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Diagnosis of Chronic Pancreatitis Incorporating Endosonographic Features, Demographics, and Behavioral Risk

Lee, Linda S. MD*; Tabak, Ying P. PhD; Kadiyala, Vivek MD*; Sun, Xiaowu PhD; Suleiman, Shadeah BS*; Johannes, Richard S. MD*†; Banks, Peter A. MD*; Conwell, Darwin L. MD

doi: 10.1097/MPA.0000000000000768
Original Articles
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Objectives Diagnosing chronic pancreatitis remains challenging. Endoscopic ultrasound (EUS) is utilized to evaluate pancreatic disease. Abnormal pancreas function test is considered the “nonhistologic” criterion standard for chronic pancreatitis. We derived a prediction model for abnormal endoscopic pancreatic function test (ePFT) by enriching EUS findings with patient demographic and pancreatitis behavioral risk characteristics.

Methods Demographics, behavioral risk characteristics, EUS findings, and peak bicarbonate results were collected from patients evaluated for pancreatic disease. Abnormal ePFT was defined as peak bicarbonate of less than 75 mEq/L. We fit a logistic regression model and converted it to a risk score system. The risk score was validated using 1000 bootstrap simulations.

Results A total of 176 patients were included; 61% were female with median age of 48 years (interquartile range, 38–57 years). Abnormal ePFT rate was 39.2% (69/176). Four variables formulated the risk score: alcohol or smoking status, number of parenchymal abnormalities, number of ductal abnormalities, and calcifications. Abnormal ePFT occurred in 10.7% with scores 4 or less versus 92.0% scoring 20 or greater. The model C-statistic was 0.78 (95% confidence interval, 0.71–0.85).

Conclusions Number of EUS pancreatic duct and parenchymal abnormalities, presence of calcification, and smoking/alcohol status were predictive of abnormal ePFT. This simple model has good discrimination for ePFT results.

From the *Division of Gastroenterology, Hepatology and Endoscopy, Brigham and Women’s Hospital, Boston, MA; †Department of Clinical Research, CareFusion, San Diego, CA; and ‡Division of Gastroenterology, Hepatology, and Nutrition, Ohio State University Medical Center, Columbus, OH.

Received for publication March 26, 2016; accepted October 5, 2016.

Address correspondence to: Linda S. Lee, MD, Brigham and Women’s Hospital, 75 Francis St, Boston, MA 02115 (e-mail: lslee@partners.org).

Supported by an American College of Gastroenterology Clinical Research Award (to D.L.C.), an unrestricted research grant from ChiRhoClin, Inc (to D.L.C.), and by the National Institutes of Diabetes and Digestive and Kidney Diseases and National Cancer Institute under award U01DK108327 (to D.L.C.).

The authors declare no conflict of interest.

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