Postoperative pancreatic fistula(POPF)is a well-known complication after pancreatoduodenectomy[1].It is difficult to prevent due to a number of factors.The very placement and tightening of sutures in pancreatic tissue...Postoperative pancreatic fistula(POPF)is a well-known complication after pancreatoduodenectomy[1].It is difficult to prevent due to a number of factors.The very placement and tightening of sutures in pancreatic tissue is challenging.Perfusion of the anastomosis edges is unpredictable.Another risk factor is the large amounts of fluids(comprising gastric and intestinal secretions,bile,and pancreatic juice)collected in the intestine near the pancreatic anastomosis,which increase the pressure in the first loop of the anastomosed intestine,and may ultimately rupture the pancreatoenteric anastomosis.Effective peristalsis,required to pass these fluids to subsequent sections of the intestine,takes time to return after such an extensive procedure.Increased pressure in the intestinal loop may also contribute to ischemia,by increasing the tension of the intestinal wall,constricting or even blocking its blood vessels.All these are aggravated by the chemical effects of intestinal contents.Any surgical errors may add the risk of POPF.展开更多
Celiac disease(CD) is a chronic immune-mediated disorder triggered by the ingestion of gluten in genetically predisposed individuals. Before activating the immune system, gluten peptides are transferred by the epithel...Celiac disease(CD) is a chronic immune-mediated disorder triggered by the ingestion of gluten in genetically predisposed individuals. Before activating the immune system, gluten peptides are transferred by the epithelial barrier to the mucosal lamina propria, where they are deamidated by intestinal tissue transglutaminase 2. As a result, they strongly bind to human leucocyte antigens(HLAs), especially HLA-DQ2 and HLA-DQ8, expressed on antigen-presenting cells. This induces an inflammatory response, which results in small bowel enteropathy. Although gluten is the main external trigger activating both innate and adaptive(specific) immunity, its presence in the intestinal lumen does not fully explain CD pathogenesis. It has been hypothesized that an early disruption of the gut barrier in genetically susceptible individuals, which would result in an increased intestinal permeability, could precede the onset of gluten-induced immune events. The intestinal barrier is a complex functional structure, whose functioning is dependent on intestinal microbiotahomeostasis, epithelial layer integrity, and the gutassociated lymphoid tissue with its intraepithelial lymphocytes(IELs). The aim of this paper was to review the current literature and summarize the role of the gut microbiota, epithelial cells and their intercellular junctions, and IELs in CD development.展开更多
文摘Postoperative pancreatic fistula(POPF)is a well-known complication after pancreatoduodenectomy[1].It is difficult to prevent due to a number of factors.The very placement and tightening of sutures in pancreatic tissue is challenging.Perfusion of the anastomosis edges is unpredictable.Another risk factor is the large amounts of fluids(comprising gastric and intestinal secretions,bile,and pancreatic juice)collected in the intestine near the pancreatic anastomosis,which increase the pressure in the first loop of the anastomosed intestine,and may ultimately rupture the pancreatoenteric anastomosis.Effective peristalsis,required to pass these fluids to subsequent sections of the intestine,takes time to return after such an extensive procedure.Increased pressure in the intestinal loop may also contribute to ischemia,by increasing the tension of the intestinal wall,constricting or even blocking its blood vessels.All these are aggravated by the chemical effects of intestinal contents.Any surgical errors may add the risk of POPF.
基金Supported by the Children’s Memorial Health Institute Grants,No.236/15,No.243/16 and No.S147/2016
文摘Celiac disease(CD) is a chronic immune-mediated disorder triggered by the ingestion of gluten in genetically predisposed individuals. Before activating the immune system, gluten peptides are transferred by the epithelial barrier to the mucosal lamina propria, where they are deamidated by intestinal tissue transglutaminase 2. As a result, they strongly bind to human leucocyte antigens(HLAs), especially HLA-DQ2 and HLA-DQ8, expressed on antigen-presenting cells. This induces an inflammatory response, which results in small bowel enteropathy. Although gluten is the main external trigger activating both innate and adaptive(specific) immunity, its presence in the intestinal lumen does not fully explain CD pathogenesis. It has been hypothesized that an early disruption of the gut barrier in genetically susceptible individuals, which would result in an increased intestinal permeability, could precede the onset of gluten-induced immune events. The intestinal barrier is a complex functional structure, whose functioning is dependent on intestinal microbiotahomeostasis, epithelial layer integrity, and the gutassociated lymphoid tissue with its intraepithelial lymphocytes(IELs). The aim of this paper was to review the current literature and summarize the role of the gut microbiota, epithelial cells and their intercellular junctions, and IELs in CD development.
