Intestinal Permeability

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Robin C Spiller - One of the best experts on this subject based on the ideXlab platform.

Jon Meddings - One of the best experts on this subject based on the ideXlab platform.

  • increased Intestinal Permeability is associated with later development of crohn s disease
    Gastroenterology, 2020
    Co-Authors: Jon Meddings, Williams Turpin, Sunho Lee, Juan Antonio Raygoza Garay, Karen L Madsen, Larbi Bedrani, Namita Power
    Abstract:

    Background & Aims Increased Intestinal Permeability has been associated with Crohn’s disease (CD), but it is not clear whether it is a cause or result of the disease. We performed a prospective study to determine whether increased Intestinal Permeability is associated with future development of CD. Methods We assessed the Intestinal Permeability, measured by the urinary fractional excretion of lactulose-to-mannitol ratio (LMR) at recruitment in 1420 asymptomatic first-degree relatives (6–35 years old) of patients with CD (collected from 2008 through 2015). Participants were then followed up for a diagnosis of CD from 2008 to 2017, with a median follow-up time of 7.8 years. We analyzed data from 50 participants who developed CD after a median of 2.7 years during the study period, along with 1370 individuals who remained asymptomatic until October 2017. We used the Cox proportional hazards model to evaluate time-related risk of CD based on the baseline LMR. Results An abnormal LMR (>0.03) was associated with a diagnosis of CD during the follow-up period (hazard ratio, 3.03; 95% CI, 1.64–5.63; P = 3.97 × 10–4). This association remained significant even when the test was performed more than 3 years before the diagnosis of CD (hazard ratio, 1.62; 95% CI, 1.051–2.50; P = .029). Conclusions Increased Intestinal Permeability is associated with later development of CD; these findings support a model in which altered Intestinal barrier function contributes to pathogenesis. Abnormal gut barrier function might serve as a biomarker for risk of CD onset.

  • Intestinal Permeability in children with food allergy on specific elimination diets
    Applied Immunohistochemistry & Molecular Morphology, 2013
    Co-Authors: Jon Meddings, Kirsi M Jarvinen, George N Konstantinou, Mariecel Pilapil, Marieclaire Arrieta, Sally Noone, Hugh A Sampson, Anna Nowakwegrzyn
    Abstract:

    BACKGROUND Children with food allergy have been shown to have increased small Intestinal Permeability (IP) following ingestion of the offending food as well as during elimination diets. We investigated IP in asymptomatic food-allergic children during an elimination diet to identify clinical characteristics associated with altered IP.

  • reducing small Intestinal Permeability attenuates colitis in the il10 gene deficient mouse
    Gut, 2009
    Co-Authors: Marieclaire Arrieta, Karen Madsen, Jason Doyle, Jon Meddings
    Abstract:

    Background: Defects in the small Intestinal epithelial barrier have been associated with inflammatory bowel disease but their role in the causation of disease is still a matter of debate. In some models of disease increased Permeability appears to be a very early event. The interleukin 10 (IL10) gene-deficient mouse spontaneously develops colitis after 12 weeks of age. These mice have been shown to have increased small Intestinal Permeability that appears early in life. Furthermore, the development of colitis is dependent upon luminal agents, as animals do not develop disease if raised under germ-free conditions. Aims: To determine if the elevated small bowel Permeability can be prevented, and if by doing so colonic disease is prevented or attenuated. Methods: IL10 gene-deficient (IL10 − / − ) mice) were treated with AT-1001 (a zonulin peptide inhibitor), a small peptide previously demonstrated to reduce small Intestinal Permeability. Small Intestinal Permeability was measured, in vivo, weekly from 4 to 17 weeks of age. Colonic disease was assessed at 8 weeks in Ussing chambers, and at 17 weeks of age inflammatory cytokines and myeloperoxidase were measured in the colon. Colonic Permeability and histology were also endpoints. Results: Treated animals showed a marked reduction in small Intestinal Permeability. Average area under the lactulose/mannitol time curve: 5.36 (SE 0.08) in controls vs 3.97 (SE 0.07) in the high-dose AT-1001 group, p Conclusions: This work suggests that increased Intestinal Permeability may be an important aetiological event in the development of colitis in IL10 − / − mice.

