Showing papers in "World Journal of Gastroenterology in 2010"
TL;DR: Therapy for SIBO must be complex, addressing all causes, symptoms and complications, and fully individualised, it should include treatment of the underlying disease, nutritional support and cyclical gastro-intestinal selective antibiotics.
Abstract: Human intestinal microbiota create a complex polymicrobial ecology. This is characterised by its high population density, wide diversity and complexity of interaction. Any dysbalance of this complex intestinal microbiome, both qualitative and quantitative, might have serious health consequence for a macro-organism, including small intestinal bacterial overgrowth syndrome (SIBO). SIBO is defined as an increase in the number and/or alteration in the type of bacteria in the upper gastrointestinal tract. There are several endogenous defence mechanisms for preventing bacterial overgrowth: gastric acid secretion, intestinal motility, intact ileo-caecal valve, immunoglobulins within intestinal secretion and bacteriostatic properties of pancreatic and biliary secretion. Aetiology of SIBO is usually complex, associated with disorders of protective antibacterial mechanisms (e.g. achlorhydria, pancreatic exocrine insufficiency, immunodeficiency syndromes), anatomical abnormalities (e.g. small intestinal obstruction, diverticula, fistulae, surgical blind loop, previous ileo-caecal resections) and/or motility disorders (e.g. scleroderma, autonomic neuropathy in diabetes mellitus, post-radiation enteropathy, small intestinal pseudo-obstruction). In some patients more than one factor may be involved. Symptoms related to SIBO are bloating, diarrhoea, malabsorption, weight loss and malnutrition. The gold standard for diagnosing SIBO is still microbial investigation of jejunal aspirates. Non-invasive hydrogen and methane breath tests are most commonly used for the diagnosis of SIBO using glucose or lactulose. Therapy for SIBO must be complex, addressing all causes, symptoms and complications, and fully individualised. It should include treatment of the underlying disease, nutritional support and cyclical gastro-intestinal selective antibiotics. Prognosis is usually serious, determined mostly by the underlying disease that led to SIBO.
506 citations
TL;DR: In adults, S. boulardii can be strongly recommended for the prevention of AAD and the traveler's diarrhea and randomized trials support the use of this yeast probiotic for prevention of enteral nutrition-related diarrhea and reduction of Helicobacter pylori treatment-related symptoms.
Abstract: This article reviews the evidence for efficacy and safe ty of Saccharomyces boulardii (S. boulardii ) for various disease indications in adults based on the peerreviewed, randomized clinical trials and pre-clinical studies from the published medical literature (Medline, Clinical Trial websites and meeting abstracts) between 1976 and 2009. For meta-analysis, only randomized, blinded controlled trials unrestricted by language were included. Pre-clinical studies, volunteer studies and uncontrolled studies were excluded from the review of efficacy and meta-analysis, but included in the systemat ic review. Of 31 randomized, placebo-controlled treatment arms in 27 trials (encompassing 5029 study patients), S. boulardii was found to be significantly effica cious and safe in 84% of those treatment arms. A meta-analysis found a significant therapeutic efficacy for S. boulardii in the prevention of antibiotic-associated diarrhea (AAD) (RR = 0.47, 95% CI: 0.35-0.63, P < 0.001). In adults, S. boulardii can be strongly recommended for the prevention of AAD and the traveler’s diarrhea. Randomized trials also support the use of this yeast probiotic for prevention of enteral nutrition-related diarrhea and reduction of Heliobacter pylori treatment-related symptoms. S. boulardii shows promise for the prevention of C. difficile disease recurrences; treatment of irritable bowel syndrome, acute adult diarrhea, Crohn’s disease, giardiasis, human immunodeficiency virus-related diarrhea; but more supporting evidence is recommended for these indications. The use of S. boulardii as a therapeutic probiotic is evidence-based for both efficacy and safety for several types of diarrhea.
389 citations
TL;DR: The current paper reviews the relevance of this intimate hepatic blood flow regulatory system in health and disease and exclusively focuses on the endogenous interrelationship between the hepatic arterial and portal venous inflow circuits in liver resection and transplantation, as well as inflammatory and chronic liver diseases.
Abstract: The interest in the liver dates back to ancient times when it was considered to be the seat of life processes. The liver is indeed essential to life, not only due to its complex functions in biosynthesis, metabolism and clearance, but also its dramatic role as the blood volume reservoir. Among parenchymal organs, blood flow to the liver is unique due to the dual supply from the portal vein and the hepatic artery. Knowledge of the mutual communication of both the hepatic artery and the portal vein is essential to understand hepatic physiology and pathophysiology. To distinguish the individual importance of each of these inflows in normal and abnormal states is still a challenging task and the subject of ongoing research. A central mechanism that controls and allows constancy of hepatic blood flow is the hepatic arterial buffer response. The current paper reviews the relevance of this intimate hepatic blood flow regulatory system in health and disease. We exclusively focus on the endogenous interrelationship between the hepatic arterial and portal venous inflow circuits in liver resection and transplantation, as well as inflammatory and chronic liver diseases. We do not consider the hepatic microvascular anatomy, as this has been the subject of another recent review.
377 citations
TL;DR: In this article, the rationale for liver biopsy, as well as the histopathological lesions, the microscopically observable patterns of injury, and the differential diagnoses of NAFLD and NASH are discussed.
