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Bacterial Overgrowth (bacterial + overgrowth)
Kinds of Bacterial Overgrowth Selected AbstractsEditorial: Small Intestinal Bacterial Overgrowth in Dogs, Less Common Than You Think?JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 1 2003Stanley L. Marks BVSc No abstract is available for this article. [source] Small Intestinal Bacterial Overgrowth: A Possible Risk Factor for Metabolic Bone DiseaseNUTRITION REVIEWS, Issue 4 2003Article first published online: 16 SEP 200 Small intestinal bacterial overgrowth (SIBO) is one of the causes of malabsorption syndromes. The prevalence of metabolic bone disease in patients with SIBO is unknown, but a recent prospective case-control study indicated significant contribution of SIBO to the development of metabolic bone disease. We review this and other reports in the literature and discuss the possible mechanisms causing metabolic bone disease in patients with SIBO. [source] Increased bacterial permeation in long-lasting ileoanal pouchesINFLAMMATORY BOWEL DISEASES, Issue 8 2006Anton J. Kroesen MD Abstract Background and Aims: Bacterial overgrowth appears to play an important role in the pathogenesis of ileoanal pouches. Therefore, the capability of bacterial permeation and its determinants is of great interest. The aim of this study was to examine bacterial permeation in the ileoanal pouch and to correlate the results with the degree of inflammation, the epithelial resistance, the mucosal transport function, and the age of the ileoanal pouches. Materials and Methods: Biopsies were taken from 54 patients before colectomy (n = 13; preileal pouch-anal anastomosis [IPAA]), and closure of ileostomy (n = 7; deviation), <1 year after closure of ileostomy (n = 8; intact pouch I), >1 year after closure of ileostomy (n = 16; intact pouch II), in the case of pouchitis (n = 11), and in 11 controls. Tissues were mounted in a miniaturized Ussing chamber. Escherichia coli was added to the mucosal side of the Ussing chamber, and the permeation was proven by serosal presence of E. coli. Epithelial and subepithelial resistance was determined by transmural impedance analysis. Active Na+ -glucose cotransport and active Cl, secretion were measured. Specimens were analyzed by fluorescent in situ hybridization with oligonucleotide probes targeting the bacterial 16s ribosomal RNA. The bacteria in and on the tissue were enumerated. Results: Bacterial permeation occurred in 2 of 13 pre-IPAA, 2 of 7 deviations, 0 of 8 intact pouch I, 9 of 16 intact pouch II, 5 of 11 pouchitis specimens, and 0 of 11 ileum controls. The frequency of bacterial permeation in the intact pouch II group is higher than in the intact pouch I group (P < 0.001). Epithelial resistance, mannitol fluxes, electrogenic chloride secretion, sodium-glucose cotransport of the bacterially permeated specimens versus nonpermeated of the intact pouch II group, and the pouchitis group and subepithelial resistance remained unchanged. Intramural bacteria could be detected by fluorescence in situ hybridization mainly in long-lasting pouches, but there was no correlation with bacterial permeation. Conclusions: The long-lasting ileoanal pouch is associated with increased bacterial permeability. This is not correlated with a disturbed function of the pouch mucosa but could be a precursor of pouchitis. [source] Differential expression of antimicrobial peptides in margins of chronic woundsEXPERIMENTAL DERMATOLOGY, Issue 7 2010Stefanie Dressel Please cite this paper as: Differential expression of antimicrobial peptides in margins of chronic wounds. Experimental Dermatology 2010; 19: 628,632. Abstract:, Skin wounds usually heal without major infections, although the loss of the mechanical epithelial barrier exposes the tissue to various bacteria. One reason may be the expression of antimicrobial peptides (AMP) of which some [human ,-defensins (hBD) and LL-37] were recently shown to support additionally certain steps of wound healing. There are no studies which have compared expression patterns of different classes of AMP in chronic wounds. The aim of our study was therefore to analyse the expression profile of hBD-2, hBD-3, LL-37, psoriasin and RNase 7 by immunohistochemistry from defined wound margins of chronic venous ulcers. We detected a strong induction of psoriasin and hBD-2 in chronic wounds in comparison with healthy skin. Except for stratum corneum, no expression of RNase 7 and LL-37 was detected in the epidermis while expression of hBD-3 was heterogeneous. Bacterial swabs identified Staphylococcus aureus and additional bacterial populations, but no association between colonization and AMP expression was found. The differential expression of AMP is noteworthy considering