PANCREAS ALERTS

 

Ann Surg 2000; 231:205-12.

Clinical and pathologic correlation of 84 mucinous cystic neoplasms of the pancreas: can one reliably differentiate benign from malignant (or premalignant) neoplasms?

Sarr MG, Carpenter HA, Prabhakar LP, Orchard TF, Hughes-S, van Heerden JA, DiMagno EP.

Department of Surgery, Mayo Clinic. Rochester, Minnesota, USA.

This study was carried out in order to understand the long-term follow-up of mucinous cystic neoplasms of the pancreas after complete resection, and to determine the recurrence rates based upon a novel system of classification of benign mucinous cystadenomas, noninvasive proliferative mucinous cystic neoplasms, and invasive mucinous cystadenocarcinomas. The current thinking is that all mucinous cystic neoplasms of the pancreas are potentially malignant and that mucinous cystadenomas, when completely removed, are biologically benign. Cystadenocarcinomas are thought to be less aggressively malignant than ordinary ductal adenocarcinomas, but reported recurrence rates vary widely and are unpredictable. All patients who underwent "curative" resection for mucinous cystic neoplasms at the Mayo Clinic in Rochester from 1940 to 1997 were identified. All available pathology slides, gross specimens, and clinical records were reviewed and patients with inadequate documentation were eliminated. Neoplasms were reclassified as mucinous cystadenomas, noninvasive proliferative mucinous cystic neoplasms, or invasive cystadenocarcinomas based on specific histologic criteria. Of 84 patients with mucinous cystic neoplasms of the pancreas, 54 were classified as cystadenomas, 23 as noninvasive proliferative mucinous cystic neoplasms, and 7 as cystadenocarcinomas. There was no recurrent disease in any of the 77 patients with the noninvasive type, but 5 of the 6 patients surviving resection for cystadenocarcinomas died of recurrent cystadenocarcinoma within 5 years. The authors concluded that when the neoplasm is completely resected and subjected to adequate histopathologic examination based on these objective criteria, absence of tissue invasion predicts a curative operation and detailed follow-up may be unnecessary. In contrast, a histologic diagnosis of invasive cystadenocarcinoma portends a dismal prognosis, similar to that of typical ductal adenocarcinoma of the pancreas.

 

 

Gut 2000; 46:233-8.

Role of procalcitonin and granulocyte colony stimulating factor in the early prediction of infected necrosis in severe acute pancreatitis.

Muller CA, Uhl W, Printzen G, Gloor B, Bischofberger H, Tcholakov O, Buechler MW.

Department of Visceral and Transplantation Surgery, University Hospital of Bern. Bern, Switzerland.

During recent years, the search for a marker suitable for predicting the severe course of acute pancreatitis has been the goal of several groups. In 1997, Rau and co-workers (Gut. 1997; 41:832-40) reported that serum determination of procalcitonin was capable of individuating those patients with infected necrosis.

Muller and co-workers now report the data of a prospective study on 64 consecutive patients with acute pancreatitis [29 were suffering from acute oedematous pancreatitis (AIP), and 35 from necrotising disease (NP)] in differentiating between infected pancreatic necrosis (IPN) and sterile pancreatic necrosis. In this study, procalcitonin (PCT) and granulocyte colony stimulating factor (G-CSF) in the serum were examined and compared with C reactive protein (CRP); monitoring was performed daily and related to the onset of the symptoms. Within the first week, all three variables were significantly higher in patients with NP than in those with AIP (p<0.001). During the course of the study, 12 of the 35 patients with NP developed late IPN. Neither the peak nor the lowest concentrations during the monitoring period were of any value for predicting IPN. The author concluded that serum PCT, G-CSF, and CRP concentrations are of similar value for early differentiation between mild and severe acute pancreatitis, but these parameters are not suitable for the early prediction of IPN.