- [Modern treatment of mesenteric ischemia]. [Journal Article]
- PMPresse Med 2018 May 15
- Acute mesenteric ischemia is a highly morbid affliction which requires urgent care. Acute mesenteric ischemia consists in an ischemia injury of the small bowel, secondary to vascular insufficiency, e...
Acute mesenteric ischemia is a highly morbid affliction which requires urgent care. Acute mesenteric ischemia consists in an ischemia injury of the small bowel, secondary to vascular insufficiency, either occlusive (thrombosis, embolism, arterial, venous) or non-occlusive (low flow or vasospasm). Given that the superior mesenteric artery supplies the small bowel as well as the right part of the colon, any ischemic process involving the right colon should be considered an acute mesenteric ischemia until proven otherwise. Acute mesenteric ischemia should always be suspected in the setting of a sudden, unusual and intense abdominal pain requiring opioids. Chronic mesenteric ischemia can also be revealed by postprandial abdominal pain associated with significant weight loss. The clinical presentation of mesenteric ischemia is nonspecific. Thus, a suspected diagnosis must be confirmed by imaging usually consisting in an abdominal computed tomography scan. Imaging will also provide guidance with regards to treatment decision. Organ failure, serum lactate elevation as well as bowel loop dilationper imaging are predictive of irreversible intestinal necrosis. In the presence of any of these predictive factors, surgical management should be considered. The modern treatment of mesenteric ischemia in Intestinal Stroke Centers has allowed rates of resection-free survival in nearly two-thirds of patients. The management of mesenteric ischemia relies in a combination of: (1) a medical protocol including oral/enteral antibiotics; (2) the revascularization of viable bowel and (3) the surgical resection of necrosic, non viable intestinal tissue. The inception and development of Intestinal Stroke Centers has been the cornerstone of significantly improved management and survival rates as well as crucial asset in research, specifically in the field of biomarkers associated with early diagnosis.
- Inhibition of Ubiquitin-activating Enzyme Protects against Organ Injury after Intestinal Ischemia-Reperfusion. [Journal Article]
- AJAm J Physiol Gastrointest Liver Physiol 2018 May 17
- Intestinal ischemia-reperfusion (I/R) occurs in various clinical settings, such as transplantation, acute mesenteric arterial occlusion, trauma and shock. I/R injury causes severe systemic inflammati...
Intestinal ischemia-reperfusion (I/R) occurs in various clinical settings, such as transplantation, acute mesenteric arterial occlusion, trauma and shock. I/R injury causes severe systemic inflammation, leading to multiple organ dysfunction associated with high mortality. The ubiquitin proteasome pathway has been indicated in the regulation of inflammation, particularly through NF-κB signaling pathway. PYR-41 is a small molecular compound that selectively inhibits ubiquitin-activating enzyme E1. A mouse model of intestinal I/R injury by clamping the superior mesenteric artery for 45 minutes was performed to evaluate the effect of PYR-41 treatment on organ injury and inflammation. PYR-41 was administered intravenously at the beginning of reperfusion. Blood and organ tissues were harvested at 4 h after reperfusion. PYR-41 treatment improved the morphologic structure of gut and lung after I/R, as judged by H&E staining. It also reduced number of apoptotic TUNEL-positive cells and caspase-3 activity in the organs. PYR-41 treatment decreased the expression of proinflammatory cytokines IL-6 and IL-1β as well as chemokines KC and MIP-2 in the gut and lung, which leads to inhibition of neutrophils infiltrating into these organs. The serum levels of IL-6, AST and LDH were reduced by the treatment. The IκB degradation in the gut increased after I/R was inhibited by PYR-41 treatment. Thus, ubiquitination may be a potential therapeutic target for treating patients suffering from intestinal I/R.
- Knockdown of TNF‑α alleviates acute lung injury in rats with intestinal ischemia and reperfusion injury by upregulating IL‑10 expression. [Journal Article]
- IJInt J Mol Med 2018 May 14
- Intestinal ischemia and reperfusion (II/R) injury often triggers severe injury in remote organs, with the lungs being considered the main target. Excessive elevation of proinflammatory cytokines is a...
