Dataset Information

Acute Pancreatitis Recurrences Augment Long-Term Pancreatic Cancer Risk.

ABSTRACT:

Introduction

In animal models, inflammation caused by experimental acute pancreatitis (AP) promotes pancreatic carcinogenesis that is preventable by suppressing inflammation. Recent studies noted higher long-term risk of pancreatic ductal adenocarcinoma (PDAC) after AP. In this study, we evaluated whether the long-term PDAC risk after AP was influenced by the etiology of AP, number of recurrences, and if it was because of progression to chronic pancreatitis (CP).

Methods

This retrospective study used nationwide Veterans Administration database spanning 1999-2015. A 2-year washout period was applied to exclude patients with preexisting AP and PDAC. PDAC risk was estimated in patients with AP without (AP group) and with underlying CP (APCP group) and those with CP alone (CP group) and compared with PDAC risk in patients in a control group, respectively, using cause-specific hazards model.

Results

The final cohort comprised 7,147,859 subjects (AP-35,550 and PDAC-16,475). The cumulative PDAC risk 3-10 years after AP was higher than in controls (0.61% vs 0.18%), adjusted hazard ratio (1.7 [1.4-2.0], P < 0.001). Adjusted hazard ratio was 1.5 in AP group, 2.4 in the CP group, and 3.3 in APCP group. PDAC risk increased with the number of AP episodes. Elevated PDAC risk after AP was not influenced by the etiology of AP (gallstones, smoking, or alcohol).

Discussion

There is a higher PDAC risk 3-10 years after AP irrespective of the etiology of AP, increases with the number of episodes of AP and is additive to higher PDAC risk because of CP.

SUBMITTER: Munigala S

PROVIDER: S-EPMC10045975 | biostudies-literature | 2023 Apr

REPOSITORIES: biostudies-literature

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Acute Pancreatitis Recurrences Augment Long-Term Pancreatic Cancer Risk.

Munigala Satish S Almaskeen Sami S Subramaniam Divya S DS Bandi Sriya S Bowe Benjamin B Xian Hong H Sheth Sunil G SG Burroughs Thomas E TE Agarwal Banke B

The American journal of gastroenterology 20221220 4

<h4>Introduction</h4>In animal models, inflammation caused by experimental acute pancreatitis (AP) promotes pancreatic carcinogenesis that is preventable by suppressing inflammation. Recent studies noted higher long-term risk of pancreatic ductal adenocarcinoma (PDAC) after AP. In this study, we evaluated whether the long-term PDAC risk after AP was influenced by the etiology of AP, number of recurrences, and if it was because of progression to chronic pancreatitis (CP).<h4>Methods</h4>This retr ...[more]

PMID: 36473072

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Project description:PurposeThe necrosis-fibrosis hypothesis describes a continuum between single attacks of acute pancreatitis (SAP), recurrent acute pancreatitis (RAP) and chronic pancreatitis (CP) with endocrine and exocrine pancreatic insufficiency. For prevention purposes we evaluated clinico-radiological parameters and pancreatic volumetry to compare SAP and RAP and provide prognostic relevance on short-term mortality, need for intervention and the hospitalization duration.Materials and methodsWe retrospectively investigated 225 consecutive patients (150 males, range 19-97years) with acute pancreatitis (74%SAP, 26%RAP) according to the revised Atlanta classification. All patients received an intravenous contrast-enhanced CT after a median time of 5 (IQR 5-7) days after onset of symptoms. Two experienced observers rated the severity of AP by 3 CT scores (CTSI, mCTSI, EPIC). Moreover, total pancreatic volumes and additional parenchymal necrosis volumes were assessed, when appropriate. Clinical parameters were etiology of AP, lipase on admission, CRP 48 hours after admission (CRP48), and the presence of organ dysfunction, assessed by the modified Marshall score. The modified Marshall score included systolic blood pressure, serum creatinine, and the ratio of arterial oxygen partial pressure to fractional inspired oxygen (PaO2/FiO2 ratio) and was assessed on admission and 48 hours after admission to find patients with persistent organ failure. Outcome parameters were total hospitalization duration, short-term mortality and need for intervention.ResultsLipase, CRP48, etiology of AP, EPIC, PaO2/FiO2 ratio, and the presence of a pleural effusion differed significantly in both groups (p<0.05). In 109 patients with interstitial edematous AP, the total pancreatic volume was significantly smaller in patients with RAP compared to those with SAP (69±35cm3; (RAP) vs 106±45cm3; (SAP), p<0.001). All outcome parameters including the mortality rates (SAP vs. RAP: 15% vs. 7%) were comparable in both groups (p>0.05). In the necrotizing RAP group, only the necrotic volume correlated significantly with total hospitalization time (r = 0.72, p<0.001), whereas the systolic blood pressure was the only, but weak predictor for short-term mortality (β-coefficient: -0.05, p = 0.03) and the need for intervention (β-coefficient: -0.02, p = 0.048) in the total RAP group. In patients with SAP, the modified Marshall score was the strongest predictor of short-term mortality, followed by the mCTSI on multivariate logistic regression (Marshall score: β-coefficient: 1.79, p<0.001; mCTSI: β-coefficient: 0.40, p<0.001). CTSI was the best predictor for required intervention in necrotizing SAP (β-coefficient: 0.46, p<0.001), followed by the volume of intrapancreatic necrosis (β-coefficient: 0.17, p = 0.03).ConclusionTotal pancreatic volume differed significantly between interstitial RAP and SAP and intrapancreatic necrosis volume revealed prognostic value for the total hospitalization duration in necrotizing RAP. Although all outcome parameters were comparable between SAP and RAP, only systolic blood pressure and pancreatic volumetry were prognostic in RAP. In SAP, only the modified Marshall score and mCTSI revealed prognostic value for short-term mortality, whereas CTSI was predictive for the need for intervention.

