Pancreatic cancer is one of the most aggressive malignant diseases due high rate of recurrence and the lack effective medical therapy. Surgery remains the only option for curable treatment but unfortunately, less than 20% of patients are eligibles at the time of diagnosis therefore identifying the risk factors represent a big step for cancer research. Pancreatic cancer is frequently associated with diabetes or glucose intolerance. There are two hypotheses at the base of this observation: either the diabetes cause pancreatic cancer or is a concequences of the cancer. In these theses we studied the patients diagnosticated with pancreatic cancer and with diabetes mellitus type 2. A total of 256 pancreatic cancer cases were identified and 71 patients had diabetes mellitus and 21 patients had glucose intolerance. Mean age 62.2 years, 81% cases were male and in 71% cancer originated form the pancreatic head. In 51.4% cases the diagnosis was in stage IV of the disease. Patients with pancreatic cancer and diabetes mellitus had reduced survival compared with those without diabetes but the difference was not statistically significant. Diabetes mellitus is associated with a decreased survival among patients with pancreatic cancer and reveal a link between chronic glucose intolerance and pancreatic cancer survival. The complex relationship between pancreatic cancer and diabetes requires more clinical research in order to developed new therapeutical posibilities.
Introduction: Malignant tumors are associated with a low incidence of postoperative pancreatic fistulas. The presence of peritumoral fibrosis is considered the protective factor for the development of postoperative pancreatic fistulas after pancreatic resections for pancreatic ductal adenocarcinomas. Methods: We analyzed a series of 109 consecutive patients with pancreatic resections for malignant pathology: pancreatic ductal adenocarcinomas and periampullary adenocarcinomas. The incidence of postoperative pancreatic fistulas has been reported in tumor histological type, in the presence of peritumoral fibrosis, and in the association between adenocarcinomas and areas of acute pancreatitis. The data obtained were processed with the statistical analysis program SPSS, and statistically significant p were considered at a value <0.05. Results: For the entire study group, the incidence of postoperative pancreatic fistulas was 11.01%. The lowest incidence was observed in the group of patients with pancreatic ductal adenocarcinomas (4.06% vs. 25.72% in the group with periampullary adenocarcinoma), with a p = 0.002. The presence of peritumoral fibrous tissue was observed in 49.31% of cases without pancreatic fistulas, and in 54.54% of cases that developed this postoperative complication (p = 0.5). Also, the peritumoral fibrous tissue had a uniform distribution depending on the main diagnosis (56.14% in pancreatic ductal adenocarcinoma group vs. 37.04% in periampullary adenocarcinoma group, with a p = 0.08). In the group of patients who associated areas of acute pancreatitis on the resections, the incidence of postoperative pancreatic fistulas was 7.8 times higher (30% vs. 3.8%, p = 0.026). Conclusions: Peritumoral fibrous tissue was not a factor involved in the developing of postoperative pancreatic fistulas. The association of adenocarciomas with areas of acute pancreatitis has led to a significant increase in postoperative pancreatic fistulas, which is a significant and independent risk factor.
Background and Objectives: Postoperative pancreatic fistula after cephalic pancreatoduodenectomy (CPD) is still the leading cause of postoperative morbidity, entailing long hospital stay and costs or even death. The aim of this study was to propose the use of morphologic parameters based on a preoperative multisequence computer tomography (CT) scan in predicting the clinically relevant postoperative pancreatic fistula (CRPF) and a risk score based on a multiple regression analysis. Materials and Methods: For 78 consecutive patients with CPD, we measured the following parameters on the preoperative CT scans: the density of the pancreas on the unenhanced, arterial, portal and delayed phases; the unenhanced density of the liver; the caliber of the main pancreatic duct (MPD); the preoperatively estimated pancreatic remnant volume (ERPV) and the total pancreatic volume. We assessed the correlation of the parameters with the clinically relevant pancreatic fistula using a univariate analysis and formulated a score using the strongest correlated parameters; the validity of the score was appreciated using logistic regression models and an ROC analysis. Results: When comparing the CRPF group (28.2%) to the non-CRPF group, we found significant differences of the values of unenhanced pancreatic density (UPD) (44.09 ± 6.8 HU vs. 50.4 ± 6.31 HU, p = 0.008), delayed density of the pancreas (48.67 ± 18.05 HU vs. 61.28 ± 16.55, p = 0.045), unenhanced density of the liver (UDL) (44.09 ± 6.8 HU vs. 50.54 ± 6.31 HU, p = 0.008), MPD (0.93 ± 0.35 mm vs. 3.14 ± 2.95 mm, p = 0.02) and ERPV (46.37 ± 10.39 cm3 vs. 34.87 ± 12.35 cm3, p = 0.01). Based on the odds ratio from the multiple regression analysis and after calculating the optimum cut-off values of the variables, we proposed two scores that both used the MPD and the ERPV and differing in the third variable, either including the UPD or the UDL, producing values for the area under the receiver operating characteristic curve (AUC) of 0.846 (95% CI 0.694–0.941) and 0.774 (95% CI 0.599–0.850), respectively. Conclusions: A preoperative CT scan can be a useful tool in predicting the risk of clinically relevant pancreatic fistula.
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