Posterior Superior Mesenteric Artery First Dissection Versus Classical Approach in Pancreaticoduodenectomy: Outcomes of a Case-Matched Study.

OBJECTIVES: Posterior superior mesenteric artery (SMA) first dissection in pancreaticoduodenectomy (PD) may allow for early assessment of resectability and aberrant anatomy. Study objectives were to compare resection margins, perioperative outcomes, disease-free survival (DFS) and overall survival (OS) in patients undergoing a posterior SMA first dissection PD to a classical technique PD. METHODS: Patients (n = 77) who underwent a posterior SMA first PD for adenocarcinoma were case matched for patient and tumor characteristics with patients undergoing a classical approach PD from 2006 to 2014 (n = 177). RESULTS: The SMA first patients had an improved negative resection margin rate (27 [35.1%] vs 14 [18.2%], P = 0.042) and a higher lymph node yield (median 28 [22-34] vs 21 [17-27], P < 0.001) compared with the classical approach group. No difference was demonstrated in serious complications or 30-day mortality between the SMA first and classical approach patients (Clavien-Dindo 3/4 16 [20.8%] vs 11 [14.3%], P = 0.336; 30-day mortality 3 [3.9%] vs 3 [3.9%], P = 1.00 respectively). Median DFS and OS was similar in SMA first compared with classical approach patients (DFS, 1.6 vs 1.1 years, P = 0.122; OS, 2.5 vs 1.5 years, P = 0.220 respectively). CONCLUSIONS: A posterior SMA first approach is a comparably safe technique that may improve oncological results in PD compared with classical approach dissection.

Toll-like receptor-mediated responses of primary intestinal epithelial cells during the development of colitis.

The interleukin-2-deficient (IL-2(-/-)) mouse model of ulcerative colitis was used to test the hypothesis that colonic epithelial cells (CEC) directly respond to bacterial antigens and that alterations in Toll-like receptor (TLR)-mediated signaling may occur during the development of colitis. TLR expression and activation of TLR-mediated signaling pathways in primary CEC of healthy animals was compared with CEC in IL-2(-/-) mice during the development of colitis. In healthy animals, CEC expressed functional TLR, and in response to the TLR4 ligand LPS, proliferated and secreted the cytokines IL-6 and monocyte chemoattractant protein-1 (MCP-1). However, the TLR-responsiveness of CEC in IL-2(-/-) mice was different with decreased TLR4 responsiveness and augmented TLR2 responses that result in IL-6 and MCP-1 secretion. TLR signaling in CEC did not involve NF-kappaB (p65) activation with the inhibitory p50 form of NF-kappaB predominating in CEC in both the healthy and inflamed colon. Development of colitis was, however, associated with the activation of MAPK family members and upregulation of MyD88-independent signaling pathways characterized by increased caspase-1 activity and IL-18 production. These findings identify changes in TLR expression and signaling during the development of colitis that may contribute to changes in the host response to bacterial antigens seen in colitis.