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| 1 | Tumor necrosis factor-α and interleukin-6 in cirrhotic patients with spontaneous bacterial peritonitis显示文摘AIM:To evaluate the role of tumor necrosis factor-α(TNF-α) and interleukin-6(IL-6) in cirrhotic patients who have hepatic and renal impairment with spontaneous bacterial peritonitis(SBP).METHODS:We prospectively studied 120 cirrhotic patients with SBP and 80 cirrhotic patients with sterile ascitic fluid.They included 144 males and 56 females with ages ranging between 34 and 62 years.The diagnosis of cirrhosis was established by clinical and laboratory criteria that did not require histological confirmation.The severity of underlying liver disease was evaluated using Pugh's modification of Child's criteria(Child-Pugh scores).Ascitic fluid was sent to the laboratory for cell count,culture,sensitivity testing,and measurement of chemical elements(i.e.,albumin,glucose).Specimens were inoculated into aerobic and anaerobic blood culture bottles.Serum and ascitic fluid were also collected in sterile tubes at study entry(before the initiation of antibiotic treatment) and 48 h later.Assays for TNF-α and IL-6 in the serum and ascitic fluid were performed with an immunoenzymometric assay using manufacture's instructions.RESULTS:Cytokine levels in serum and ascitic fluid were significantly higher in the patients with SBP.(plasma TNF-α:135.35 ng/mL ± 11.21 ng/mL vs 92.86 ng/mL ± 17.56 ng/mL,P < 0.001;plasma IL-6:32.30 pg/mL ± 7.07 pg/mL vs 12.11 pg/mL ± 6.53 pg/mL,P < 0.001;ascitic fluid TNF-α:647.54 ± 107.11 ng/mL vs 238.43 ng/mL ± 65.42 ng/mL,P < 0.001);ascitic fluid IL-6:132.84 ng/mL ± 34.13 vs 40.41 ± 12.85 pg/mL,P < 0.001).About 48(40%) cirrhotic patients with SBP developed renal and hepatic impairment and showed significantly higher plasma and ascitic fluid cytokine levels at diagnosis of infection.[(plasma TNF-α:176.58 ± 17.84 vs 135.35 ± 11.21 ng/mL)(P < 0.001) and(IL-6:57.83 ± 7.85 vs 32.30 ± 7.07 pg/mL)(P < 0.001);ascitic fluid TNF-α:958.39 ± 135.72 vs 647.54 ± 107.11 ng/mL,(P < 0.001),ascitic fluid IL-6:654.74 ± 97.43 vs 132.84 ± 34.13 pg/mL,(P < 0.001)].Twenty nine patients(60.4%) with SBP and renal impairment died whereas,only four patients(5.55%) with SBP but without renal impairment died from gastrointestinal hemorrhage(P < 0.0005).CONCLUSION:It appears that TNF-α production may enhance liver cell injury and lead to renal impairment.This correlated well with the poor prognosis and significantly increased mortality associated with SBP in cirrhotic patients. | Muhammed AM Suliman Fawzy MH Khalil Salam SA Alkindi Anil V Pathare Ali AA Almadhani Neveen AAI Soliman | 2012 | World Journal of Gastrointestinal Pathophysiology2012，3，5： | 39 |
| 2 | Implication of miRNAs for inflammatory bowel disease treatment:Systematic review显示文摘Inflammatory bowel disease(IBD)is believed to develop via a complex interaction between genetic,environmental factors and the mucosal immune system.Crohn’s disease and ulcerative colitis are two major clinical forms of IBD.MicroRNAs(miRNAs)are a class of small,endogenous,noncoding RNA molecules,and evolutionary conserved in animals and plants.It controls protein production at the post-transcriptional level by targeting mRNAs for translational repression or degradation.MiRNAs are important in many biological processes,such as signal transduction,cellular proliferation,differentiation and apoptosis.Considerable attention has been paid on the key role of miRNAs in autoimmune and inflammatory disease,especially IBD.Recent studies have identified altered miRNA profiles in ulcerative colitis,Crohn’s disease and inflammatory bowel diseaseassociated colorectal cancer.In addition,emerging data have implicated that special miRNAs which suppress functional targets play a critical role in regulating key pathogenic mechanism in IBD.MiRNAs were found involving in regulation of nuclear transcription factor kappa B pathway(e.g.,miR-146a,miR-146b,miR-122,miR-132,miR-126),intestinal epithelial barrier function(e.g.,miR-21,miR-150,miR-200b)and the autophagic activity(e.g.,miR-30c,miR-130a,miR-106b,miR-93,miR-196).This review aims at discussing recent advances in our understanding of miRNAs in IBD pathogenesis,their role as disease biomarkers,and perspective for future investigation and clinical application. | Wei-Xu Chen Li-Hua Ren Rui-Hua Shi | 2014 | World Journal of Gastrointestinal Pathophysiology2014，5，2： | 31 |
