Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
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J. Gastrointest. Surg. · Mar 2007
The effect of L-arginine and aprotinin on intestinal ischemia-reperfusion injury.
Intestinal ischemia/reperfusion (I/R) results in local mucosal injury, systemic injuries, and organ dysfunction. These injuries are characterized by altered microvascular and epithelial permeability and villous damage. Activation of neutrophils, platelets, and endothelial factors are known to be involved in this process. Cytokines such as TNF-alpha, IL-1, IL-6, and oxygen-derived free radicals are believed to be important pathogenic mediators. Capillary no-reflow is also known to play a role in I/R. The aim of our study was to examine the role of L-arginine, a known nitric oxide (NO) donor, and aprotinin, a protease inhibitor with multiple effects, on intestinal I/R. ⋯ Administration of L: -arginine and aprotinin may lead to amelioration of intestinal I/R injury. We did not note a synergistic or additive effect of these two substances. These findings warrant further studies in clinical settings for future treatment efforts.
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J. Gastrointest. Surg. · Jan 2007
Anastomotic leakage is associated with poor long-term outcome in patients after curative colorectal resection for malignancy.
The impact of anastomotic leakage on long-term outcomes after curative surgery for colorectal cancer has not been well documented. This study aimed to investigate the effect of anastomotic leakage on survival and tumor recurrence in patients who underwent curative resection for colorectal cancer. Prospectively collected data of the 1,580 patients (904 men) of a median age of 70 years (range: 24-94), who underwent potentially curative resection for colorectal cancer between 1996 and 2004, were reviewed. ⋯ In rectal cancer, anastomotic leakage was an independent factor for a higher local recurrence rate (hazard ratio: 2.55, 95% CI: 1.07-6.06, p = 0.034). In conclusion, anastomotic leakage is associated with a poor survival and a higher tumor recurrence rate after curative resection of colorectal cancer. Efforts should be undertaken to avoid this complication to improve the long-term outcome.
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J. Gastrointest. Surg. · Dec 2006
In vitro evidence for role of ERK, p38, and JNK in exocrine pancreatic cytokine production.
Elucidation of mechanisms of acinar cell cytokine production is essential for a better understanding of acute pancreatitis pathogenesis. We hypothesize that the stress kinases ERK, p38, and JNK play an important role in acinar cell cytokine production. Rat pancreatic fragments were incubated with 100 nM concentration of the cholecystokinin analog caerulein or 100 nM caerulein and specific ERK inhibitor (100 microM PD98059), specific p38 inhibitor (10 microM SB203580), or specific JNK inhibitor (20 microM SP600125). ⋯ Increased activation of ERK, p38, and JNK in pancreatic fragments was not associated with significant increases in total ERK, total p38, or total JNK concentrations. The stress kinases ERK and p38 play an important role in caerulein-stimulated exocrine pancreatic overproduction of cytokines. The role of JNK needs further evaluation in this experimental model.
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J. Gastrointest. Surg. · Dec 2006
Case ReportsDurability of portal venous reconstruction following resection during pancreaticoduodenectomy.
Venous resection and reconstruction is becoming more common during pancreaticoduodenectomy (PD). There are multiple options for reconstruction of the mesenteric venous system ranging from primary repair to grafting with autologous or synthetic material. Few studies report on the patency rates and long-term morbidity of these repairs. ⋯ In those patients with thrombosis outside the acute time period, morbidity was limited to ascites in three patients and splenic vein thrombosis with uncomplicated esophageal varices in another patient. Mesenteric venous resection and reconstruction during PD has a high patency rate, and those reconstructions that do thrombose are associated with a low morbidity. The majority of reconstruction thromboses that occurred late were associated with recurrence.
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J. Gastrointest. Surg. · Nov 2006
Randomized Controlled TrialDoes pancreatic duct stenting decrease the rate of pancreatic fistula following pancreaticoduodenectomy? Results of a prospective randomized trial.
Pancreatic duct stenting remains an attractive strategy to reduce the incidence of pancreatic fistulas following pancreaticoduodenectomy (PD) with encouraging results in both retrospective and prospective studies. We performed a prospective randomized trial to test the hypothesis that internal pancreatic duct stenting reduces the development of pancreatic fistulas following PD. Two hundred thirty-eight patients were randomized to either receive a pancreatic stent (S) or no stent (NS), and stratified according to the texture of the pancreatic remnant (soft/normal versus hard). ⋯ A nonstatistically significant increase in the pancreatic fistula rate in the S group persisted after adjusting for the operating surgeon and technical details of the operation (e.g., anastomotic technique, anastomotic orientation, pancreatic duct size, and number of intra-abdominal drains placed). In patients with soft pancreata, 63% percent of the pancreatic fistulas in stented patients required adjustment to the clinical pathway (including two deaths), compared to 47% of the pancreatic fistulas in patients in the NS group (P = 0.3). Internal pancreatic duct stenting does not decrease the frequency or the severity of postoperative pancreatic fistulas.