cute pancreatitis is one of the most common gastrointestinal conditions that results in hospital admission in the United States. The incidence of acute pancreatitis is estimated at 110 to 140 per 100 000 population, with an estimated more than 300 000 US emergency department visits per year. 1,2 Admissions due to acute pancreatitis have increased from 9.48 cases per 1000 hospitalizations in 2002 to 12.19 in 2013, with a median hospital cost of nearly $7000 per hospitalization. 3,4 Acute pancreatitis is a complex disease with a variable course that is often difficult to predict early in its development (eBox in the Supplement). Approximately 80% of patients develop mild to moderately severe disease (absence of organ failure >48 hours). 5,6 However, one-fifth of patients develop severe disease, with a mortality rate of approximately 20%. 5,7 The purpose of this review is to summarize evidence regarding the recognition of disease severity, fluid and nutrition management, and risk-reduction methods for the prevention of recurrent disease. MethodsPubMed and the Cochrane databases were searched for Englishlanguage studies published from January 2009 through August 2020 for randomized clinical trials (RCTs), meta-analyses, systematic reviews, and observational studies. Manual searches were performed of the references of selected articles, reviews, metaanalyses, and practice guidelines. Select studies prior to 2009 were included for historical context. Emphasis was given to RCTs and metaanalyses. All publications and citations included were mutually agreed on by the authors and selected for clinical importance and relevance with consideration to the general medical readership of JAMA. Sixty-six articles were included, which contained 8 RCTs, 12 meta-analyses, and 5 clinical guidelines. Pathogenesis and EtiologyAcute pancreatitis is characterized by damage to the acinar cells, the functional units of the exocrine pancreas, precipitating inappropriate release and activation of trypsinogen to trypsin within the acini. This triggers the activation of other digestive enzymes, the kinin system, and the complement cascade resulting in autodigestion of the pancreatic parenchyma. 8,9 Pancreatic duct obstruction (eg, gallstone pancreatitis) is one of the more common causes of acinar damage, causing an increase in ductal pressure, interstitial edema, and accumulation of enzyme-rich fluid within the pancreatic tissue. 10 Alternatively, primary acinar injury may be caused by a variety of other factors, such as calcium, which regulates trypsin activation. Inappropriate release of IMPORTANCE In the United States, acute pancreatitis is one of the leading causes of hospital admission from gastrointestinal diseases, with approximately 300 000 emergency department visits each year. Outcomes from acute pancreatitis are influenced by risk stratification, fluid and nutritional management, and follow-up care and risk-reduction strategies, which are the subject of this review.OBSERVATIONS MEDLINE was searched via PubMed as was the Cochrane data...

Background: Current diagnosis and staging of pancreatic ductal adenocarcinoma (PDAC) has important limitations and better biomarkers are needed to guide initial therapy. We investigated the performance of circulating tumour cells (CTCs) as an adjunctive biomarker at the time of disease presentation.

Background Occult metastatic tumors, below imaging thresholds, are a limitation of staging systems that rely on cross-sectional imaging alone and are a cause of the routine understaging of pancreatic ductal adenocarcinomas (PDACs). We investigated circulating tumor cells (CTCs) as a preoperative predictor of occult metastatic disease and as a prognostic biomarker for PDAC patients. Experimental Design A total of 126 patients (100 with cancer, 26 with benign disease) were enrolled in our study and CTCs were identified and enumerated from 4 mL of venous blood using the microfluidic NanoVelcro assay. CTC enumeration was correlated with clinicopathologic variables and outcomes following both surgical and systemic therapies. Results CTCs were identified in 78% of PDAC patients and CTC counts correlated with increasing stage (ρ = 0.42, ρ < 0.001). Of the 53 patients taken for potentially curative surgery, 13 (24.5%) had occult metastatic disease intraoperatively. Patients with occult disease had significantly more CTCs than patients with local disease only (median 7 vs. 1 CTC, p < 0.0001). At a cutoff of three or more CTCs/4 mL, CTCs correctly identified patients with occult metastatic disease preoperatively (area under the receiver operating characteristic curve 0.82, 95% confidence interval (CI) 0.76–0.98, p < 0.0001). CTCs were a univariate predictor of recurrence-free survival following surgery [hazard ratio (HR) 2.36, 95% CI 1.17–4.78, p = 0.017], as well as an independent predictor of overall survival on multivariate analysis (HR 1.38, 95% CI 1.01–1.88, p = 0.040). Conclusions CTCs show promise as a prognostic biomarker for PDAC patients at all stages of disease being treated both medically and surgically. Furthermore, CTCs demonstrate potential as a preoperative biomarker for identifying patients at high risk of occult metastatic disease.

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