| 3 | Eosinophilic ascites,an unusual presentation of eosinophilic gastroenteritis:A case report and review显示文摘Eosinophilic ascites(EA)is a rare disorder of unknown etiology that has been reported in both adult and pediatric patients.It is a part of the syndrome of eosinophilic gastroenteritis,which is characterized by eosinophilic infiltration of any or all layers of the gut wall and may involve any segment of the gastrointestinal tract.Peripheral eosinophilia may or may not be present.We report a case of EA that developed post partum. | Iryna S Hepburn Subbaramiah Sridhar Robert R Schade | 2010 | World Journal of Gastrointestinal Pathophysiology2010，1，5： | 22 |
| 4 | Helicobacter pylori and neurological diseases: Married by the laws of inflammation显示文摘The purpose of this paper is to review current infor-mation about the role of inflammation caused by He-licobacter pylori(H. pylori) infection in neurological diseases such as Parkinson's disease, Alzheimer's dis-ease, Guillain-Barré syndrome, multiple sclerosis, and other inflammatory diseases including ischemic stroke. Infection with H. pylori usually persists throughout life, resulting in a chronic inflammatory response with local secretion of numerous inflammatory mediators includ-ing chemokines [interleukin(IL)-8, macrophage che-motactic protein, growth-regulated oncogene(GRO)-α, chemokine(C-X-C motif) ligand 1] and cytokines [IL-1β, tumor necrosis factor-α, IL-6, IL-12, interferon-g], which can pass into the circulation and have a systemic effect. The persistence of detectable systemic and lo-cal concentrations of inflammatory mediators is likely to alter the outcome of neurological diseases. These proinflammatory factors can induce brain inflammation and the death of neurons and could eventually be asso-ciated to Parkinson's disease and also may be involved in the development of Alzheimer's disease. However,most neurological diseases are the result of a combina-tion of multiple factors, but the systemic inflammatory response is a common component and determinant in the onset, evolution, and outcome of diseases. How-ever, more studies are needed to allow understanding of the effects and mechanisms by which the inflamma-tory response generated by H. pylori infection affects neurological diseases. | Lourdes álvarez-Arellano Carmen Maldonado-Bernal | 2014 | World Journal of Gastrointestinal Pathophysiology2014，5，4： | 23 |
| 5 | Mesenteric ischemia:Pathogenesis and challengingdiagnostic and therapeutic modalities显示文摘Mesenteric ischemia(MI) is an uncommon medical condition with high mortality rates. ΜΙ includes inadequate blood supply, inflammatory injury and eventually necrosis of the bowel wall. The disease can be divided into acute and chronic MI(CMI), with the first being subdivided into four categories. Therefore, acute MI(AMI) can occur as a result of arterial embolism, arterial thrombosis, mesenteric venous thrombosis and nonocclusive causes. Bowel damage is in proportion to the mesenteric blood flow decrease and may vary from minimum lesions, due to reversible ischemia, to transmural injury, with subsequent necrosis and perforation. CMI is associated to diffuse atherosclerotic disease in more than 95% of cases, with all major mesenteric arteries presenting stenosis or occlusion. Because of a lack of specific signs or due to its sometime quiet presentation, this condition is frequently diagnosed only at an advanced stage. Computed tomography(CT) imaging and CT angiography contribute to differential diagnosis and management of AMI. Angiography is also the criterion standard for CMI, with mesenteric duplex ultrasonography and magnetic resonance angiography also being of great importance. Therapeutic approach of MI includes both medical and surgical treatment. Surgical procedures include restoration of the blood flow with arteriotomy, endarterectomy or anterograde bypass, while resection of necrotic bowel is always implemented. The aim of this review was to evaluate the results of surgical treatment for MI and to present the recent literature in order to provide an update on the current concepts of surgical management of the disease. Mesh words selected include MI, diagnostic approach and therapeutic management. | Aikaterini Mastoraki Sotiria Mastoraki Evgenia Tziava Stavroula Touloumi Nikolaos Krinos Nikolaos Danias Andreas Lazaris Nikolaos Arkadopoulos | 2016 | World Journal of Gastrointestinal Pathophysiology2016，7，1： | 23 |
