Acute Pancreatitis Increases Risk for Pancreatic Ductal Adenocarcinoma

Patients with acute pancreatitis (AP) have an increased long-term risk for pancreatic ductal adenocarcinoma (PDAC), according to study results published in American Journal of Gastroenterology.

Researchers conducted a retrospective cohort study and used data from the Department of Veterans Affairs (VA) of medical encounters from September 1999 through December 2015. Eligible participants had more than 2 years’ duration between their first and last visit in the VA system.

The primary outcome was pancreatic cancer and was defined according to primary or secondary diagnoses codes (≥1 codes) for adenocarcinoma of the pancreas. The primary predictor variable of interest was AP, which was defined based on inpatient diagnoses codes for AP.

A total of 7,147,859 participants were included, of whom 35,550 (0.5%) had at least 1 episode of AP and 16,475 (0.2%) were diagnosed with PDAC. This group included 133 patients in the AP group (0.5%), 82 in the chronic pancreatitis (CP) group (0.7%), 92 in the AP with underlying CP (APCP) group (1.1%), and 16,168 (0.2%) control individuals. The median age in the cohort was 62 years (IQR, 53-72), 94% were men, 82% were White, 36% currently smoked cigarettes, and 15% heavily drank alcohol.

Patients with AP had an increased risk for PDAC in the following 3 to 10 years vs participants in the control group (adjusted hazard ratio [aHR], 1.65; 95% CI, 1.40-1.95; P <.001), according to Cox-regression analyses. In patients who had underlying CP, AP was associated with an increased risk for PDAC even (aHR, 4.71; 95% CI, 3.80-5.82; P <.001, APCP group vs control group). The PDAC risk was significantly increased in the APCP group compared with the AP group (aHR, 2.24; 95% CI, 1.69-2.96; P <.001) and CP patient group (aHR, 1.94; 95% CI, 1.39-2.71; P <.001).

In the 35,550 patients who had more than 2 years of follow-up after AP, 79% had 1 episode of AP, 13.6% had 2 episodes, and the other participants had at least 3 episodes. The risk for PDAC was 0.4% in individuals with 1 episode of AP, 1.1% after 2 episodes, and 2.1% with at least 3 episodes of AP.

No significant difference was found in the cumulative incidence of PDAC in patients with gallstone and nongallstone pancreatitis (P =.19). Among control participants, the PDAC risk was increased in current smokers (aHR, 1.43; 95% CI, 1.38-1.48, P <.001) and heavy alcoholic drinkers (aHR, 1.22; 95% CI, 1.17-1.28; P <.001).

Study limitations include the retrospective design and use of administrative data. Also, 92% of veterans are men, which limits the generalizability of the results.

“Our data provide additional evidence supporting a higher long-term PDAC risk following AP both in patients without and with underlying CP,” conclude the study authors. They add, “This increased PDAC risk is intrinsic to AP and likely due to acute inflammation, increases with the number of AP episodes, is independent of the etiology of AP, and is additive with that due to CP.”