Main duct IMPNs are more likely to progress to malignancy than branch duct ones and frequently require surgery.3 Branch duct IPMNs that are small (ie, branch duct size <3 cm and not associated with main duct

dilatation or a mass or mural module) can often be monitored over time and left alone when they fail to progress.4 However, those of us who manage patients with these pancreatic curiosities live in fear of missing a “rogue” branch duct lesion that harbors an adenocarcinoma. Making a cytologic or—even better—histologic diagnosis greatly aids our decision making, which should be a team effort among the gastroenterologist, a body-imaging radiologist, and an experienced pancreatic surgeon. If the gastroenterologist is not a skilled exponent of EUS, then a suitably Selleckchem HSP inhibitor qualified colleague should be recruited to the team. Historically, ERCP has not had a major role to play in the diagnosis of IPMN because the branch ducts are not easily accessed for sampling, and

contrast injection into the main duct may be Apoptosis inhibitor greatly hampered by the presence of thick mucus. It has been suggested that the incidence of postprocedure pancreatitis may be significantly increased when main duct IPMNs are studied by ERCP,5 possibly because contrast is forced out into side branches by the gelatinous (mucinous) plug occupying the lumen of the main duct. Modern thin-caliber endoscopes that can be inserted through the instrument channel of a standard duodenoscope have rendered pancreatoscopy a practical investigation in suitably equipped centers. However, pancreatoscopy is only useful within significantly dilated main PDs, where frondlike, villous lesions (often likened to

sea anemones), gently waving in the pancreatic tide, can be identified and sampled. Although main duct IPMNs can be impressive, branch duct IPMNs are often subtle, with a few fronds entering the main duct or sometimes not being visible at all. In our experience, getting a really good pancreatoscopic view of branch duct lesions is the exception rather than the rule. Most investigators rely instead on endoscopic brush cytology at ERCP and/or EUS-guided FNA cytology of mural nodules or associated pancreatic masses to guide their decision making. Serologic Isotretinoin and fluid collection markers of evolving pancreatic malignancy, such as carcinoembryonic antigen and CA19-9, have not proved useful for diagnosis or monitoring in IPMN.6 and 7 In this issue of the Gastrointestinal Endoscopy, a group from Japan 8 reports on their experience with PD lavage cytology and histology (by using a cell-block method) for distinguishing benign from malignant IPMNs. This was a single-center, prospective study: their technique was not compared with any “standard” approach. They selected patients with suspected pancreatic branch duct IPMNs identified by CT or magnetic resonance imaging (MRI). Those with mural nodules seen on subsequent EUS underwent endoscopic retrograde pancreatography followed by PD lavage cytology.