the high bacterial load of chronic ulcers. Clinically, supplementation of AMP with the capability to enhance wound healing besides restricting bacterial overgrowth could present a physiological support for treatment of disturbed wound healing. [source] Helicobacter Hypothesis for Idiopathic Parkinsonism: Before and BeyondHELICOBACTER, Issue 5 2008R. John Dobbs Abstract We challenge the concept of idiopathic parkinsonism (IP) as inevitably progressive neurodegeneration, proposing a natural history of sequential microbial insults with predisposing host response. Proof-of-principle that infection can contribute to IP was provided by case studies and a placebo-controlled efficacy study of Helicobacter eradication. "Malignant" IP appears converted to "benign", but marked deterioration accompanies failure. Similar benefit on brady/hypokinesia from eradicating "low-density" infection favors autoimmunity. Although a minority of UK probands are urea breath test positive for Helicobacter, the predicted probability of having the parkinsonian label depends on the serum H. pylori antibody profile, with clinically relevant gradients between this "discriminant index" and disease burden and progression. In IP, H. pylori antibodies discriminate for persistently abnormal bowel function, and specific abnormal duodenal enterocyte mitochondrial morphology is described in relation to H. pylori infection. Slow intestinal transit manifests as constipation from the prodrome. Diarrhea may flag secondary small-intestinal bacterial overgrowth. This, coupled with genetically determined intense inflammatory response, might explain evolution from brady/hypokinetic to rigidity-predominant parkinsonism. [source] Increased intestinal permeability and tight junction alterations in nonalcoholic fatty liver disease,HEPATOLOGY, Issue 6 2009Luca Miele 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.) [source] Increased lipopolysaccharide binding protein in cirrhotic patients with marked immune and hemodynamic derangementHEPATOLOGY, Issue 1 2003Agustín Albillos Intestinal bacterial overgrowth and translocation, both common in cirrhosis with ascites, may lead to the activation of monocytes and lymphocytes, increased levels of proinflammatory cytokines, and enhanced synthesis of nitric oxide present in cirrhosis. Bacterial endotoxin promotes the synthesis of lipopolysaccharide (LPS)-binding protein (LBP), and forms a LPS-LBP complex that binds to CD14. This study was designed to evaluate LBP levels and their correlation to the immune response and the hemodynamic status in cirrhotic patients. Plasma LBP, endotoxin, soluble CD14 (sCD14), cytokines, renin, nitrites, and systemic vascular resistance were determined before and 4 weeks after norfloxacin or placebo in 102 cirrhotic patients and 30 controls. LBP was elevated in 42% of ascitic cirrhotic patients (15.7 ± 0.7 versus 6.06 ± 0.5 ,g/mL, P < .01). In 60% of high LBP patients, endotoxin was within normal range. Among ascitic patients, those with high LBP showed greater (P < .05) levels of sCD14, tumor necrosis factor , (TNF-,), interleukin 6 (IL-6), nitrites + nitrates (NOx)/creatinine, and renin, and lower vascular resistance. In the cirrhotic patients with high LBP, norfloxacin normalized (P < .01) LBP (from 16.6 ± 0.5 to 5.82 ± 0.8 , g/mL) and sCD14; reduced the level of cytokines, NOx/creatinine, and renin; and increased vascular resistance; but lacked effect in patients with normal LBP. Portal pressure was unchanged after norfloxacin in another group of 18 cirrhotic patients with high and 19 with normal LBP. In conclusion, the subset of ascitic cirrhotic patients with marked immune and hemodynamic derangement is identified by increased LBP levels. Amelioration of these abnormalities by norfloxacin suggests the involvement of enteric bacteria or their products in the triggering of the process. [source] Effect of propranolol on the factors promoting bacterial translocation in cirrhotic rats with ascitesHEPATOLOGY, Issue 1 2000María Pérez-Paramo Bacterial translocation appears to be an important mechanism in the pathogenesis of spontaneous infections in cirrhosis. Cirrhotic patients are commonly treated with ,-adrenoceptor blockers, but the impact of this treatment in the factors promoting bacterial translocation has not been investigated. This study was aimed at investigating in cirrhotic rats with ascites the effect of propranolol on intestinal bacterial load, transit, and permeability of the bowel and on the rate of bacterial translocation. Bacterial translocation to mesenteric lymph nodes and intestinal bacterial overgrowth, permeability (urinary excretion of 99mTc-diethylenetriaminepentaacetic acid [99mTc-DTPA]), and transit (geometric center ratio of 51Cr) were assessed