Project description:BackgroundTwenty-three percent of patients are diagnosed with diabetes mellitus after the first episode of acute pancreatitis. The incidence of post-acute pancreatitis diabetes mellitus is significantly higher than that of type 1 diabetes mellitus. Some studies have concluded that the all-cause mortality and worse prognosis of diabetes after pancreatitis are higher. We predicted that number of recurrences of pancreatitis would be significantly associated with the incidences of metabolic syndrome, abdominal obesity, and post-acute pancreatitis diabetes mellitus.MethodsPatients admitted to our hospital for hypertriglyceridemic acute pancreatitis from 2013-2021 were selected for a cross-sectional study. Statistical analysis methods were used to analyze the effect of recurrences on the long-term prognosis of patients with hypertriglyceridemic acute pancreatitis.ResultsIn this study, 101 patients with hypertriglyceridemic acute pancreatitis were included: 60 (59.41%) in the recurrent acute pancreatitis group and 41 (40.59%) in the only one episode of acute pancreatitis group. Among all hypertriglyceridemic acute pancreatitis patients, approximately 61.4% were diagnosed with abdominal obesity, 33.7% of patients are diagnosed with metabolic syndrome, 34.7% of patients are diagnosed with diabetes mellitus, and 21.8% of patients are diagnosed with post-acute pancreatitis diabetes mellitus. Recurrent acute pancreatitis were independent risk factors for post-acute pancreatitis diabetes mellitus in patients with hypertriglyceridemic acute pancreatitis (odds ratio [OR] = 3.964, 95% confidence interval [CI] = 1.230-12.774) and the risk of post-acute pancreatitis diabetes mellitus in patients with three or more recurrent episodes was 6.607 times higher than that in patients without recurrent episodes (OR = 6.607, 95% CI = 1.412-30.916).ConclusionsRecurrence is an independent risk factor for the development of post-acute pancreatitis diabetes mellitus and is significantly associated with the number of recurrences.