Intestinal ischemia and reperfusion (II/R) injury often triggers severe injury in remote organs, with the lungs being considered the main target. Excessive elevation of proinflammatory cytokines is a major contributor in the occurrence and development of II/R‑induced acute lung injury (ALI). Therefore, the present study aimed to investigate whether blocking tumor necrosis factor‑α (TNF‑α) expression could protect the lungs from injury following II/R, and to explore the possible underlying mechanism involving interleukin‑10 (IL‑10). Briefly, II/R was induced in rats by 40 min occlusion of the superior mesenteric artery and celiac artery, followed by 8, 16 or 24 h of reperfusion. Subsequently, lentiviral vectors containing TNF‑α short hairpin (sh)RNA were injected into the right lung tissues, in order to induce TNF‑α knockdown. The severity of ALI was determined according to lung injury scores and lung edema (lung wet/dry weight ratio). The expression levels of TNF‑α were analyzed by quantitative polymerase chain reaction (qPCR), western blotting and immunofluorescence (IF) staining. IL‑10 expression, in response to TNF‑α knockdown, was detected in lung tissues by qPCR and IF. The results detected marked inflammatory responses, and increased levels of lung wet/dry weight ratio and TNF‑α expression, in the lungs of II/R rats. Conversely, treatment with TNF‑α shRNA significantly alleviated the severity of ALI and upregulated the expression levels of IL‑10 in lung tissues. These findings suggested that TNF‑α RNA interference may exert a protective effect on II/R‑induced ALI via the upregulation of IL‑10. Therefore, TNF‑α knockdown may be considered a potential strategy for the prevention or treatment of ALI induced by II/R in future clinical trials.
- Released Mitochondrial DNA Following Intestinal Ischemia Reperfusion Induces the Inflammatory Response and Gut Barrier Dysfunction. [Journal Article]
- SRSci Rep 2018 May 09; 8(1):7350
- Ischemia-reperfusion (I/R) injury is a challenging clinical problem, especially injuries involving the gastrointestinal tract. Mitochondrial DNA (mtDNA) is released upon cell death and stress, and ca...
Ischemia-reperfusion (I/R) injury is a challenging clinical problem, especially injuries involving the gastrointestinal tract. Mitochondrial DNA (mtDNA) is released upon cell death and stress, and can induce the inflammatory response. We aimed to investigate the role of mtDNA in the pathogenesis of intestinal I/R. Intestinal I/R model was established with clamping of the superior mesenteric artery, and IEC-6 cells were incubated under hypoxia/reoxygenation (H/R) conditions to simulate I/R injury. Using in vitro models, H/R up-regulated oxidative stress, disrupted mitochondrial activity and the mitochondrial membrane potential, induced apoptosis and elevated the mtDNA levels in the supernatant of intestinal epithelial cells, and the co-culture of mtDNA with human primary dendritic cells significantly elevated TLR9-MyD88 expression and enhanced the production of inflammatory cytokines and chemokines. MtDNA was also released in a mouse model of intestinal I/R and was associated with the increased secretion of inflammatory cytokines and increased gut barrier injury compared with that of the sham group. We concluded that mtDNA contributes to I/R injury and may serve as a biomarker of intestinal I/R. We further suggest that oxidized mtDNA originated from IECs during intestinal I/R exacerbates the acute proinflammatory process by eliciting the production of proinflammatory cytokines and chemokines.
- Endoscopic Follow-up of Intestinal Transplant Recipients. [Review]
- GCGastroenterol Clin North Am 2018; 47(2):381-391
- The growing population of intestinal transplant recipients present a unique challenge to the gastroenterologists responsible for their support and evaluation. Improvements in patient and graft surviv...
The growing population of intestinal transplant recipients present a unique challenge to the gastroenterologists responsible for their support and evaluation. Improvements in patient and graft survival are largely attributed to surgical advancements, refined antirejection therapy, and enhanced endoscopic surveillance protocols that better perceive rejection and other complications. This article reviews the endoscopic management and interventions provided for transplant recipients at the University of Illinois Hospital with complications, such as acute rejection, ischemia, bleeding, fistula, post-transplant lymphoproliferative disorder, and gastroparesis. Further research is needed on promising strategies currently used for related diseases to treat and sustain the intestinal graft.