| 6 | New-found link between microbiota and obesity显示文摘Due to the grave pathological role of obesity, worldwide research is being continued to find out the causative factors involved in it. Recent advances in this field reveal a possible relationship between the compositional pattern of gut microbiota and genesis of obesity. Several study results have shown that short-chain fatty acids(SCFAs, microbiota-induced fermentation products) and lipopolysaccharides(LPS, an integral component of Gram negative microorganisms) play the key role in linking the two. Though several SCFAs are produced as microbiota-fermentation products, three of them, i.e., butyrate, propionate and acetate have been found to be definitely involved in obesity; though individually they are neither purely obesogenic nor antiobesogenic. Out of these, butyrate and propionate are predominantly antiobesogenic. Butyrate, though a major energy source for colonocytes, has been found to increase mitochondrial activity, prevent metabolic endotoxemia, improve insulin sensitivity, possess antiinflammatory potential, increase intestinal barrier function and protect against diet-induced obesity without causing hypophagia. Propionate has been found to inhibit cholesterol synthesis, thereby antagonizing the cholesterol increasing action of acetate, and to inhibit the expression of resistin in adipocytes. Moreover, both these SCFAs have been found to cause weight regulation through their stimulatory effect on anorexigenic gut hormones and to increase the synthesis of leptin. Unlike butyrate and propionate, acetate, which is substantially absorbed, shows more obesogenic potential, as it acts as a substrate for hepatic and adipocyte lipogenesis. High fat diet increases the absorption of LPS, which, in turn, has been found to be associated with metabolic endotoxemia and to induce inflammation resulting in obesity. Multiple independent and interrelated mechanisms have been found to be involved in such linking processes which are discussed in this review work along with some possible remedial measures for prevention of weight gain and obesity. | Chandra Kanti Chakraborti | 2015 | World Journal of Gastrointestinal Pathophysiology2015，6，4： | 22 |
| 7 | Intestinal microbiota: The explosive mixture at the origin of inflammatory bowel disease?显示文摘Inflammatory bowel diseases(IBDs), namely Crohn's disease and ulcerative colitis, are lifelong chronic disorders arising from interactions among genetic, immunological and environmental factors. Although the origin of IBDs is closely linked to immune response alterations, which governs most medical decision-making, recent findings suggest that gut microbiota may be involved in IBD pathogenesis. Epidemiologic evidence and several studies have shown that a dysregulation of gut microbiota(i.e., dysbiosis) may trigger the onset of intestinal disorders such as IBDs. Animal and human investigations focusing on the microbiota-IBD relationship have suggested an altered balance of the intestinal microbial population in the active phase of IBD. Rigorous microbiota typing could, therefore, soon become part of a complete phenotypic analysis of IBD patients. Moreover, individual susceptibility and environmental triggers such as nutrition, medications, age or smoking could modify bacterial strains in the bowel habitat. Pharmacological manipulation of bowel microbiota is somewhat controversial. The employment of antibiotics, probiotics, prebiotics and synbiotics has been widely addressed in theliterature worldwide, with the aim of obtaining positive results in a number of IBD patient settings, and determining the appropriate timing and modality of this intervention. Recently, novel treatments for IBDs, such as fecal microbiota transplantation, when accepted by patients, have shown promising results. Controlled studies are being designed. In the near future, new therapeutic strategies can be expected, with non-pathogenic or modified food organisms that can be genetically modified to exert anti-inflammatory properties. | Roberto Bringiotti Enzo Ierardi Rosa Lovero Giuseppe Losurdo Alfredo Di Leo Mariabeatrice Principi | 2014 | World Journal of Gastrointestinal Pathophysiology2014，5，4： | 20 |
