education level, country of birth, alcohol-related comorbidity and Charlson Comorbidity Index.

Results: Among 66,251 cases and 198,456 controls (1.97 million person-years), mortality patterns differed markedly by etiology. Cancer mortality was increased early in both groups (non-gallstone sHR 2.27, 95% CI 2.08-2.48; gallstone 2.05, 95% CI 1.87-2.24) but remained elevated beyond 5 years only in non-gallstone acute pancreatitis (sHR 1.38, 95% CI 1.28-1.49). Cardiovascular mortality showed modest increases in non-gallstone acute pancreatitis (0–<2 years sHR 1.13, 95% CI 1.04-1.22; ≥5 years 1.10, 95% CI 1.03-1.17), with no sustained excess risk in gallstone etiology. Other-cause mortality was consistently increased in non-gallstone acute pancreatitis (≥5 years sHR 1.38, 95% CI 1.30-1.46) but not in gallstone etiology. Absolute excess mortality was driven primarily by non-gallstone etiology across all causes.

Conclusion: Cause-specific mortality after acute pancreatitis differs substantially by etiology. Non-gallstone acute pancreatitis is associated with sustained excess mortality across multiple causes, whereas gallstone acute pancreatitis shows no long-term increase in cause-specific mortality. These findings support etiology-specific risk stratification and follow-up.

Biography:

Daniel Selin is an attending surgeon and head of division of emergency surgery and trauma care at Mälarsjukhuset county hospital in Eskilstuna, Sweden. His research is focused on epidemiological aspects of acute pancreatitis, particularly long-term morbidity and mortality.

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