- Acute lower limb ischemia and intestinal necrosis due to arterial tumor embolism from advanced lung cancer: a case report and literature review. [Journal Article]
- SCSurg Case Rep 2018 May 02; 4(1):42
- CONCLUSIONS: ATE is rare but should be considered as a differential diagnosis for unidentified arterial occlusion.
- Author Correction: Role of iRhom2 in intestinal ischemia-reperfusion-mediated acute lung injury. [Published Erratum]
- SRSci Rep 2018 May 01; 8(1):7087
- A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has not been fixed in the paper.
A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has not been fixed in the paper.
- What's new in short bowel syndrome? [Journal Article]
- COCurr Opin Clin Nutr Metab Care 2018 Apr 26
- CONCLUSIONS: Multimodal treatment of acute meseteric ischemia may avoid intestinal resection and is an effective prevention strategy for SBS. New understandings in intestinal adaptation can help us to optimize this adaptation, including with hormonal therapy. GLP-2 analog is now the treatment of reference in SBS patients with chronic intestinal failure.
- Selection and Determination of Treatment for the Spontaneous Isolated Dissection of the Superior Mesenteric Artery. [Journal Article]
- AVAnn Vasc Dis 2018 Mar 25; 11(1):101-105
- Objective: This study aimed to clarify the selection and determination of appropriate treatment for acute symptomatic spontaneous isolated dissection of the superior mesenteric artery (SIDSMA). Metho...
Objective: This study aimed to clarify the selection and determination of appropriate treatment for acute symptomatic spontaneous isolated dissection of the superior mesenteric artery (SIDSMA). Methods: Data from 10 consecutive patients, who were diagnosed with symptomatic SIDSMA using computed tomography angiography and were managed in our hospital from January 2010 to October 2015, were retrospectively collected and analyzed. Results: There were nine males and one female; mean patient age was 50.3 (range, 35-64) years. All patients experienced acute abdominal pain, and three patients experienced concomitant vomiting. Only one patient exhibited symptoms of suspected peritonitis and intestinal ischemia. Three patients showed improved abdominal pain before admission to our hospital. One patient experienced severe abdominal pain that could not be managed using morphine; he underwent right external iliac to superior mesenteric artery bypass with a great saphenous vein graft. No patient presented with intestinal necrosis. All patients survived, and no patient developed complications during the follow-up period of up to 42 (24.5±16.5) months. Conclusion: Conservative management appears to be the most feasible treatment for SIDSMA. However, open surgery can be performed in patients presenting with any symptoms of intestinal ischemia.
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- Nrf2 protects against acute lung injury and inflammation by modulating TLR4 and Akt signaling. [Journal Article]
- FRFree Radic Biol Med 2018 Apr 17; 121:78-85
- Lung injury, which is associated with systemic inflammatory responses, is a common problem with significant morbidity and mortality. Here, we examined the involvement of toll-like receptor 4 (TLR4) a...
Lung injury, which is associated with systemic inflammatory responses, is a common problem with significant morbidity and mortality. Here, we examined the involvement of toll-like receptor 4 (TLR4) and nuclear factor erythroid 2-related factor 2 (Nrf2) on intestinal ischemia-reperfusion (I/R)-induced lung injury in vivo and in vitro. Analysis of lung tissues in Nrf2-knockout mice by western blotting, immunohistochemistry, and TUNEL assay, and analysis of bronchoalveolar lavage fluid showed that Nrf2 deficiency upregulated TLR4, enhanced I/R-induced lung injury, apoptosis, inflammation, and autophagy, and increased the I/R-induced inactivation of Akt. In mouse lung epithelial cells subjected to oxygen and glucose deprivation/reperfusion (OGD/Rep), Nrf2 silencing increased the OGD/Rep-induced upregulation of TLR4 and MyD88 and downregulation of HO-1, and exacerbated OGD/Rep-induced apoptosis, autophagy, and the downregulation of phospho-Akt. TLR4 silencing and Akt inhibition experiments indicated that OGD/Rep-induced cell death by suppressing Akt signaling, and Nrf2 protected lung cells by modulating TLR4 and Akt signaling. These results indicated that the Nrf2/TLR4/Akt axis plays a role in inflammation-associated lung damage, suggesting potential therapeutic targets for the treatment of lung injury.