ARTICLE IN PRESS
A weird polyp, 8 years after the Whipple procedure Laetitia Courtin-Tanguy, MD,a,b,c Aude Merdrignac, MD,a,b,c Bernard Meunier, MD,a,b and Laurent Sulpice, MD, PhD,a,b,c,d Rennes, France
From the CHU Rennes, Service de Chirurgie He patobiliaire et Digestive,a Universite Rennes1, Faculte de me decine,b INSERM, U991, Foie me tabolismes et cancer,c and INSERM, U1414, Centre d’investigation Clinique,d Rennes, France
A 62-YEAR-OLD MAN underwent a pancreaticoduodenectomy in 2008 for a main duct intraductal papillary mucinous pancreatic neoplasm (IPMN). The pathologic examination showed an invasive carcinoma, classified pT3N1 (1/23), with a curative resection. The patient received adjuvant chemotherapy by gemcitabine (18 cycles). During the follow-up, the patient presented with iron-deficiency anemia. An upper gastrointestinal endoscopy and a colonoscopy were normal. A computed tomography scan in 2014 revealed an endoscopically unreachable 10-mm polypoid lesion in the jejunal loop, close to the pancreaticojejunal anastomosis (Fig 1, A). A control computed tomography scan at 1 year showed an increase in size to 25 mm (Fig 1, B). An operative treatment was decided upon. Due to the tumor’s proximity to the pancreatojejunal anastomosis, the operation required its removal, along with 3 and 1.5 cm of jejunum and pancreatic parenchyma, respectively. The intraoperative frozen section examination of the pancreatic section showed chronic pancreatitis without suspect lesion. A pancreatico-gastric anastomosis was done. The postoperative course was uneventful, and the patient was discharged on postoperative day 8. The final pathologic examination described the polypoid lesion as a villous proliferation, similar to that observed in IPMN (Fig 2). The reviewing pathologist also described a 6-mm mucinous Accepted for publication May 31, 2016. Reprint requests: Laurent Sulpice, MD, PhD, CHU Pontchaillou, Universit e de Rennes 1, Service de chirurgie hepatobiliaire et digestive, 2 rue henri Le Guilloux, Rennes 35033, France. E-mail:
[email protected]. Surgery 2016;j:j-j. 0039-6060/$ - see front matter Ó 2016 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.surg.2016.05.034
infiltrative adenocarcinoma in the remnant pancreatic parenchyma. The 2 lesions had a CK7/CK20 phenotype, corresponding to a gastric phenotype. This result was confirmed by a second IPMN expert pathologist. A multidisciplinary collaborating meeting decided a resumption of chemotherapy. DISCUSSION IPMN are intraepithelial lesions that develop at the expense of the main pancreatic duct, its branch ducts, or both (mixed type) without ovarian stroma and can progress to pancreatic carcinoma.1 IPMN are classified in 3 evolving groups: benign lesions (hyperplasia or moderate dysplasia), in situ carcinomas (high grade of dysplasia), and invasive carcinomas.2 The IPMN prognosis depends on the malignant transformation. Of 30–60% of IPMN cases, mostly main duct or mixed types, 17–43% are invasive cancers. Patients with in situ or invasive stage I malignant resected IPMN have a good prognosis with an actuarial survival rate at 5 years of 88% and 36%, respectively. Prognosis also depends on histologic type3: gastric phenotype (with the best prognosis, representing 80% of IPMN), intestinal, pancreatobiliary, and oncocytic phenotypes. These subtypes can be characterized by different mucin expression patterns. The 5-year survival rate is 30% for invasive IPMN at the time of initial operation, and locally advanced patients have the same poor prognosis as patients with pancreatic adenocarcinoma at the same stage.2,4 This is related closely to local recurrence and metastatic spread. Half of patients relapse during the first 2 years. These recurrences are metastasis (40%), usually in the liver (72%); recurrences in the remnant pancreas (29%); and peritoneal carcinomatosis (20%). An invasive component larger than 2 cm and the presence of SURGERY 1
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Surgery j 2016
Fig 1. Computed tomography images showing the lesion (white arrow) in 2014 (A) and in 2015 (B).
Fig 2. (A and B) Histopathology in 2008 showing the degenerated duct intraductal papillary mucinous pancreatic neoplasm. (C) Operative specimen in 2015 after conditioning by a pathologist. (D) Its corresponding histopathology, showing the lesion in the jejunal loop and the adenocarcinoma.
positive lymph nodes are related to shorter survival (P = .03 and P = .01, respectively).4 Operations play a pivotal role in the treatment of IPMN, depending on the risk of degeneration.5 However, because of immediate complications and the functional effects of pancreatic operations, surgical indications for IPMN must be selective and currently still are debated. Thereby, procedures to save the pancreas should be the rule if possible. Prolonged monitoring after operations should be proposed routinely, as illustrated in the present case, due to the longterm risk of relapse, particularly in the case of invasive IPMN, a lesion in the pancreatic section, or residual lesion in the remnant pancreas. If recurrence occurs, a new operation could be discussed.
REFERENCES 1. Werner J, Fritz S, B€ uchler MW. Intraductal papillary mucinous neoplasms of the pancreas---a surgical disease. Nat Rev Gastroenterol Hepatol 2012;9:253-9. 2. Maire F, Hammel P, Terris B, Paye F, Scoazec JY, Cellier C, et al. Prognosis of malignant intraductal papillary mucinous tumours of the pancreas after surgical resection. Comparison with pancreatic ductal adenocarcinoma. Gut 2002;51:717-22. 3. Distler M, Kersting S, Niedergethmann M, Aust DE, Franz M, R€ uckert F, et al. Pathohistological subtype predicts survival in patients with intraductal papillary mucinous neoplasm (IPMN) of the pancreas. Ann Surg 2013;258:324-30. 4. Turrini O, Waters JA, Schnelldorfer T, Lillemoe KD, Yiannoutsos CT, Farnell MB, et al. Invasive intraductal papillary mucinous neoplasm: predictors of survival and role of adjuvant therapy. HPB (Oxford) 2010;12:447-55. 5. Tanaka M, Fernandez-del Castillo C, Adsay V, Chari S, Falconi M, Jang JY, et al. International consensus guidelines 2012 for the management of IPMN and MCN of the pancreas. Pancreatology 2012;12:183-97.