review of literature on clinical pancreatology - The Pancreapedia

patients for operation and when counseling patients about operative risk, but they do notpreclude obese individuals from undergoing definitive pancreatic operations [458].To examine the influence <strong>of</strong> obesity, as measured by body mass index (BMI) onclinicopathologic factors and survival after pancreatectomy to treat adenocarcinoma aretrospective <strong>review</strong> and statistical analysis using prospectively collected data wasperformed. Two hundred eighty-five consecutive patients with data available for BMIcalculation who underwent potentially curative pancreas resection to treat adenocarcinomafrom 1999 to 2006. It was identified a subset <strong>of</strong> obese patients (BMI >35) who were at 12-foldrisk <strong>of</strong> lymph node metastasis compared with nonobese patients (BMI < 35). The estimateddisease-free and overall survival rates were decreased in the obese patients, and the risk <strong>of</strong>cancer recurrence and death after pancreatectomy was nearly twice that in nonobesepatients. It was concluded that obese patients with a BMI <strong>of</strong> more than 35 are more likely tohave node-positive pancreatic cancer and decreased survival after surgical resection. Datasuggest that the negative influence <strong>of</strong> BMI <strong>of</strong> more than 35 on cancer-related end points isunrelated to the potential complexity <strong>of</strong> performing major oncologic surgery in obese patients[459].Diabetes in pancreatic cancerIn Korea, the prevalence <strong>of</strong> pancreatic cancer (PC) in general population has been reportedas 7 in 100,000. However, that in diabetes mellitus (DM) has not been elucidated yet. Onestudy was designed to estimate the prevalence <strong>of</strong> PC among diabetes mellitus patients, andcharacterize and compare the patients with diabetes mellitus with and without PC. 5,082patients (4,890 diabetes mellitus without PC, 78 PC with diabetes mellitus, and 114 PCwithout diabetes mellitus) were enrolled during a period <strong>of</strong> 4 years between 2004 and 2008.The prevalence <strong>of</strong> PC in diabetes mellitus patients was 1.6 percent and that <strong>of</strong> diabetesmellitus in PC patients was 41 percent. No significant differences in the clinicalcharacteristics except HbAIc and ALP were observed between PC patients with diabetesmellitus and without diabetes mellitus. Among 78 PC patients with diabetes mellitus, diabetesmellitus was diagnosed in 19 (29 %) and 29 (37 %) patients concomitantly or within 2 yearsprior to the diagnosis <strong>of</strong> PC, respectively. Among the cases with recent onset diabetesmellitus (less than 2 years duration), the disease duration <strong>of</strong> diabetes mellitus before thediagnosis <strong>of</strong> PC was less than 1 year in 14 patients (18 %) and 1 to 2 years in 15 patients(19 %). Diabetes mellitus patients with PC were found to have significantly higher ALT, totalbilirubin, and ALP levels than in diabetes mellitus patients without PC. It was concluded thatthe prevalence <strong>of</strong> pancreatic cancer in diabetes mellitus patients was 1.6 percent and washigher than in the general population. Recent onset diabetes mellitus was frequent in PCpatients (less than 2 years duration) [460].Coeliac axis stenosisPatients with celiac axis stenosis are asymptomatic due to the rich collateral blood supplythrough superior mesenteric artery. However, ligating and dividing gastroduodenal arteryduring pancreatoduodenectomy can cause ischemic threat especially to liver, less frequentlystomach and spleen, or failure <strong>of</strong> anastomoses. It was presented a case <strong>of</strong> 27-year-oldfemale who underwent duodenopancreatectomy for pseudopapillary tumor <strong>of</strong> the head <strong>of</strong>pancreas. Celiac axis stenosis was found peroperatively and proven during angiography.Although an attempt <strong>of</strong> endovascular dilatation <strong>of</strong> celiac axis was unsuccessful, blood supplyto the liver was sufficient and therefore it was not performed any other intervention toimprove blood flow to the liver. Postoperative course was uneventful. Celiac axis stenosiscan be caused by tumor infiltration or lymphadenopathy in malignant disease,atherosclerosis or compression <strong>of</strong> the median arcuate ligament. The stenosis can be