Background and Objectives Outcomes after recurrence of resected pancreatic neuroendocrine tumors (PNETs) are not well described. We aim to assess the rate and sites of recurrence, and its effect on clinical outcomes. Methods Retrospective chart review of patients (n = 83) who underwent surgical resection of PNETs at 2 institutions. Patients were treated from September 2002 to July 2010. Results There were 13 (16%) recurrences. The most common site of recurrence was the liver (9 patients, 9.6%). The most common treatment of recurrences was chemotherapy (5 patients, 36%). The 1‐, 3‐, and 5‐year disease‐free survival was 90.9%, 82.7%, and 72.5%, respectively. Median recurrence‐free survival was 127 months. The median follow‐up for all PNET patients was 25.8 months (range, 1‐140 months). The 3‐year survival was 97%. The median follow‐up of patients after the diagnosis of a recurrence was 13.8 months. The overall survival for those with and without recurrence was 96.3% and 100%, respectively (P = .36). The age ( P = .002) and lymph node ratio ( P < .001) were predictors of recurrence on multivariate analysis. Conclusions Age and lymph node ratio are significant predictors of recurrence after the resection of PNETs with hepatic metastases being the most common. Survival of patients with recurrence is not significantly different from patients without recurrence.

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Purpose Outcomes and predictors of acute surgical conversion during endovascular aortic aneurysm repair (EVAR) were examined using the American College of Surgeons-National Safety and Quality Improvement Project (ACS-NSQIP) Database (2005 to 2008). Methods Acute intraoperative surgical conversions occurring during elective EVAR were identified using Current Procedural Terminology codes. Nonemergent EVAR and primary open surgical repairs of infrarenal aneurysms were examined for comparison. Perioperative morbidity was categorized as wound, pulmonary, venous thromboembolic, genitourinary, cardiovascular, operative, and septic. Mortality, overall morbidity, and length of stay (LOS) were examined. Results We identified 72 acute conversions, 2414 open repairs, and 6332 EVAR without acute conversion. Demographics and comorbidities were generally similar among operative groups. Mean operative time was 274 minutes for acute conversion vs 226 minutes for primary open repair and 162 minutes for EVAR (conversion vs EVAR and open repair vs EVAR P < .0001 for each; conversion vs open repair P = .0014; analysis on rank operative time). Blood transfusion was required in 69% of acute conversions (mean volume, 6.0 units) vs 73% of open repairs (mean volume, 3.3 units) and 12% of EVARs (mean volume, 2.6 units; P < .0001 for each pair-wise comparison; analysis on rank number of units among those transfused). Major morbidity was 28% for acute conversions, 28% for open repairs, and 12% for EVARs. Mortality was 4.2% for acute conversions, 3.2% for open repairs, and 1.3% for EVARs. Median (quartile 1, quartile 3) LOS was 7 (5, 9) days for acute conversion and open repair, and 2 (1, 3) days for EVAR. Morbidity and mortality were significantly higher for acute conversion and open repair vs EVAR. The OR (95% confidence interval) for morbidity was 2.9 (1.7–4.8) after conversion and 2.8 (2.5–3.2) after open repair (P < .0001 for both) and for mortality was 3.4 (1.0–10.9; P = .0437) for conversion and 2.5 (1.9–3.5; P < .0001) for open repair. Morbidity and mortality were similar between acute conversion and open repair. A similar pattern among repair groups was demonstrated for LOS, with similar LOS for acute conversions and open repair, which were significantly longer than those observed for EVAR. No significant demographic or medical risk factor predictors of acute conversion during EVAR were identified. Conclusion Acute surgical conversion was a rare complication affecting 1.1% of EVAR cases, with no broadly identifiable at-risk population. When conversion did occur, morbidity and mortality rates paralleled those observed for elective open repair.

Introduction: Abdominal aortic aneurysms (AAA) are characterized by localized inflammation, extracellular matrix degradation, and apoptosis of smooth muscle cells, which together lead to progressive and irreversible aortic dilation. Major risk factors for AAA include smoking and aging, both of which prominently alter gene expression via epigenetic mechanisms, including histone methylation (me) and acetylation (ac).However, little is known about epigenomic dynamics during AAA formation. Here, we profiled histone modification patterns in aortic tissues during AAA formation in two distinct mouse models; (1) angiotensin II (AngII) infusion in low density lipoprotein receptor (LDLR) knockout (KO) mice, and (2) calcium chloride (CaCl 2 ) application in wild type mice. Methods and Results:AAA formed in both models, in conjunction with enhanced macrophage infiltration, elastin degradation and matrix metalloproteinases expression as evaluated by immunohistochemistry. To investigate the histone modification patterns during AAA formation, total histone proteins were extracted from AAA tissues, and histone H3 modifications were quantified using profiling kits. Intriguingly, we observed dynamic changes in histone H3 modifications of lysine (K) residues at different time points during AAA formation. In mature aneurysmal tissues at 3 weeks after AngII infusion, we detected reduced K4/K27/K36 monomethylation, K9 trimethylation K9, and K9/K56 acetylation (<70%), and increased K4 trimethylation (>130%). Conversely, in CaCl 2 -induced AAA, K4/K9/K27/K36/K79 monomethylation and K9/K18/K56 acetylation were reduced in AAA tissues, whereas K27 di-/tri-methylation and K14 acetylation were upregulated. Interestingly, K4/K27/K36 monomethylation, K9 trimethylation, and K9/K56 acetylation were commonly downregulated in both animal models, while no H3 modifications were uniformly upregulated. Western blot of AAA tissues confirmed Greenway et al.Profiling of Histone H3 Modifications in AAA markedly reduced levels of key H3 modifications, including H3K4me1, H3K9me3, and H3K56ac. Furthermore, pathway enrichment analysis using an integrative bioinformatics approach identified specific molecular pathways, including endocytosis, exon guidance and focal adhesion signaling, that may potentially be linked to these histone H3 modifications during AAA formation.Conclusions: Dynamic modifications of histone H3 occur during AAA formation in both animal models. We identified 6 discreet H3 modifications that are consistently downregulated in both models, suggesting a possible role in AAA pathobiology. Identifying the functional mechanisms may facilitate development of novel strategies for AAA prevention or treatment.

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