  • Intestinal Permeability in patients with irritable bowel syndrome after a waterborne outbreak of acute gastroenteritis in walkerton ontario
    Alimentary Pharmacology & Therapeutics, 2004
    Co-Authors: John K Marshall, Jon Meddings, Marroon Thabane, Amit X Garg, William F Clark, Stephen M Collins
    Abstract:

    Summary Background : Post-infectious irritable bowel syndrome is a common clinical phenomenon of uncertain aetiology. Aim : To test the association between Intestinal Permeability and irritable bowel syndrome symptoms 2 years after a large waterborne outbreak of bacterial gastroenteritis. Methods : Consecutive adults with Rome I irritable bowel syndrome and controls without irritable bowel syndrome attending a community clinic were enrolled. Intestinal Permeability was measured as the ratio of fractional urinary excretions of lactulose and mannitol, and compared among cases vs. controls and predictors of abnormal Intestinal Permeability were assessed. Results : A total of 218 subjects (132 irritable bowel syndrome cases and 86 non-irritable bowel syndrome controls) completed the study protocol. About 27 (12%) had been diagnosed with the irritable bowel syndrome before the outbreak and 115 (53%) had been ill during the outbreak. Lactulose–mannitol ratios were increased among cases vs. controls (Mann–Whitney mean rank 118.8 vs. 95.3, P = 0.007), and cases were more likely to have a ratio >0.020 (P = 0.007). Among cases, those with increased Intestinal Permeability were more likely to report increased stool frequency. Both irritable bowel syndrome symptoms and male gender, but not diarrhoeal illness during the outbreak, were significant predictors of abnormal Permeability. Conclusions : Irritable bowel syndrome symptoms are associated with a subtle increase in Intestinal Permeability irrespective of prior gastroenteritis. This may improve understanding of the aetiology of both sporadic and post-infectious irritable bowel syndrome.

  • Intestinal Permeability and postheparin plasma diamine oxidase activity in the prediction of crohn s disease relapse
    Inflammatory Bowel Diseases, 1999
    Co-Authors: Robert J Hilsden, Jon Meddings, James A Hardin, Grant D Gall, Lloyd R Sutherland
    Abstract:

    A method of detecting presymptomatic relapse of Crohn's disease could allow for the selective use of maintenance or intensified medical therapy in those with an increased risk of relapse. The aim of this study was to evaluate three potential laboratory markers of relapse: Intestinal and gastroduodenal Permeability and plasma diamine oxidase activity. Intestinal Permeability (lactulose/mannitol test), gastroduodenal Permeability (urinary sucrose excretion), and postheparin plasma diamine oxidase activity were serially measured in 61 adults with Crohn's disease in remission (CDAI 150 and increased by at least 100 points or the need for steroids or surgery). Fourteen patients (23%) relapsed. A cut-off of 0.030 for the lactulose/mannitol ratio was defined. Those with ratios above the cutoff had a 7.0 times greater risk of relapse (p < 0.001). Three subjects who went from a normal ratio to an abnormal ratio relapsed, whereas none of 32 subjects with a repeatedly normal ratio relapsed. Sucrose excretion and plasma diamine oxidase activity did not predict relapse. Serial testing of Intestinal Permeability, but not of gastroduodenal Permeability or plasma diamine oxidase activity, was useful in predicting relapse in asymptomatic patients.

Adrian G Cummins - One of the best experts on this subject based on the ideXlab platform.

  • improvement in Intestinal Permeability precedes morphometric recovery of the small intestine in coeliac disease
    Clinical Science, 2001
    Co-Authors: Adrian G Cummins, Fiona M Thompson, Ross N Butler, John Cassidy, David Gillis, Mark Lorenzetti, Emma Southcott, Peter Wilson
    Abstract:

    It is often difficult to assess small bowel recovery in adults with coeliac disease on a gluten-free diet (GFD). This prospective study compares changes in Intestinal Permeability with changes in Intestinal biopsy at various intervals after commencing a GFD. Intestinal Permeability was measured by lactulose/rhamnose absorption from 1 week to 24 months after commencing a GFD. Intestinal morphometry was measured by villus area, crypt length and mitotic count per crypt at diagnosis and after commencing a GFD. Median Intestinal Permeability values decreased from 0.47 (n = 35) at diagnosis to 0.25 (n = 17) after 1 week and to 0.16 (n = 18) after 2 months of a GFD. Rhamnose absorption improved significantly at an early stage, from 6.6% (untreated) to 15.4% at 3 months of a GFD, whereas the decrease in lactulose permeation took longer: from 3.4% (untreated) to 0.8% after 12 months of a GFD. Mean villus area (n = 29) was reduced to 16% of control values at diagnosis, and improved to a maximum of 48% after 6 months on a GFD, but did not change thereafter. Mean crypt length and mitotic count per crypt were increased by 222% and 356% respectively at diagnosis, and these parameters remained elevated at 172% and 216% above control values after 6 months of a GFD. We conclude that Intestinal Permeability improves within 2 months after starting a GFD, but that measurable Intestinal biopsy improvement requires ingestion of a GFD for at least 3-6 months, and even then remains incomplete.