in 29 rats with carbon tetrachloride (CCl4 ) cirrhosis and 20 controls. These variables were then measured in 12 placebo- and in 13 propranolol-treated ascitic cirrhotic rats. Bacterial translocation was present in 48% of the cirrhotic rats and in none of the controls. Cirrhotic rats with intestinal bacterial overgrowth had a significantly higher rate of translocation and slower intestinal transit than those without it. Among the 15 rats with overgrowth and a 99mTc-DTPA excretion greater than 10%, 15 had translocation and 2 had bacterial peritonitis. Only 1 of the 14 rats with either intestinal overgrowth or a 99mTc-DTPA excretion greater than 10% presented translocation. Compared with the placebo group, propranolol-treated animals had significantly lower portal pressure, faster intestinal transit, and lower rates of bacterial overgrowth and translocation. In ascitic cirrhotic rats, bacterial translocation results from intestinal overgrowth and severe damage to gut permeability. In this setting, intestinal overgrowth is associated with intestinal hypomotility. Propranolol accelerates the intestinal transit, decreasing the rates of bacterial overgrowth and translocation. [source] Chronic pouchitis is not related to small intestine bacterial overgrowthINFLAMMATORY BOWEL DISEASES, Issue 8 2008Aleksandra Lisowska MD Abstract Background: Restorative ileal pouch-anal anastomosis (IPAA) potentially may lead to upper gastrointestinal tract motility disturbances. In addition, a bacterial etiology of IPAA complication,pouchitis,has been suggested. The oro-anal transit time is significantly reduced in this patient group. Therefore, we investigated the hypothesis if IPAA constitutes a significant risk for small intestine bacterial overgrowth (SIBO). Methods: Twenty-eight patients age 23,71 years with IPAA operated due to ulcerative colitis without subjective symptoms of pouchitis were evaluated as outpatients according to the prescheduled follow-up after operation and included in the study. The modified Pouchitis Disease Activity Index (PDAI) was determined in all IPAA patients, including clinical, endoscopic, and histopathological (Moskowitz criteria) parameters. In addition, anorectal manometry was performed. The presence of SIBO was determined with the use of a glucose breath test (GBT). Results: In 1 subject (3.6%) an abnormal GBT result was recorded consistent with SIBO. In addition, 2 borderline values (7.1%) were documented. Both patients with SIBO as subjects with borderline values presented with low PDAI values. All patients with PDAI >7 had normal GBT results. In patients with SIBO the maximal tolerated rectal volume was significantly higher than in subjects without SIBO (P < 0.007). Similarly, the PDAI value was significantly lower (P < 0.014). Conclusions: Asymptomatic chronic pouchitis is not related to SIBO. However, excessive colonization of the small intestine does occur in some IPAA patients and needs to be kept in the differential diagnosis. (Inflamm Bowel Dis 2008) [source] Bacterial flora in irritable bowel syndrome: role in pathophysiology, implications for managementJOURNAL OF DIGESTIVE DISEASES, Issue 1 2007Eamonn M M QUIGLEY Irritable bowel syndrome (IBS) may, in part at least, result from a dysfunctional interaction between the indigenous flora and the intestinal mucosa which, in turn, leads to immune activation in the colonic mucosa. Some propose a role for bacterial overgrowth as a common causative factor in the pathogenesis of symptoms in IBS; other evidence points to more subtle qualitative changes in the colonic flora; both hypotheses remain to be confirmed but the likelihood that bacterial overgrowth will prove to be a major factor in IBS now seems remote. Nevertheless, short-term therapy with either antibiotics or probiotics does seem to reduce symptoms among IBS patients. It seems most likely that the benefits of antibiotic therapy are mediated through subtle and, perhaps, localized, quantitative and/or qualitative changes in the colonic flora. How probiotics exert their effects remain to be defined but an anti-inflammatory effect seems likely. While this approach to the management of IBS is in its infancy, it is evident that manipulation of the flora, whether through the administration of antibiotics or probiotics, deserves further attention in IBS. [source] Phosphatidylcholine Reverses Ethanol-Induced Increase in Transepithelial Endotoxin Permeability and Abolishes Transepithelial Leukocyte ActivationALCOHOLISM, Issue 3 2009Katja Mitzscherling Background:, Chronic alcohol abuse increases both intestinal bacterial overgrowth and intestinal permeability to macromolecules. Intestinal permeability of endotoxin, a component of the outer cell membrane of Gram-negative