| 8 | Early phase of acute pancreatitis: Assessment and management显示文摘Acute pancreatitis(AP) is a potentially life-threatening disease with a wide spectrum of severity. The overall mortality of AP is approximately 5%. According to the revised Atlanta classification system, AP can be classified as mild, moderate, or severe. Severe AP often takes a clinical course with two phases, an early and a late phase, which should both be considered separately. In this review article, we first discuss general aspects of AP, including incidence, pathophysiology, etiology, and grading of severity, then focus on the assessment of patients with suspected AP, including diagnosis and risk stratification, followed by the management of AP during the early phase, with special emphasis on fluid therapy, pain management, nutrition, and antibiotic prophylaxis. | Veit Phillip Jrg M Steiner Hana Algül | 2014 | World Journal of Gastrointestinal Pathophysiology2014，5，3： | 19 |
| 9 | Escherichia coli in chronic inflammatory bowel diseases: An update on adherent invasive Escherichia coli pathogenicity显示文摘Escherichia coli(E. coli), and particularly the adherent invasive E. coli(AIEC) pathotype, has been increasingly implicated in the ethiopathogenesis of Crohn's disease(CD). E. coli strains with similar pathogenic features to AIEC have been associated with other intestinal disorders such as ulcerative colitis, colorectal cancer, and coeliac disease, but AIEC prevalence in these diseases remains largely unexplored. Since AIEC was described one decade ago, substantial progress has been made in deciphering its mechanisms of pathogenicity. However, the molecular bases that characterize the phenotypic properties of this pathotype are still not well resolved. A review of studies focused on E. coli populations in inflammatory bowel disease(IBD) is presented here and we discuss about the putative role of this species on each IBD subtype. Given the relevance of AIEC in CD pathogenesis, we present the latest research findings concerning AIEC host-microbe interactions and pathogenicity. We also review the existing data regarding the prevalence and abundance of AIEC in CD and its association with other intestinal diseases from humans and animals, in order to discuss the AIEC disease- and hostspecificity. Finally, we highlight the fact that dietarycomponents frequently found in industrialized countries may enhance AIEC colonization in the gut, which merits further investigation and the implementation of preventative measures. | Margarita Martinez-Medina Librado Jesus Garcia-Gil | 2014 | World Journal of Gastrointestinal Pathophysiology2014，5，3： | 19 |
| 10 | 为表面的食道的有鳞的房间瘤的内视镜的 submucosal 解剖显示文摘 Endoscopic resection is an effective treatment for noninvasive esophageal squamous cell neoplasms(ESCNs).Endoscopic mucosal resection(EMR)has been developed for small localized ESCNs as an alternative to surgical therapy because it shows similar effectiveness and is less invasive than esophagectomy.However,EMR is limited in resection size and therefore piecemeal resection is performed for large lesions,resulting in an imprecise histological evaluation and a high frequency of local recurrence.Endoscopic submucosal dissection(ESD)has been developed in Japan as one of the standard endoscopic resection techniques for ESCNs.ESD enables esophageal lesions,regardless of their size,to be removed en bloc and thus has a lower local recurrence rate than EMR.The development of new devices and the establishment of optimal strategies for esophageal ESD have resulted in fewer complications such as perforation than expected.However,esophageal stricture after ESD may occur when the resected area is larger than three-quarters of the esophageal lumen or particularly when it encompasses the entire circumference;such a stricture requires multiple sessions of endoscopic balloon dilatation.Recently,oral prednisolone has been reported to be useful in preventing post-ESD stricture.In addition,a combination of chemoradiotherapy(CRT)and ESD might be an alternative therapy for submucosal esophageal cancer that has a risk of lymph node metastasis because esophagectomy is extremely invasive;CRT has a higher local recurrence rate than esophagectomy but is less invasive.ESD is likely to play a central role in the treatment of superficial esophageal squamous cell neoplasms in the future. | Kuniomi Honda Hirotada Akiho | 2012 | World Journal of Gastrointestinal Pathophysiology2012，3，2： | 18 |
