World Journal of Gastrointestinal Pathophysiology最新文献

Aim: To assess whether higher sensitivity of colonic epithelium to hypoxia at the serosal side is associated with oxygen transfer asymmetry.

Methods: Rats were fed either with normal chow or a low-sodium diet. Tissues were mounted as flat sheets in a modified, airtight Ussing chamber with oxygen meters in each hemichamber. Mucosal samples from normal diet animals were studied under control conditions, in low-chloride solution and after adding chloride secretion inhibitors and chloride secretagogues. Samples from sodium-deprived rats were studied before and after ouabain addition. In separate experiments, the correlation between short-circuit current and oxygen consumption was analyzed. Finally, hypoxia was induced in one hemichamber to assess the relationship between its oxygen content and the oxygen pressure difference between both hemichambers.

Results: In all studied conditions, oxygen consumption was larger in the serosal hemichamber than in the mucosal one (P = 0.0025 to P < 0.0001). Short-circuit current showed significant correlation with both total oxygen consumption (r = 0.765; P = 0.009) in normoxia and oxygen consumption in the serosal hemichamber (r = 0.754; P = 0.011) during mucosal hypoxia, but not with oxygen consumption in the mucosal hemichamber. When hypoxia was induced in the mucosal hemichamber, an oxygen pressure difference of 13 kPa with the serosal hemichamber was enough to keep its oxygen content constant. However, when hypoxia was induced in the serosal hemichamber, the oxygen pressure difference with the mucosal hemichamber necessary to keep its oxygen content constant was 40 kPa (P < 0.0001).

Conclusion: Serosal oxygen supply is more readily available to support short-circuit current. This may be partly due to a rectifying behavior of transepithelial oxygen transfer.

Gastrointestinal involvement in plasma cell neoplasms, either as primary localizations (extramedullary plasmacytomas) or as secondary involvement in systemic multiple myeloma, is a well-known event. Accurate histological examination is crucial in defining the diagnosis. In this report, an uncommon case of duodenal localization of myeloma with plasmablastic features is described, with emphasis on the role of clinical data and findings from ancillary immunostaining techniques to avoid misdiagnosis.

Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease associated with insulin resistance and metabolic syndrome. The spectrum of disease ranges from simple steatosis to steatohepatitis and progression to cirrhosis. Compelling evidence over the past several years has substantiated a significant link between NAFLD and cardiovascular disease ranging from coronary artery disease to subclinical carotid atherosclerosis. Close follow up, treatment of risk factors for NAFLD, and cardiovascular risk stratification are necessary to predict morbidity and mortality in this subset of patients.

Portal hypertension in the rat by triple partial portal vein ligation produces an array of splanchnic and systemic disorders, including hepatic steatosis. In the current review these alterations are considered components of a systemic inflammatory response that would develop through three overlapping phenotypes: The neurogenic, the immune and the endocrine. These three inflammatory phenotypes could resemble the functions expressed during embryonic development of mammals. In turn, the inflammatory phenotypes would be represented in the embryo by two functional axes, that is, a coelomic-amniotic axis and a trophoblastic yolk-sac or vitelline axis. In this sense, the inflammatory response developed after triple partial portal vein ligation in the rat would integrate both functional embryonic axes on the liver interstitial space of Disse. If so, this fact would favor the successive development of steatosis, steatohepatitis and fibrosis. Firstly, these recapitulated embryonic functions would produce the evolution of liver steatosis. In this way, this fat liver could represent a yolk-sac-like in portal hypertensive rats. After that, the systemic recapitulation of these embryonic functions in experimental prehepatic portal hypertension would consequently induce a gastrulation-like response in which a hepatic wound healing reaction or fibrosis occur. In conclusion, studying the mechanisms involved in embryonic development could provide key results for a better understanding of the nonalcoholic fatty liver disease etiopathogeny.

Chronic granulomatous disease (CGD) is a primary immune deficiency that is commonly diagnosed under the age of 5 years (95%) and is rarely seen in adulthood. CGD may manifest as inflammatory bowel disease (IBD) in childhood. Without proper diagnosis, these patients may be monitored for years as IBD; some may even be regarded as steroid-resistant ulcerative colitis (UC) and end up having a colectomy. In this case report, we described a patient who had been followed-up for years as UC and subsequently underwent colectomy, but was finally diagnosed in adulthood as primary immune deficiency.

Celiac disease, also known as "celiac sprue", is a chronic inflammatory disorder of the small intestine, produced by the ingestion of dietary gluten products in susceptible people. It is a multifactorial disease, including genetic and environmental factors. Environmental trigger is represented by gluten while the genetic predisposition has been identified in the major histocompatibility complex region. Celiac disease is not a rare disorder like previously thought, with a global prevalence around 1%. The reason of its under-recognition is mainly referable to the fact that about half of affected people do not have the classic gastrointestinal symptoms, but they present nonspecific manifestations of nutritional deficiency or have no symptoms at all. Here we review the most recent data concerning epidemiology, pathogenesis, clinical presentation, available diagnostic tests and therapeutic management of celiac disease.

Aim: To identify the prevalence, and clinical and pathologic characteristic of colonic polyps among Iranian patients undergoing a comprehensive colonoscopy, and determine the polyp detection rate (PDR) and adenoma detection rate (ADR).

Methods: In this cross-sectional study, demographics and epidemiologic characteristics of 531 persons who underwent colonoscopies between 2014 and 2015 at Mehrad gastrointestinal clinic were determined. Demographics, indication for colonoscopy, colonoscopy findings, number of polyps, and histopathological characteristics of the polyps were examined for each person.

Results: Our sample included 295 (55.6%) women and 236 (44.4%) men, with a mean age of 50.25 ± 14.89 years. Overall PDR was 23.5% (125/531). ADR and colorectal cancer detection rate in this study were 12.8% and 1.5%, respectively. Polyps were detected more significantly frequently in men than in women (52.8% vs 47.2%, P < 0.05). Polyps can be seen in most patients after the age of 50. The average age of patients with cancer was significantly higher than that of patients with polyps (61.3 years vs 56.4 years, P < 0.05). The majority of the polyps were adenomatous. More than 50% of the polyps were found in the rectosigmoid part of the colon.

Conclusion: The prevalence of polyps and adenomas in this study is less than that reported in the Western populations. In our patients, distal colon is more susceptible to developing polyps and cancer than proximal colon.

Recent study shows that germ-free and antibiotic-treated animals are highly susceptible to gut epithelial injury. This paper addresses that impaired inactivation of digestive proteases may be the key factor for the increased susceptibility.

Fibrosis represents a major challenge in Crohn's disease (CD), and many CD patients will develop fibrotic strictures requiring treatment throughout their lifetime. There is no drug that can reverse intestinal fibrosis, and so endoscopic balloon dilatation and surgery are the only effective treatments. Since patients may need repeated treatments, it is important to obtain the diagnosis at an early stage before strictures become symptomatic with extensive fibrosis. Several markers of fibrosis have been proposed, but most need further validation. Biomarkers can be measured either in biological samples obtained from the serum or bowel of CD patients, or using imaging tools and tests. The ideal tool should be easily obtained, cost-effective, and reliable. Even more challenging is fibrosis occurring in ulcerative colitis. Despite the important burden of intestinal fibrosis, including its detrimental effect on outcomes and quality of life in CD patients, it has received less attention than fibrosis occurring in other organs. A common mechanism that acts via a specific signaling pathway could underlie both intestinal fibrosis and cancer. A comprehensive overview of recently introduced biomarkers of fibrosis in CD is presented, along with a discussion of the controversial areas remaining in this field.