bacteria, plays a crucial role in the development of alcohol-induced liver disease (ALD). As impaired bile flow leads to endotoxemia and the bile component phosphatidylcholine (PC) is therapeutically active in ALD, we tested the hypothesis that conjugated primary bile salts (CPBS) and PC inhibit ethanol-enhanced transepithelial permeability of endotoxin and the subsequent transepithelial activation of human leukocytes. Methods:, For this purpose, we used a model in which intestinal epithelial cells (Caco-2) were basolaterally cocultivated with mononuclear leukocytes. Cells were challenged apically with endotoxin from Escherichia coli K12 and were incubated with or without the addition of CPBS (1.5 mM), PC (0.38 mM), pooled human bile (2%) in combination with ethanol (0 to 66 mM). Results:, Ethanol decreased integrity of intestinal epithelial cell monolayer and enhanced transepithelial permeability of endotoxin. Both the transepithelial permeability of endotoxin and the transepithelial stimulation of leukocytes were nearly completely abolished after the apical supplementation of PC with CPBS, but not by CPBS alone. Ethanol up to 66 mM was not able to reverse this effect. Conclusions:, A considerable part of the therapeutic and preventive effect of PC supplementation in ALD might result from a reduction of ethanol-enhanced permeability of endotoxin through the intestinal barrier. [source] Clinical trial: the combination of rifaximin with partially hydrolysed guar gum is more effective than rifaximin alone in eradicating small intestinal bacterial overgrowthALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2010M. Furnari Aliment Pharmacol Ther 2010; 32: 1000,1006 Summary Background, Abnormal intestinal clearance is involved in the pathogenesis of small intestinal bacterial overgrowth (SIBO). It is known that partially hydrolysed guar gum affects intestinal motility. Eradication therapy of SIBO is based on antibiotic treatment: no data are available on the role of fibre supplementation in eradicating SIBO. Aim, To assess whether the combination of partially hydrolysed guar gum and rifaximin is more effective than rifaximin alone in the treatment of SIBO. Methods, A 50 g-glucose breath test was given to 500 consecutive patients. Patients with a positive glucose breath test and predisposing conditions to SIBO entered into the study, and were randomized to receive rifaximin 1200 mg/day or rifaximin 1200 mg/day plus partially hydrolysed guar gum 5 g/day for 10 days. Patients completed a symptom questionnaire and glucose breath test both in basal condition and 1 month after withdrawal of therapy. Results, Seventy-seven patients had SIBO. Eradication rate of SIBO was 62.1% in the rifaximin group (both on per-protocol and intention-to-treat analyses), and 87.1% (per-protocol, P = 0.017) and 85.0% (intention-to-treat, P = 0.036) in the rifaximin-plus-partially hydrolysed guar gum group. Clinical improvement was observed in 86.9% and 91.1% of eradicated cases in rifaximin and rifaximin-plus-partially hydrolysed guar gum groups respectively (P = 0.677). Conclusion, The combination of rifaximin with partially hydrolysed guar gum seems to be more useful in eradicating SIBO compared with rifaximin alone. [source] Lactose intolerance in patients with chronic functional diarrhoea: the role of small intestinal bacterial overgrowthALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2010J. ZHAO Aliment Pharmacol Ther,31, 892,900 Summary Background, Many studies report a high prevalence of lactose intolerance in patients with functional, gastrointestinal disease. Aim, To evaluate the role of small intestinal bacterial overgrowth (SIBO) in condition of lactose intolerance and the mechanism by which SIBO may impact lactose tolerance in affected patients. Methods, Consecutive out-patients with chronic functional diarrhoea (CFD) and healthy controls underwent a validated 20 g lactose hydrogen breath test (HBT). Patients completed also a 10 g lactulose HBT with concurrent assessment of small bowel transit by scintigraphy. Results, Lactose malabsorption was present in 27/31 (87%) patients with CFD and 29/32 (91%) healthy controls (P = 0.708). From the patient group 14/27 (52%) had lactose intolerance and 13/27 (48%) experienced no symptoms (lactose malabsorption controls). Only 5 (17%) healthy controls reported symptoms (P < 0.01). The oro-caecal transit time was similar between patient groups with or without symptoms (P = 0.969). SIBO was present in 11 (41%) subjects and was more prevalent in lactose intolerance than in lactose malabsorption [9/14 (64%) vs. 2/13 (15%), P = 0.018]. Symptom severity was similar in lactose intolerance patients with and without SIBO (P = 0.344). Conclusions, Small intestinal bacterial