BACKGROUND: Disturbance of gastrointestinal function is a common complication in the early phase of acute pancreatitis (AP). Intestinal gas may reflect the function of the gut. Using plain abdominal radiographs, we in...BACKGROUND: Disturbance of gastrointestinal function is a common complication in the early phase of acute pancreatitis (AP). Intestinal gas may reflect the function of the gut. Using plain abdominal radiographs, we investigated whether intestinal gas volume is related to AP. METHODS: Plain abdominal radiographs of 68 patients with AP within 24 hours after admission and 21 normal controls were digitized and transmitted to a computer. The region of intestinal gas was identified by an image manipulation software and the gas volume score (GVS) was calculated. The relationships between the GVS values and various clinical factors of AP were analyzed. RESULTS: The GVS in the AP group was 0.084±0.016, in the mild AP (MAP) group 0.070±0.005, and in the severe AP (SAP) group 0.094±0.013; all values were higher than that in the control group (P<0.01). The GVS in the SAP group was higher than that in the MAP group. The GVSs were correlated to the Ranson’s scores (r=0.762, P<0.01) and the acute physiology and chronic health evaluation II (APACHE II) scores (r=0.801, P<0.01). In addition, the GVS in patients with secondary pancreatic and/or peripancreatic infection was 0.107±0.014, higher than that in patients without secondary infection (P<0.01). GVS was not related to gender, age, etiology or clinical outcome of AP. CONCLUSIONS: Intestinal gas volume is significantly elevated in patients with AP. It is closely related to Ranson’s and APACHE II score and secondary pancreatic and/or peripancreatic infection. GVS may be a new prognostic tool for assessing the severity of AP in the early course of the disease.展开更多
Chronic alcohol abuse damages nearly every organ in the body. The harmful effects of ethanol on thebrain, the liver and the pancreas are well documented. Although chronic alcohol consumption causes serious impairments...Chronic alcohol abuse damages nearly every organ in the body. The harmful effects of ethanol on thebrain, the liver and the pancreas are well documented. Although chronic alcohol consumption causes serious impairments also in the gastrointestinal tract like altered motility, mucosal damage, impaired absorption of nu-trients and inflammation, the effects of chronically consumed ethanol on the enteric nervous system are less detailed. While the nitrergic myenteric neurons play an essential role in the regulation of gastrointestinal peristalsis, it was hypothesised, that these neurons are the first targets of consumed ethanol or its metabolites generated in the different gastrointestinal segments. To reinforce this hypothesis the effects of ethanol on the gastrointestinal tract was investigated in different rodent models with quantitative immunohistochemistry, in vivo and in vitro motility measurements, western blot analysis, evaluation of nitric oxide synthase enzyme activity and bio-imaging of nitric oxide synthesis. These results suggest that chronic alcohol consumption did not result significant neural loss, but primarily impaired the nitrergic pathways in gut region-dependent way leading to disturbed gastrointestinal motility. The gut segment-specific differences in the effects of chronic alcohol consumption highlight the significance the ethanol-induced neuronal microenvironment involving oxidative stress and intestinal microbiota.展开更多
基金supported by a grant from the National Natural Science Foundation of China (81070297)
文摘BACKGROUND: Disturbance of gastrointestinal function is a common complication in the early phase of acute pancreatitis (AP). Intestinal gas may reflect the function of the gut. Using plain abdominal radiographs, we investigated whether intestinal gas volume is related to AP. METHODS: Plain abdominal radiographs of 68 patients with AP within 24 hours after admission and 21 normal controls were digitized and transmitted to a computer. The region of intestinal gas was identified by an image manipulation software and the gas volume score (GVS) was calculated. The relationships between the GVS values and various clinical factors of AP were analyzed. RESULTS: The GVS in the AP group was 0.084±0.016, in the mild AP (MAP) group 0.070±0.005, and in the severe AP (SAP) group 0.094±0.013; all values were higher than that in the control group (P<0.01). The GVS in the SAP group was higher than that in the MAP group. The GVSs were correlated to the Ranson’s scores (r=0.762, P<0.01) and the acute physiology and chronic health evaluation II (APACHE II) scores (r=0.801, P<0.01). In addition, the GVS in patients with secondary pancreatic and/or peripancreatic infection was 0.107±0.014, higher than that in patients without secondary infection (P<0.01). GVS was not related to gender, age, etiology or clinical outcome of AP. CONCLUSIONS: Intestinal gas volume is significantly elevated in patients with AP. It is closely related to Ranson’s and APACHE II score and secondary pancreatic and/or peripancreatic infection. GVS may be a new prognostic tool for assessing the severity of AP in the early course of the disease.
基金Supported by The János Bolyai Research Scholarship of the Hungarian Academy of Sciences(Mária Bagyánszki)by the Hungarian Scientific Research Fund,OTKA grant PD 108309(Nikolett Bódi)
文摘Chronic alcohol abuse damages nearly every organ in the body. The harmful effects of ethanol on thebrain, the liver and the pancreas are well documented. Although chronic alcohol consumption causes serious impairments also in the gastrointestinal tract like altered motility, mucosal damage, impaired absorption of nu-trients and inflammation, the effects of chronically consumed ethanol on the enteric nervous system are less detailed. While the nitrergic myenteric neurons play an essential role in the regulation of gastrointestinal peristalsis, it was hypothesised, that these neurons are the first targets of consumed ethanol or its metabolites generated in the different gastrointestinal segments. To reinforce this hypothesis the effects of ethanol on the gastrointestinal tract was investigated in different rodent models with quantitative immunohistochemistry, in vivo and in vitro motility measurements, western blot analysis, evaluation of nitric oxide synthase enzyme activity and bio-imaging of nitric oxide synthesis. These results suggest that chronic alcohol consumption did not result significant neural loss, but primarily impaired the nitrergic pathways in gut region-dependent way leading to disturbed gastrointestinal motility. The gut segment-specific differences in the effects of chronic alcohol consumption highlight the significance the ethanol-induced neuronal microenvironment involving oxidative stress and intestinal microbiota.