| 11 | Treatment strategy for gastric non-invasive intraepithelial neoplasia diagnosed by endoscopic biopsy显示文摘Treatment strategies,whether as follow-up or'total incisional biopsy'for gastric noninvasive intraepithelial neoplasia diagnosed by examination of an endoscopic forceps biopsy specimen,are controversial due to problems associated with the diagnostic accuracy of endoscopic forceps biopsy and questions about the safety and efficacy of endoscopic treatment.Based on the histological findings of the biopsy specimen,it is difficult to differentiate between reactive or regenerative changes,inflammation and neoplastic changes,intraepithelial and invasive tumors.Therefore,gastric neoplasia diagnosed as noninvasive intraepithelial often develop into invasive carcinoma during follow-up.Recent advances in endoscopic modalities and treatment devices,such as image-enhanced endoscopy and highfrequency generators,may make endoscopic treatment,such as endoscopic submucosal dissection(ESD),a therapeutic option for gastric intraepithelial neoplasia,including low-grade neoplasms.Future studies are required to evaluate whether ESD is a valid strategy for gastric intraepithelial neoplasm with regard to safety and cost effectiveness. | Tsutomu Nishida Shusaku Tsutsui Motohiko Kato Takuya Inoue Shunsuke Yamamoto Yoshito Hayashi Tomofumi Akasaka Takuya Yamada Shinichiro Shinzaki Hideki Iijima Masahiko Tsujii Tetsuo Takehara | 2011 | World Journal of Gastrointestinal Pathophysiology2011，2，6： | 18 |
| 12 | 肠的上皮的障碍的主人微生物引起的相互作用和规定工作: 从生理学到病理显示文摘 The gastrointestinal tract is the largest reservoir of commensal bacteria in the human body, providing nutrients and space for the survival of microbes while concurrently operating mucosal barriers to confine the microbial population. The epithelial cells linked by tight junctions not only physically separate the microbiota from the lamina propria, but also secrete proinflammatory cytokines and reactive oxygen species in response to pathogen invasion and metabolic stress and serve as a sentinel to the underlying immune cells. Accumulating evidence indicates that commensal bacteria are involved in various physiological functions in the gut and microbial imbalances (dysbiosis) may cause pathology. Commensal bacteria are involved in the regulation of intestinal epithelial cell turnover, promotion of epithelial restitution and reorganization of tight junctions, all of which are pivotal for fortifying barrier function. Recent studies indicate that aberrant bacterial lipopolysaccharide-mediated signaling in gut mucosa may be involved in the pathogenesis of chronic inflammation and carcinogenesis. Our perception of enteric commensals has now changed from one of opportunistic pathogens to active participants in maintaining intestinal homeostasis. This review attempts to explain the dynamic interaction between the intestinal epithelium and commensal bacteria in disease and health status. | Linda Chia-Hui Yu Jin-Town Wang Yen-Hsuan Ni | 2012 | World Journal of Gastrointestinal Pathophysiology2012，3，1： | 17 |
| 13 | Update on pathogenesis and clinical management of acute pancreatitis显示文摘Acute pancreatitis (AP), defined as the acute nonbacterial inflammatory condition of the pancreas, is derived from the early activation of digestive enzymes found inside the acinar cells, with variable compromise of the gland itself, nearby tissues and other organs. So, it is an event that begins with pancreatic injury, elicits an acute inflammatory response, encompasses a variety of complications and generally resolves over time. Different conditions are known to induce this disorder, although the innermost mechanisms and how they act to develop the disease are still unknown. We summarize some well established aspects. A phase sequence has been proposed: etiology factors generate other conditions inside acinar cells that favor the AP development with some systemic events; genetic factors could be involved as susceptibility and modifying elements. AP is a disease with extremely different clinical expressions. Most patients suffer a mild and limited disease, but about one fifth of cases develop multi organ failure, accompanied by high mortality. This great variability in presentation, clinical course and complications has given rise to the confusion related to AP related terminology. However, consensus meetings have provided uniform definitions, including the severity of the illness. The clinical