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The focus of the review is on roles of autophagy and pancreatic secretory trypsin inhibitor (PSTI), an endogenous trypsin inhibitor, in trypsinogen activation in acute pancreatitis. Acute pancreatitis is a disease in which tissues in and around the pancreas are autodigested by pancreatic digestive enzymes. This reaction is triggered by the intrapancreatic activation of trypsinogen. Autophagy causes trypsinogen and cathepsin B, a trypsinogen activator, to colocalize within the autolysosomes. Consequently, if the resultant trypsin activity exceeds the inhibitory activity of PSTI, the pancreatic digestive enzymes are activated, and they cause autodigestion of the acinar cells. Thus, autophagy and PSTI play important roles in the development and suppression of acute pancreatitis, respectively.

The prognostic value of the prognostic nutrition index (PNI) in pancreatic ductal adenocarcinoma (PDAC) is still controversial. This study aimed to assess the correlation between PNI and the outcome for PDAC patients and to generate a new score from PNI and serum markers.This study investigated 151 patients who underwent pancreatic resection for PDAC between April 2002 and June 2012. Disease-free survival (DFS), overall survival, and clinicopathological parameters were analyzed according to the PNI value.The low PNI patients had poorer 5-year DFS rate than high-PNI patients (10.7% and 34.8%, respectively). Multivariate analyses revealed that independent risk factors for poor DFS were high carcinoembryonic antigen (hazard ratio [HR], 1.53; P = 0.038), high carbohydrate antigen 19-9 (HR, 1.67; P = 0.017), positive lymph node metastasis (HR, 1.98; P = 0.017), R1 or 2 resection (HR, 3.50; P0.001), and low PNI (HR, 0.37 [high/low]; P = 0.029]. Scoring based on the formula -0.49 × (PNI) + 0.41 × (carcinoembryonic antigen) + 0.67 × (carbohydrate antigen 19-9) was significantly associated with poor DFS (P0.001) and overall survival (P = 0.0019).Low PNI and serum marker score are significantly associated with poor DFS.

Activating Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations are the most common and frequent changes observed in pancreatic cancer. This study aimed to determine the frequency and extent of intratumoral and metastatic lymph node KRAS mutation heterogeneity of resected pancreatic ductal adenocarcinoma.Tumor tissues macrodissected from tumor centers, invasion fronts (n = 97), and lymph nodes (n = 11) were subjected to DNA extraction and mutation analysis of KRAS codons 12 and 13 by pyrosequencing.Activating mutations in codon 12 of KRAS were detected in 90 (92.8%) tumor centers. No mutations were detected in KRAS codon 13 in any patient. After a comparison of tumor centers and invasion fronts, intratumoral heterogeneity of KRAS was observed only in 4 (4.1%) cases. Additional invasion front tumor analysis revealed the same mutation status consistent with each tumor center. No heterogeneity was observed between primary tumors and metastatic lymph nodes.Intratumoral heterogeneity of the KRAS mutational status is rare in pancreatic ductal adenocarcinoma. In addition, no KRAS heterogeneity between primary tumors and metastatic lymph nodes was detected in this study. This finding is consistent with the hypothesis that oncogenic activation of KRAS is the first driver mutation in pancreatic cancer.

Local recurrence of pancreatic cancer (PC) can occur in the pancreatic remnant. In addition, new primary PC can develop in the remnant. There are limited data available regarding this so-called remnant PC. The aim of this review was to describe the characteristics and therapeutic strategy regarding remnant PC. A literature search was performed using Medline published in English according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. The incidence of remnant PC has been reported to be 3% to 5%. It is difficult to distinguish local recurrence from new primary PC. Genetic diagnosis such as Kirsten rat sarcoma viral oncogene homolog mutation may resolve this problem. For patients with remnant PC, repeated pancreatectomy can be performed. Residual total pancreatectomy is the most common procedure. Recent studies have described the safety of the operation because of recent surgical progress and perioperative care. The patients with remnant PC without distant metastasis have shown good long-term outcomes, especially those who underwent repeated pancreatectomy. Adjuvant chemotherapy may contribute to longer survival. In conclusion, this review found that both local recurrence and new primary PC can develop in the pancreatic remnant. Repeated pancreatectomy for the remnant PC is a feasible procedure and can prolong patient survival.

To evaluate the clinical applicability of the determination of disseminated intravascular coagulation (DIC) parameters in acute pancreatitis.The subjects for this study were 139 consecutive patients with acute pancreatitis. DIC parameters were assessed at the initial observation of these patients.The levels of the DIC parameters at admission were significantly associated with the severity and the prognosis of acute pancreatitis. Antithrombin III (AT-III), fibrin/fibrinogen degradation products-E, platelet count, D-dimer, and thrombin-AT-III complex at admission showed better area under the receiver operating characteristics curve values compared with C-reactive protein. An AT-III value of 69% at admission was the best cut-off value to predict fatal outcome (sensitivity, 81%; specificity, 86%).The aggravated coagulation parameters predict a fatal outcome in patients with acute pancreatitis. AT-III level (69%) was the most accurate marker for poor outcome of acute pancreatitis at admission.