overgrowth increases the likelihood of lactose intolerance in patients with CFD as a direct result of lactose fermentation in the small intestine, independent of oro-caecal transit time and visceral sensitivity. [source] Small-intestinal bacterial overgrowth in cirrhosis is related to the severity of liver diseaseALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 12 2009C. PANDE Summary Background, Small-intestinal bacterial overgrowth (SIBO) is known to be present in patients with cirrhosis, predisposing to various complications. Aim, To determine the frequency of SIBO in cirrhotics and correlate with severity of cirrhosis. Methods, Small-intestinal bacterial overgrowth was determined by glucose,hydrogen breath test (GHBT). A basal breath-hydrogen >20 ppm or a rise by ,12 ppm above baseline following glucose administration was taken as positive test. Prevalence of SIBO in cirrhotics was compared with healthy controls and correlated with severity of cirrhosis. Results, Of the 53 cirrhotics, 26 (49%) had SIBO, compared to one (8%) control (P = 0.010). The prevalence of SIBO increased with severity of cirrhosis (Child,Pugh A 20%, B 52% and C 73%; P = 0.013). On multivariate analysis, SIBO was independently associated with serum bilirubin and ascites. The best cut-off of serum bilirubin was ,2 mg/dL [AUROC 0.77 (95% CI 0.64,0.90)] predicting SIBO with sensitivity 65%, specificity 81%, positive predictive value 77%, negative predictive value 71% and accuracy 74%. Patients having combination of ascites and serum bilirubin ,2 mg/dL had 82% chance, while patients having neither had only 10% chance of having SIBO. Conclusions, Small-intestinal bacterial overgrowth was prevalent in about half of cirrhotics. Its frequency increased with increase in severity of cirrhosis. Ascites and raised serum bilirubin reliably predicted presence of SIBO. [source] Review article: small intestinal bacterial overgrowth, bile acid malabsorption and gluten intolerance as possible causes of chronic watery diarrhoeaALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 10 2009X. FAN Summary Background, Chronic watery diarrhoea is one of the most common symptoms prompting GI evaluation. Recently, new diagnostic considerations have emerged as possible factors in chronic diarrhoea. Aim, To review available data regarding diagnosis and treatment of chronic diarrhoea with an emphasis on bacterial overgrowth and bile acid malabsorption. Methods, A systematic search of the English language literature of chronic diarrhoea was performed focused on three possible aetiologies of diarrhoea: small intestinal bacterial overgrowth (SIBO), idiopathic bile salt malabsorption (IBAM), gluten responsive enteropathy. Results, Recent studies suggest that SIBO and bile acid malabsorption may have been underestimated as possible causes of chronic watery diarrhoea. Gluten intolerance with negative coeliac serology is a contentious possible cause of watery diarrhoea, but requires further research before acceptance as an entity. Conclusion, In patients with otherwise unexplained chronic watery diarrhoea, small intestinal bacterial overgrowth and bile salt malabsorption should be considered and investigated. [source] Genes or environment to determine alcoholic liver disease and non-alcoholic fatty liver diseaseLIVER INTERNATIONAL, Issue 9 2006C. P. Day Abstract: While the vast majority of heavy drinkers and individuals with obesity, insulin resistance, and the metabolic syndrome will have steatosis, only a minority will ever develop steatohepatitis, fibrosis, and cirrhosis. Genetic and environmental risk factors for advanced alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD) seem likely to include factors that influence the severity of steatosis and oxidative stress, the cytokine milieu, the magnitude of the immune response, and/or the severity of fibrosis. For ALD, the dose and pattern of alcohol intake, along with obesity are the most important environmental factors determining disease risk. For NAFLD, dietary saturated fat and antioxidant intake and small bowel bacterial overgrowth may play a role. Family studies and interethnic variations in susceptibility suggest that genetic factors are important in determining disease risk. For ALD, functional polymorphisms in the alcohol dehydrogenases and aldehyde dehydrogenase alcohol metabolising genes play a role in determining susceptibility in Oriental populations. No genetic associations with advanced NAFLD have been replicated in large studies. Preliminary data suggest that polymorphisms in the genes encoding microsomal triglyceride transfer protein, superoxide dismutase 2, the CD14 endotoxin receptor, TNF-,, transforming growth factor-,, and angiotensinogen may be associated with steatohepatitis