Management and outcomes following pancreaticoduodenectomy for ampullary adenocarcinoma.

INTRODUCTION: The purpose of this study was to evaluate outcomes following pancreaticoduodenectomy(PD) for ampullary adenocarcinoma(AAC). METHODS: We evaluated patients having undergone PD for AAC and the impact of clinical/histopathologic factors and adjuvant therapy(AT) on survival. RESULTS: 52 patients underwent potentially curative PD. Perineural and lymphovascular invasion were associated with decreased survival. There was no difference in survival between patients treated with PD vs. PD+AT, however, AT was more often administered to patients with N1 vs. N0 and stage II/III vs. I disease. Among patients receiving AT, we observed a trend towards improved survival when radiation was included. Recurrence occurred in 7/18(39%) stage I patients, only 2(7%) of which received AT. CONCLUSION: AT did not improve survival, however was more commonly administered in advanced disease. Stage I patients had high recurrence rates but rarely received AT. Prospective evaluation of appropriate AT regimens and use in early stage patients should be considered.

Neutrophil inhibition contributes to cardioprotection by postconditioning.

BACKGROUND: Postconditioning (postcon) reduces infarct size, myocardial superoxide ((•)O(2)) generation, and neutrophil (PMN) accumulation. It is unknown whether inhibition of PMNs influence cardioprotection by postcon. The present study tested the following hypotheses: (1) myocardial salvage by postcon is modified by inhibition of PMNs and (2) postcon directly inhibits PMN (•)O(2) generation. METHODS: For hypothesis 1, a deductive approach was used to determine infarct size in vivo with and without PMNs in rats, and for hypothesis 2, blood sampled from the anterior interventricular vein (AIV) in a canine model was used. Protocol 1: anesthetized rats, subjected to 30 min of coronary artery occlusion and 3 h of reperfusion, were randomized to control (n = 13), postcon (n = 13), PMN-depletion: (n = 9), and postcon in PMN-depleted rats (n = 9). Protocol 2: blood was sampled at baseline, 2 h and 24 h from the AIV, draining the area at risk (AAR) in anesthetized dogs with 60 min coronary occlusion ± postcon; whole blood was analyzed for (•)O(2) by luminol-enhanced chemiluminescence. RESULTS: Postcon and PMN depletion reduced infarct size (42.6 ± 2.1%, P < 0.05 vs. control, and 43.9 ± 3.0%, P < 0.05 vs. control, respectively) vs. control (58.8 ± 0.9%), with no further decrease with postcon in PMN-depleted rats (37.2 ± 2.9%, P = 0.34 vs. postcon). PMN accumulation in AAR was less in postcon (21.2 ± 0.3%, P < 0.05 vs. control) and PMN-depleted (9.4 ± 0.3%, P < 0.05 vs. control) vs. control (30.5 ± 1.2%), with a further decrease in the postcon + PMN depletion group (5.4 ± 0.6%, P < 0.05 vs. control). In dogs, (•)O(2) release by PMNs increased at 2 h and 24 h of R, which was reduced to baseline levels by postcon. CONCLUSIONS: These data imply PMN involvement in cardioprotection by postconditioning.