management is mainly based on the disease′s severity and must be directed to correct the underlying predisposing factors and control the inflammatory process itself. The first step is to determine if it is mild or severe. We review the principal aspects to be considered in this treatment, as reflected in several clinical practice guidelines. For the last 25 years, there has been a global increase in incidence of AP, along with many advances in diagnosis and treatment. However, progress in knowledge of its pathogenesis is scarce. | Dulce M Cruz-Santamaría Carlos Taxonera Manuel Giner | 2012 | World Journal of Gastrointestinal Pathophysiology2012，3，3： | 16 |
| 14 | Risk factors for osteoporosis in inflammatory bowel disease patients显示文摘Inflammatory bowel disease(IBD) patients exhibit higher risk for bone loss than the general population. The chronic inflammation causes a reduction in bone mineral density(BMD), which leads to osteopenia and osteoporosis. This article reviewed each risk factor for osteoporosis in IBD patients. Inflammation is one of the factors that contribute to osteoporosis in IBD patients, and the main system that is involved in bone loss is likely RANK/RANKL/osteoprotegerin. Smoking is a risk factor for bone loss and fractures, and many mechanisms have been proposed to explain this loss. Body composition also interferes in bone metabolism and increasing muscle mass may positively affect BMD. IBD patients frequently use corticosteroids, which stimulates osteoclastogenesis. IBD patients are also associated with vitamin D deficiency, which contributes to bone loss. However, infliximab therapy is associated with improvements in bone metabolism, but it is not clear whether the effects are because of inflammation improvement or infliximab use. Ulcerative colitis patients with proctocolectomy and ileal pouches and Crohn's disease patients with ostomy are also at risk for bone loss, and these patients should be closely monitored. | Carla Andrade Lima Andre Castro Lyra Raquel Rocha Genoile Oliveira Santana | 2015 | World Journal of Gastrointestinal Pathophysiology2015，6，4： | 15 |
| 15 | 胰腺的癌症诊断由免费并且 exosomal miRNA显示文摘 Patients with pancreatic adenocarcinoma(PaCa) have a dismal prognosis. This is in part due to late diagnosis prohibiting surgical intervention, which provides the only curative option as PaCa are mostly chemo- and radiation resistance. Hope is raised on a reliable noninvasive/minimally invasive diagnosis that is still missing. Recently two diagnostic options are discussed, serum MicroRNA(miRNA) and serum exosomes. Serum miRNA can be free or vesicle-, particularly, exosomesenclosed. This review will provide an overview on the current state of the diagnostic trials on free serum miRNA and proceed with an introduction of exosomes that use as a diagnostic tool in serum and other body fluids has not received sufficient attention, although serum exosome miRNA in combination with protein marker expression likely will increase the diagnostic and prognostic power. By their crosstalk with host cells, which includes binding-initiated signal transduction, as well as reprogramming target cells via the transfer of proteins, mRNA and miRNA exosomes are suggested to become a most powerful therapeutics. I will discuss which hurdles have still to be taken as well as the different modalities, which can be envisaged to make therapeutic use of exosomes. PaCa are known to most intensely crosstalk with the host as apparent by desmoplasia and frequent paraneoplastic syndromes. Thus, there is hope that the therapeutic application of exosomes brings about a major breakthrough. | Margot Zller | 2013 | World Journal of Gastrointestinal Pathophysiology2013，4，4： | 15 |
| 16 | Genetic update on inflammatory factors in ulcerative colitis: Review of the current literature显示文摘Ulcerative colitis(UC) is one of the main types of inflammatory bowel disease, which is caused by dysregulated immune responses in genetically predisposed individuals. Several genetic factors, including interleukin and interleukin receptor gene polymorphisms and other inflammation-related genes play central role in mediating and modulating the inflammation in the human body, thereby these can be the main cause of development of the disease. It is clear these data are very important for understanding the base of the disease, especially in terms of clinical utility and validity, but summarized literature is exiguous for challenge health specialist that can used in the clinical practice nowadays. This review summarizes the current literature on inflammationrelated genetic polymorphisms which are associated with UC. We performed an electronic search of Pubmed Database among publications of the last 10 years, using the following medical subject heading terms: UC, ulcerative colitis, inflammation, genes, polymorphisms, and susceptibility. | Patricia Sarlos Erzsebet Kovesdi Lili Magyari Zsolt Banfai Andras Szabo Andras Javorhazy Bela Melegh | 2014 | World Journal of Gastrointestinal Pathophysiology2014，5，3： | 15 |