and/or fibrosis. [source] Review article: potential gastrointestinal effects of long-term acid suppression with proton pump inhibitorsALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 6 2000Laine This review examines the evidence for the development of adverse effects due to prolonged gastric acid suppression with proton pump inhibitors. Potential areas of concern regarding long-term proton pump inhibitor use have included: carcinoid formation; development of gastric adenocarcinoma (especially in patients with Helicobacter pylori infection); bacterial overgrowth; enteric infections; and malabsorption of fat, minerals, and vitamins. Prolonged proton pump inhibitor use may lead to enterochromaffin-like cell hyperplasia, but has not been demonstrated to increase the risk of carcinoid formation. Long-term proton pump inhibitor treatment has not been documented to hasten the development or the progression of atrophic gastritis to intestinal metaplasia and gastric cancer, although long-term studies are required to allow definitive conclusions. At present, we do not recommend that patients be tested routinely for H. pylori infection when using proton pump inhibitors for prolonged periods. Gastric bacterial overgrowth does increase with acid suppression, but important clinical sequelae, such a higher rate of gastric adenocarcinoma, have not been seen. The risk of enteric infection may increase with acid suppression, although this does not seem to be a common clinical problem with prolonged proton pump inhibitor use. The absorption of fats and minerals does not appear to be significantly impaired with chronic acid suppression. However, vitamin B12 concentration may be decreased when gastric acid is markedly suppressed for prolonged periods (e.g. Zolllinger,Ellison syndrome), and vitamin B12 levels should probably be assessed in patients taking high-dose proton pump inhibitors for many years. Thus, current evidence suggests that prolonged gastric acid suppression with proton pump inhibitors rarely, if ever, produces adverse events. Nevertheless, continued follow-up of patients taking proton pump inhibitors for extended periods will provide greater experience regarding the potential gastrointestinal adverse effects of long-term acid suppression. [source] Altered intestinal microbiota in irritable bowel syndromeNEUROGASTROENTEROLOGY & MOTILITY, Issue 5 2010K. J. Lee Abstract, Recent studies have suggested that alterations in the composition of the intestinal microbiota may play an important role in irritable bowel syndrome (IBS) symptoms. However, an association between the composition of the intestinal microbiota and IBS symptoms has not been clearly demonstrated. In the current issue of the Journal, Tana et al. suggest that altered intestinal microbiota contributes to the symptoms of IBS through increased levels of organic acids. In fecal samples, IBS patients had significantly higher numbers of Veillonella and Lactobacillus than healthy controls. They also showed significantly higher levels of acetic acid and propionic acid. Furthermore, IBS patients with high acetic acid or propionic acid levels presented more severe symptoms, impaired quality of life and negative emotions. These results are in accordance with the concept that the gut microbiota influences the sensory, motor and immune system of the gut and interacts with higher brain centers. Small intestinal bacterial overgrowth observed in a subset of IBS patients describes quantitative changes in the small intestinal microbiota. Data on qualitative changes in the gut microbiota in IBS patients are lacking. Different members of gut bacteria may have different influence on gut function. The concepts identified here may lead to the development of novel therapeutic strategies for IBS using manipulation of the intestinal microbiota. [source] Small Intestinal Bacterial Overgrowth: A Possible Risk Factor for Metabolic Bone DiseaseNUTRITION REVIEWS, Issue 4 2003Article first published online: 16 SEP 200 Small intestinal bacterial overgrowth (SIBO) is one of the causes of malabsorption syndromes. The prevalence of metabolic bone disease in patients with SIBO is unknown, but a recent prospective case-control study indicated significant contribution of SIBO to the development of metabolic bone disease. We review this and other reports in the literature and discuss the possible mechanisms causing metabolic bone disease in patients with SIBO. [source] Pneumatosis intestinalis and diarrhea in a child following renal transplantation,PEDIATRIC TRANSPLANTATION, Issue 3 2003G. Chelimsky Abstract: Pneumatosis intestinalis is an uncommon finding beyond the neonatal period, but it has been reported in immunocompromized pediatric patients. The association