PGE 2 in Pancreatic Cyst Fluid Helps Differentiate IPMN from MCN and Predict IPMN Dysplasia C. Max Schmidt & Michele T. Yip-Schneider & Matthew C. Ralstin & Sabrina Wentz & John DeWitt & Stuart Sherman & Thomas J. Howard & Lee McHenry & Sarah Dutkevitch & Michael Goggins & Attila Nakeeb & Keith D. Lillemoe Received: 22 May 2007 / Accepted: 23 October 2007 / Published online: 20 November 2007 # 2007 The Society for Surgery of the Alimentary Tract Abstract Current management of intraductal papillary mucinous neoplasm (IPMN) according to recently published International Consensus Guidelines depends upon distinguishing it from mucinous cystic neoplasms (MCNs). We have previously shown that prostaglandin E 2 (PGE 2 ) is increased in pancreatic cancer tissue over normal controls. Thus, we hypothesized that PGE 2 level in pancreatic fluid differentiates IPMN and MCN and is a biomarker of IPMN dysplasia. Pancreatic fluid was collected in 65 patients at the time of endoscopy (EUS or ERCP) or operation (OR) and analyzed by PGE 2 enzyme-linked immunosorbent assay (ELISA). PGE 2 level was correlated with surgical pathologic diagnosis and dysplastic stage. Mean PGE 2 level (pg/μl) in IPMNs (2.2±0.6) was greater than in MCNs (0.2±0.1) (p <0.05). Mean PGE 2 level of IPMN by dysplastic stage was 0.1±0.01 (low grade), 1.2±0.6 (medium grade), 4.4±0.9 (high grade), and 5.0±2.3 (invasive). Among invasive IPMN, PGE 2 level dropped in advanced cases with pancreatic ductal obstruction by tumor (0.3±0) vs non-obstructed (8.6±2.9). PGE 2 level may help in distinguishing IPMN from MCN in patients with known mucinous lesions. PGE 2 level may also be an indicator of malignant progression of IPMN before ductal obstruction by tumor. Prospective evaluation will be necessary to evaluate the clinical role of PGE 2 level in pancreatic fluid. Keywords Prostaglandin E2 . PGE2 . Intraductal papillary mucinous neoplasm . Mucinous cystic neoplasm . Pancreatic cancer . Dysplasia . Biomarker . Pancreatic adenocarcinoma J Gastrointest Surg (2008) 12:243–249 DOI 10.1007/s11605-007-0404-8 Disclosure: This paper was presented at the Society for Surgery of the Alimentary Tract (SSAT) in Washington, DC in May 2007 C. Max Schmidt and Michele T. Yip-Schneider contributed equally to this work. Grant support: This work was supported by the NIH 1R03CA112629- 01A1 (CMS) and Central Surgical Association Enrichment Award (CMS) C. M. Schmidt : M. T. Yip-Schneider : M. C. Ralstin : S. Wentz : T. J. Howard : S. Dutkevitch : A. Nakeeb : K. D. Lillemoe Department of Surgery, Indiana University School of Medicine, Indianapolis, IN, USA C. M. Schmidt Department of Biochemistry/Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, USA C. M. Schmidt : A. Nakeeb : K. D. Lillemoe Indiana University Cancer Center, Indiana University School of Medicine, Indianapolis, IN, USA C. M. Schmidt Walther Oncology, Indianapolis, IN, USA C. M. Schmidt Richard L. Roudebush VAMC, Indianapolis, IN, USA J. DeWitt : S. Sherman : L. McHenry Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, USA M. Goggins Johns Hopkins Medical Institutions, Baltimore, MD, USA C. M. Schmidt (*) Departments of Surgery and Biochemistry and Molecular Biology, Cancer Research Institute, 1044 W. Walnut Street R4-039, Indianapolis, IN 46202, USA e-mail: maxschmi@iupui.edu