| 17 | Intra-abdominal pressure:Time ripe to revise managementguidelines of acute pancreatitis?显示文摘AIM: To systematically review evidence on pathophysiology of intra-abdominal pressure(IAP) in acute pancreatitis(AP) with its clinical correlates. METHODS: Systematic review of available evidence in English literature with relevant medical subject heading terms on Pub Med, Medline and Scopus with further search from open access sources on internet as suggested by articles retrieved. RESULTS: Intra-abdominal hypertension(IAH) is increasingly gaining recognition as a point of specific intervention with potential to alter disease outcome and improve mortality in AP. IAH can be expected in at least 17% of patients presenting with diagnosis of AP to a typical tertiary care hospital(prevalence increasing to 50% in those with severe disease). Abdominal compartment syndrome can be expected in at least 15% patients with severe disease. Recent guidelines on management of AP do not acknowledge utility of surveillance for IAP other than those by Japanese Society of Hepato-BiliaryPancreatic Surgery. We further outline pathophysiologic mechanisms of IAH; understanding of which advances our knowledge and helps to coherently align common observed variations in management related conundrums(such as fluid therapy, nutrition and antibiotic prophylaxis) with potential to further individualize treatment in AP. CONCLUSION: We suggest that IAP be given its due place in future practice guidelines and that recommendations be formed with help of a broader panel with inclusion of clinicians experienced in management of IAH. | jiten jaipuria vimal bhandari avneet singh chawla mohit singh | 2016 | World Journal of Gastrointestinal Pathophysiology2016，7，1： | 14 |
| 18 | Laboratory markers in ulcerative colitis: Current insights and future advances显示文摘Ulcerative colitis(UC)and Crohn’s disease(CD)are the major forms of inflammatory bowel diseases(IBD)in man.Despite some common features,these forms can be distinguished by different genetic predisposition,risk factors and clinical,endoscopic and histological characteristics.The aetiology of both CD and UC remains unknown,but several evidences suggest that CD and perhaps UC are due to an excessive immuneresponse directed against normal constituents of the intestinal bacterial flora.Tests sometimes invasive are routine for the diagnosis and care of patients with IBD.Diagnosis of UC is based on clinical symptoms combined with radiological and endoscopic investigations.The employment of non-invasive biomarkers is needed.These biomarkers have the potential to avoid invasive diagnostic tests that may result in discomfort and potential complications.The ability to determine the type,severity,prognosis and response to therapy of UC,using biomarkers has long been a goal of clinical researchers.We describe the biomarkers assessed in UC,with special reference to acute-phase proteins and serologic markers and thereafter,we describe the new biological markers and the biological markers could be developed in the future:(1)serum markers of acute phase response:The laboratory tests most used to measure the acute-phase proteins in clinical practice are the serum concentration of C-reactive protein and the erythrocyte sedimentation rate.Other biomarkers of inflammation in UC include platelet count,leukocyte count,and serum albumin and serum orosomucoid concentrations;(2)serologic markers/antibodies:In the last decades serological and immunologic biomarkers have been studied extensively in immunology and have been used in clinical practice to detect specific pathologies.In UC,the presence of these antibodies can aid as surrogate markers for the aberrant host immune response;and(3)future biomarkers:The development of