of pneumatosis intestinalis in children following renal transplantation has to the best of our knowledge been only reported once in children. We describe a 4-year-old female who developed intermittent emesis, weight loss, and intermittently loose bloody stools after cadaveric renal transplantation at age 3.5 years. An abdominal x-ray demonstrated extensive pneumatosis in the colon. The infectious work-up was negative. Histologically, she had increased eosinophils throughout the lamina propria in the rectum. A glucose breath test was suggestive of small bowel bacterial overgrowth. She was treated with 10 days of metronidazole with resolution of the diarrhea and occult blood in stools. One month after the treatment she had radiologic resolution of her pneumatosis. Based on this report, pneumatosis intestinalis should be considered in the differential diagnosis of children after organ transplant suffering from diarrhea, abdominal pain, or blood in the stool. [source] Inhibition of bacterial translocation by chronic ethanol consumption in the rat,APMIS, Issue 12 2001VALERIA BENDER BRAULIO Chronic ethanol ingestion has been associated with small intestine morphological changes, disrupted host mucosal defenses and bacterial overgrowth. Since bacterial translocation (BT) may result from such alterations, we have investigated the potential effect of chronic ethanol consumption on BT. For this purpose, male Wistar rats were fed a liquid diet containing 5% v/v ethanol for 4 weeks (EG, n=16), and a pair-fed group received equal daily amounts of calories in a similar diet without ethanol (PFG, n=16). On experimental day 29, distal ileum ligature and small intestine inoculation of a tetracycline-resistant E. coli strain (Tc®E. coli R6) followed by duodenal ligature was performed. After 1 or 5 h post inoculation, mesenteric lymph nodes, liver, spleen and kidney were excised. Unexpectedly, rats of the EG presented markedly less BT to the mesenteric lymph nodes (p<0.001) and to the other organs examined compared to rats of the PFG. This BT inhibition was observed at 1 and 5 h after bacterial inoculation, and may be attributed exclusively to chronic ethanol ingestion. Since alcoholism is well known to decrease host immunity, these results suggest that other factors, independent of the immune function, may be involved in the BT inhibition observed in this study. [source] Folic acid supplementation on red kidney bean-induced diarrhoea and enteric bacterial translocation into mesenteric lymph nodes in rats: a pilot studyACTA PAEDIATRICA, Issue 1 2002R Shoda Deaths following childhood diarrhoea, a major health problem in developing countries, are often associated with malnutrition and septicaemic complications. Folic acid has been used in the treatment of acute and chronic diarrhoea in the tropics. Using a rat model, we evaluated the protective effect of large doses of folic acid on diarrhoea, small intestinal bacterial overgrowth and translocation of enteric bacteria into mesenteric lymph nodes induced by a raw red kidney bean-based diet containing lectin (phytohemagglutinin). Long-Evans rats in 2 groups of 5 each (60 g to 70 g in weight, 28 d old) were used. All 10 rats, individually kept in metabolic cages, received a raw red kidney bean-based diet for 10 d, and 5 of them also received a daily folic acid supplement (160 ,g/g feed) both during and for 10 d before the experiment. The faecal weight was measured and a quantitative aerobic bacterial culture of the small intestinal mucosal scrapings and of the mesenteric lymph nodes was made. Folic acid supplementation did not reduce faecal output nor did it prevent loss of body weight associated with lectin-induced diarrhoea. However, the mean total count of enteric bacteria translocated to the mesenteric lymph nodes was significantly reduced in the supplemented rats (1.27 ± 0.61 vs 2.66 ± 0.84, p= 0.028) and a trend towards reduced bacterial count in the small intestinal mucosal scrapings (0.40 ± 0.89 vs 1.42 ± 1.31, p= 0.16) was documented. A significant positive correlation was also seen between the bacterial count in the jejunal mucosal scrapings and in the mesenteric lymph nodes. Conclusion: Although large-dose folic acid supplementation did not prevent diarrhoea and malnutrition induced by a lectin-based diet, it substantially reduced the count of enteric bacteria translocated into the mesenteric lymph nodes and showed a trend towards a reduction in indigenous bacteria adhering to jejunal mucosa. These findings could be of relevance in the prevention of septicaemic complications following many clinical conditions, including diarrhoea with malnutrition in children known to have bacteraemic and septicaemic complications. [source] | ||||||||||||||||||||||||||||