Project description:ImportanceIntraductal papillary mucinous neoplasms (IPMNs) are pancreatic cysts that can give rise to pancreatic cancer (PC). Limited population data exist on their prevalence, natural history, or risk of malignant transformation (IPMN-PC).ObjectiveTo fill knowledge gaps in epidemiology of IPMNs and associated PC risk by estimating population prevalence of IPMNs, associated PC risk, and proportion of IPMN-PC.Design, setting, and participants: This retrospective cohort study was conducted in Olmsted County, Minnesota. Using the Rochester Epidemiology Project (REP), patients aged 50 years and older with abdominal computed tomography (CT) scans between 2000 and 2015 were randomly selected (CT cohort). All patients from the REP with PC between 2000 and 2019 were also selected (PC cohort). Data were analyzed from November 2021 through August 2023.Main outcomes and measuresCIs for PC incidence estimates were calculated using exact methods with the Poisson distribution. Cox models were used to estimate age, sex, and stage-adjusted hazard ratios for time-to-event end points.ResultsThe CT cohort included 2114 patients (1140 females [53.9%]; mean [SD] age, 68.6 [12.1] years). IPMNs were identified in 231 patients (10.9%; 95% CI, 9.7%-12.3%), most of which were branch duct (210 branch-duct [90.9%], 16 main-duct [6.9%], and 5 mixed [2.2%] IPMNs). There were 5 Fukuoka high-risk (F-HR) IPMNs (2.2%), 39 worrisome (F-W) IPMNs (16.9%), and 187 negative (F-N) IPMNs (81.0%). After a median (IQR) follow-up of 12.0 (8.1-15.3) years, 4 patients developed PC (2 patients in F-HR and 2 patients in F-N groups). The PC incidence rate per 100 person years for F-HR IPMNs was 34.06 incidents (95% CI, 4.12-123.02 incidents) and not significantly different for patients with F-N IPMNs compared with patients without IPMNs (0.16 patients; 95% CI, 0.02-0.57 patients vs 0.11 patients; 95% CI, 0.06-0.17 patients; P = .62). The PC cohort included 320 patients (155 females [48.4%]; mean [SD] age, 72.0 [12.3] years), and 9.8% (95% CI, 7.0%-13.7%) had IPMN-PC. Compared with 284 patients with non-IPMN PC, 31 patients with IPMN-PC were older (mean [SD] age, 76.9 [9.2] vs 71.3 [12.5] years; P = .02) and more likely to undergo surgical resection (14 patients [45.2%] vs 60 patients [21.1%]; P = .003) and more-frequently had nonmetastatic PC at diagnosis (20 patients [64.5%] vs 130 patients [46.8%]; P = .047). Patients with IPMN-PC had better survival (adjusted hazard ratio, 0.62; 95% CI, 0.40-0.94; P = .03) than patients with non-IPMN PC.Conclusions and relevanceIn this study, CTs identified IPMNs in approximately 10% of patients aged 50 years or older. PC risk in patients with F-N IPMNs was low and not different compared with patients without IPMNs; approximately 10% of patients with PC had IPMN-PC, and they had better survival compared with patients with non-IPMN PC.

Project description:Background & aimsScreening of individuals who have a high risk of pancreatic ductal adenocarcinoma (PDAC), because of genetic factors, frequently leads to identification of pancreatic lesions. We investigated the incidence of PDAC and risk factors for neoplastic progression in individuals at high risk for PDAC enrolled in a long-term screening study.MethodsWe analyzed data from 354 individuals at high risk for PDAC (based on genetic factors of family history), enrolled in Cancer of the Pancreas Screening cohort studies at tertiary care academic centers from 1998 through 2014 (median follow-up time, 5.6 years). All subjects were evaluated at study entry (baseline) by endoscopic ultrasonography and underwent surveillance with endoscopic ultrasonography, magnetic resonance imaging, and/or computed tomography. The primary endpoint was the cumulative incidence of PDAC, pancreatic intraepithelial neoplasia grade 3, or intraductal papillary mucinous neoplasm with high-grade dysplasia (HGD) after baseline. We performed multivariate Cox regression and Kaplan-Meier analyses.ResultsDuring the follow-up period, pancreatic lesions with worrisome features (solid mass, multiple cysts, cyst size > 3 cm, thickened/enhancing walls, mural nodule, dilated main pancreatic duct > 5 mm, or abrupt change in duct caliber) or rapid cyst growth (>4 mm/year) were detected in 68 patients (19%). Overall, 24 of 354 patients (7%) had neoplastic progression (14 PDACs and 10 HGDs) over a 16-year period; the rate of progression was 1.6%/year, and 93% had detectable lesions with worrisome features before diagnosis of the PDAC or HGD. Nine of the 10 PDACs detected during routine surveillance were resectable; a significantly higher proportion of patients with resectable PDACs survived 3 years (85%) compared with the 4 subjects with symptomatic, unresectable PDACs (25%), which developed outside surveillance (log rank P < .0001). Neoplastic progression occurred at a median age of 67 years; the median time from baseline screening until PDAC diagnosis was 4.8 years (interquartile range, 1.6-6.9 years).ConclusionsIn a long-term (16-year) follow-up study of individuals at high-risk for PDAC, we found most PDACs detected during surveillance (9/10) to be resectable, and 85% of these patients survived for 3 years. We identified radiologic features associated with neoplastic progression.

Dataset Information

Acute Pancreatitis Recurrences Augment Long-Term Pancreatic Cancer Risk.

Introduction

Methods

Results

Discussion

Publications

Acute Pancreatitis Recurrences Augment Long-Term Pancreatic Cancer Risk.

Similar Datasets

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