biomarkers in UC will be very important in the future.The progress of molecular biology tools(microarrays,proteomics and nanotechnology)have revolutionised the field of the biomarker discovery.The advances in bioinformatics coupled with cross-disciplinary collaborations have greatly enhanced our ability to retrieve,characterize and analyse large amounts of data generated by the technological advances.The techniques available for biomarkers development are genomics(single nucleotide polymorphism genotyping,pharmacogenetics and gene expression analyses)and proteomics.In the future,the additionof new serological markers will add significant benefit.Correlating serologic markers with genotypes and clinical phenotypes should enhance our understanding of pathophysiology of UC. | Michele Cioffi Antonella De Rosa Rosalba Serao Ilaria Picone Maria Teresa Vietri | 2015 | World Journal of Gastrointestinal Pathophysiology2015，6，1： | 14 |
| 19 | Role of Sonic Hedgehog signaling during progression from inflammation to cancer in the stomach显示文摘Despite advances in treatment and the declining incidence,gastric cancer remains the second leading cause of cancer-related deaths in the world.Understanding the progression from inflammation to cancer in the stomach is crucial in the development of novel therapies and strategies for treating this disease.Chronic inflammation of the stomach is typically caused by Helicobacter pylori(H.pylori)and resulting lesions may lead to gastric cancer.During the progression from inflammation to cancer,the stomach epithelium changes with evidence of the disruption of normal epithelial cell differentiation and infiltrating inflammatory cells.Coincident with the development of atrophic gastritis and metaplasia,is the loss of the gastric morphogen Sonic Hedgehog(Shh).Given its critical role as a regulator of gastric tissue homeostasis,the disruption of Shh expression during inflammation correlates with the loss of normal epithelial cell differentiation,but this has only recently been rigorously tested in vivo using a unique mouse model of targeted gastric Shh deletion.While pre-neoplastic lesions such as atrophic gastritis and in-testinal metaplasia are associated with the loss of Shh within the acid-secreting glands of the stomach,there is a clear link between elevated Shh and signaling to gastric cancers.The current review focuses on the effects of aberrant Shh expression and its role in the development of gastric cancer,specifically in response to H.pylori infection. | Alexander E Sherman Yana Zavros | 2011 | World Journal of Gastrointestinal Pathophysiology2011，2，6： | 14 |
| 20 | Quality of healing of gastric ulcers: Natural products beyond acid suppression显示文摘Gastric ulcer is a chronic disease featured with unexpected complications, including bleeding, stenosis and perforation, as well as a high incidence of recurrence. Clinical treatments for gastric ulcer have allowed the rapid development of potent anti-ulcer drugs during the last several decades. Gastric ulcer healing is successful with conventional treatments including H2-receptor antagonists, and proton pump inhibitors(PPIs) have been essential for ulcer healing and prevention of complications. Additionally, Helicobacter pylori eradication therapy is effective in reducing ulcer recurrence and leads to physiological changes in the gastric mucosa which affect the ulcer healing process. However, in spite of these advancements, some patients have suf-fered from recurrence or intractability in spite of continuous anti-ulcer therapy. A new concept of the quality of ulcer healing(QOUH) was initiated that considers the reconstruction of the mucosal structure and its function for preventing ulcer recurrence. Although several gastroprotection provided these achievements of the QOUH, which PPI or other acid suppressants did not accomplish, we found that gastroprotection that originated from natural products, such as a newer formulation from either Artemisia or S-allyl cysteine from garlic, were very effective in the QOUH, as well as improving clinical symptoms with fewer side effects. In this review, we will introduce the importance of the QOUH in ulcer healing and the achievements from natural products. | Napapan Kangwan Jong-Min Park Eun-Hee Kim Ki Baik Hahm | 2014 | World Journal of Gastrointestinal Pathophysiology2014，5，1： | 14 |
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