  • the role of small Intestinal bacterial overgrowth Intestinal Permeability endotoxaemia and tumour necrosis factor α in the pathogenesis of non alcoholic steatohepatitis
    Gut, 2001
    Co-Authors: Alan J Wigg, Ian C Robertsthomson, R B Dymock, P J Mccarthy, R H Grose, Adrian G Cummins
    Abstract:

    BACKGROUND Small Intestinal bacterial overgrowth may contribute to the development of non-alcoholic steatohepatitis, perhaps by increasing Intestinal Permeability and promoting the absorption of endotoxin or other enteric bacterial products. AIMS To investigate the prevalence of small Intestinal bacterial overgrowth, increased Intestinal Permeability, elevated endotoxin, and tumour necrosis factor α (TNF-α) levels in patients with non-alcoholic steatohepatitis and in control subjects. PATIENTS AND METHODS Twenty two patients with non-alcoholic steatohepatitis and 23 control subjects were studied. Small Intestinal bacterial overgrowth was assessed by a combined 14 C-d-xylose and lactulose breath test. Intestinal Permeability was assessed by a dual lactulose-rhamnose sugar test. Serum endotoxin levels were determined using the limulus amoebocyte lysate assay and TNF-α levels using an ELISA. RESULTS Small Intestinal bacterial overgrowth was present in 50% of patients with non-alcoholic steatosis and 22% of control subjects (p=0.048). Mean TNF-α levels in non-alcoholic steatohepatitis patients and control subjects were 14.2 and 7.5 pg/ml, respectively (p=0.001). Intestinal Permeability and serum endotoxin levels were similar in the two groups. CONCLUSIONS Patients with non-alcoholic steatohepatitis have a higher prevalence of small Intestinal bacterial overgrowth, as assessed by the 14 C-d-xylose-lactulose breath test, and higher TNF-α levels in comparison with control subjects. This is not accompanied by increased Intestinal Permeability or elevated endotoxin levels.

Germano Perotti - One of the best experts on this subject based on the ideXlab platform.

  • Intestinal Permeability in cirrhotic patients with and without spontaneous bacterial peritonitis is the ring closed
    The American Journal of Gastroenterology, 2010
    Co-Authors: Emidio Scarpellini, Venanzio Valenza, Maurizio Gabrielli, Ernesto Cristiano Lauritano, Germano Perotti, G Merra, Antonio Dal Lago, Veronica Ojetti, Maria Elena Ainora, Michele Santoro
    Abstract:

    Intestinal Permeability in Cirrhotic Patients With and Without Spontaneous Bacterial Peritonitis: Is the Ring Closed?

  • increased Intestinal Permeability and tight junction alterations in nonalcoholic fatty liver disease
    Hepatology, 2009
    Co-Authors: Luca Miele, Venanzio Valenza, Giuseppe La Torre, Massimo Montalto, Giovanni Cammarota, Riccardo Ricci, Roberta Masciana, Alessandra Forgione, M L Gabrieli, Germano Perotti
    Abstract:

    The role played by the gut in nonalcoholic fatty liver disease (NAFLD) is still a matter of debate, although animal and human studies suggest that gut-derived endotoxin may be important. We investigated Intestinal Permeability in patients with NAFLD and evaluated the correlations between this phenomenon and the stage of the disease, the integrity of tight junctions within the small intestine, and prevalence of small Intestinal bacterial overgrowth (SIBO). We examined 35 consecutive patients with biopsy-proven NAFLD, 27 with untreated celiac disease (as a model of Intestinal hyperPermeability) and 24 healthy volunteers. We assessed the presence of SIBO by glucose breath testing (GBT), Intestinal Permeability by means of urinary excretion of 51Cr-ethylene diamine tetraacetate (51Cr-EDTA) test, and the integrity of tight junctions within the gut by immunohistochemical analysis of zona occludens-1 (ZO-1) expression in duodenal biopsy specimens. Patients with NAFLD had significantly increased gut Permeability (compared with healthy subjects; P < 0.001) and a higher prevalence of SIBO, although both were lower than in the untreated celiac patients. In patients with NAFLD, both gut Permeability and the prevalence of SIBO correlated with the severity of steatosis but not with presence of NASH. Conclusions: Our results provide the first evidence that NAFLD in humans is associated with increased gut Permeability and that this abnormality is related to the increased prevalence of SIBO in these patients. The increased Permeability appears to be caused by disruption of intercellular tight junctions in the intestine, and it may play an important role in the pathogenesis of hepatic fat deposition. (HEPATOLOGY 2009.)

Simon P Dunlop - One of the best experts on this subject based on the ideXlab platform.

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