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The selection from this month’s clinical journal scan is a reminder of the varied presentations and etiologies EPI. Surmelioglu and colleagues out of Istanbul looked at the development of EPI after curative gastrectomy for gastric cancer. 69 patients with gastric cancer following treatment were followed for a minimum follow-up period of 16 months. Fecal elastase (FE-1) levels were low in 33 (47.8%) of the patients, moderate in 11 (15.9%), and normal in 25 (36.2%). Having received adjuvant chemoradiotherapy (CRT) was significantly associated with being in the low or moderate FE-1 group (P < 0.001 and P = 0.012, respectively).
Interestingly the authors propose possible causative mechanisms. They note that normal pancreatic secretion is regulated by neural and endocrine control mechanisms that require intact gastro-pancreatico-duodenal anatomy. Disruptions to this include “extensive pancreatic denervation because of lymph node dissection and truncal vagotomy, the asynchronous release of pancreatic enzymes for food particles (pancreaticocibal-asynchrony) because of newly made reconstructions, and gastric reservoir and neural gastric stimulation losses.” They also include the possibility of effects of adjuvant therapies as well.
While 64% of this patient population had some form of EPI, another study from this month’s selection by Sridhar et al out of Vellore, India tells a different story. In this cross-sectional study, they looked at symptomatic and biochemical evidence of EPI on pre and post questionnaires following gastric resection for adenocarcinoma. Of 27 patients that completed pre and post questionnaires, none of the patients on short-term follow-up (mean follow up of 3 months) had clinical symptoms of EPI following gastric resection. However, more than a third of the patients developed asymptomatic EPI after gastric resection, based on FE testing. The authors conclude that pancreatic supplementation might not be necessary following gastric resection, but perhaps their follow up window was much too short to draw such a conclusion.
The selection from this month’s clinical journal scan is a reminder of the varied presentations and etiologies EPI. Surmelioglu and colleagues out of Istanbul looked at the development of EPI after curative gastrectomy for gastric cancer. 69 patients with gastric cancer following treatment were followed for a minimum follow-up period of 16 months. Fecal elastase (FE-1) levels were low in 33 (47.8%) of the patients, moderate in 11 (15.9%), and normal in 25 (36.2%). Having received adjuvant chemoradiotherapy (CRT) was significantly associated with being in the low or moderate FE-1 group (P < 0.001 and P = 0.012, respectively).
Interestingly the authors propose possible causative mechanisms. They note that normal pancreatic secretion is regulated by neural and endocrine control mechanisms that require intact gastro-pancreatico-duodenal anatomy. Disruptions to this include “extensive pancreatic denervation because of lymph node dissection and truncal vagotomy, the asynchronous release of pancreatic enzymes for food particles (pancreaticocibal-asynchrony) because of newly made reconstructions, and gastric reservoir and neural gastric stimulation losses.” They also include the possibility of effects of adjuvant therapies as well.
While 64% of this patient population had some form of EPI, another study from this month’s selection by Sridhar et al out of Vellore, India tells a different story. In this cross-sectional study, they looked at symptomatic and biochemical evidence of EPI on pre and post questionnaires following gastric resection for adenocarcinoma. Of 27 patients that completed pre and post questionnaires, none of the patients on short-term follow-up (mean follow up of 3 months) had clinical symptoms of EPI following gastric resection. However, more than a third of the patients developed asymptomatic EPI after gastric resection, based on FE testing. The authors conclude that pancreatic supplementation might not be necessary following gastric resection, but perhaps their follow up window was much too short to draw such a conclusion.
The selection from this month’s clinical journal scan is a reminder of the varied presentations and etiologies EPI. Surmelioglu and colleagues out of Istanbul looked at the development of EPI after curative gastrectomy for gastric cancer. 69 patients with gastric cancer following treatment were followed for a minimum follow-up period of 16 months. Fecal elastase (FE-1) levels were low in 33 (47.8%) of the patients, moderate in 11 (15.9%), and normal in 25 (36.2%). Having received adjuvant chemoradiotherapy (CRT) was significantly associated with being in the low or moderate FE-1 group (P < 0.001 and P = 0.012, respectively).
Interestingly the authors propose possible causative mechanisms. They note that normal pancreatic secretion is regulated by neural and endocrine control mechanisms that require intact gastro-pancreatico-duodenal anatomy. Disruptions to this include “extensive pancreatic denervation because of lymph node dissection and truncal vagotomy, the asynchronous release of pancreatic enzymes for food particles (pancreaticocibal-asynchrony) because of newly made reconstructions, and gastric reservoir and neural gastric stimulation losses.” They also include the possibility of effects of adjuvant therapies as well.
While 64% of this patient population had some form of EPI, another study from this month’s selection by Sridhar et al out of Vellore, India tells a different story. In this cross-sectional study, they looked at symptomatic and biochemical evidence of EPI on pre and post questionnaires following gastric resection for adenocarcinoma. Of 27 patients that completed pre and post questionnaires, none of the patients on short-term follow-up (mean follow up of 3 months) had clinical symptoms of EPI following gastric resection. However, more than a third of the patients developed asymptomatic EPI after gastric resection, based on FE testing. The authors conclude that pancreatic supplementation might not be necessary following gastric resection, but perhaps their follow up window was much too short to draw such a conclusion.