Abstract: Histological analysis of liver biopsies remains a standard against which other methods of assessment for the presence and amount of hepatic injury due to nonalcoholic fatty liver disease (NAFLD) are measured. Histological evaluation remains the sole method of distinguishing steatosis from advanced forms of NAFLD, i.e. nonalcoholic steatohepatitis (NASH) and fibrosis. Included in the lesions of NAFLD are steatosis, lobular and portal inflammation, hepatocyte injury in the forms of ballooning and apoptosis, and fibrosis. However, patterns of these lesions are as distinguishing as the lesions themselves. Liver injury in adults and children due to NAFLD may have different histological patterns. In this review, the rationale for liver biopsy, as well as the histopathological lesions, the microscopically observable patterns of injury, and the differential diagnoses of NAFLD and NASH are discussed.
355 citations
TL;DR: In this article, a foregut microbiome dataset was constructed using 16S rRNA gene sequences obtained from oral, esophageal, and gastric microbiomes produced by Sanger sequencing.
Abstract: AIM: To design and validate broad-range 16S rRNA primers for use in high throughput sequencing to clas-sify bacteria isolated from the human foregut microbi-ome. METHODS: A foregut microbiome dataset was con-structed using 16S rRNA gene sequences obtained from oral, esophageal, and gastric microbiomes produced by Sanger sequencing in previous studies represented by 219 bacterial species. Candidate primers evaluated were from the European rRNA database. To assess the effect of sequence length on accuracy of classification, 16S rRNA genes of various lengths were created by trimming the full length sequences. Sequences spanning various hypervariable regions were selected to simulate the amplicons that would be obtained using possible primer pairs. The sequences were compared with full length 16S rRNA genes for accuracy in taxonomic classification using online software at the Ribosomal Database Project (RDP). The universality of the primer set was evaluated using the RDP 16S rRNA database which is comprised of 433 306 16S rRNA genes, represented by 36 phyla.
350 citations
TL;DR: The role of the Toll-like receptor 4 (TLR4) complex in LPS recognition and the importance of the TLR4-induced signaling pathways are evaluated in ALD.
Abstract: Alcoholic liver disease (ALD) is one of the leading causes of liver diseases and liver-related death worldwide. Of the many factors that contribute to the pathogenesis of ALD, gut-derived lipopolysaccharide (LPS) plays a central role in induction of steatosis, inflammation, and fibrosis in the liver. In this review, we discuss the mechanisms by which alcohol contributes to increased gut permeability, the activation of Kupffer cells, and the inflammatory cascade by LPS. The role of the Toll-like receptor 4 (TLR4) complex in LPS recognition and the importance of the TLR4-induced signaling pathways are evaluated in ALD.
310 citations
TL;DR: The PPIs are a safe class of medications to use long-term in persons in whom there is a clear need for the maintenance of extensive acid inhibition, and the key is to use PPIs only when clearly indicated, and to reassess continued use so that long- term therapy is used judiciously.
Abstract: The proton pump inhibitors (PPIs) as a class are remarkably safe and effective for persons with peptic ulcer disorders. Serious adverse events are extremely rare for PPIs, with case reports of interstitial nephritis with omeprazole, hepatitis with omeprazole and lansoprazole, and disputed visual disturbances with pantoprazole and omeprazole. PPI use is associated with the development of fundic gland polyps (FGP); stopping PPIs is associated with regression of FGP. In the absence of Helicobacter pylori infection, the long-term use of PPIs has not been convincingly proven to cause or be associated with the progression of pre-existing chronic gastritis or gastric atrophy or intestinal metaplasia. Mild/modest hypergastrinemia is a physiological response to the reduction in gastric acid secretion due to any cause. The long-term use of PPIs has not been convincingly proven to cause enterochromaffin-like cell hyperplasia or carcinoid tumors. PPIs increase the risk of community acquired pneumonia, but not of hospital acquired (nosocomial) pneumonia. There is no data to support particular care in prescribing PPI therapy due to concerns about risk of hip fracture with the long-term use of PPIs. Long-term use of PPIs does not lead to vitamin B12 deficiencies, except possibly in the elderly, or in persons with Zollinger-Ellison Syndrome who are on high doses of PPI for prolonged periods of time. There is no convincingly proven data that PPIs increase the risk of Clostridium difficile-associated diarrhea in persons in the community. The discontinuation of PPIs may result in rebound symptoms requiring further and even continuous PPI use for suppression of symptoms. As with all medications, the key is to use PPIs only when clearly indicated, and to reassess continued use so that long-term therapy is used judiciously. Thus, in summary, the PPIs are a safe class of medications to use long-term in persons in whom there is a clear need for the maintenance of extensive acid inhibition.
284 citations
TL;DR: In this article, the authors analyzed the physiopathological mechanisms of portal vein thrombosis, together with the hemodynamic and functional alterations related to this condition, and described the principal factors most frequently involved in PVT development and the recent knowledge concerning diagnostic and therapeutic procedures.
Abstract: Portal vein thrombosis (PVT) is a relatively common complication in patients with liver cirrhosis, but might also occur in absence of an overt liver disease. Several causes, either local or systemic, might play an important role in PVT pathogenesis. Frequently, more than one risk factor could be identified; however, occasionally no single factor is discernable. Clinical examination, laboratory investigations, and imaging are helpful to provide a quick diagnosis, as prompt treatment might greatly affect a patient’s outcome. In this review, we analyze the physiopathological mechanisms of PVT development, together with the hemodynamic and functional alterations related to this condition. Moreover, we describe the principal factors most frequently involved in PVT development and the recent knowledge concerning diagnostic and therapeutic procedures. Finally, we analyze the implications of PVT in the setting of liver transplantation and its possible influence on patients’ future prognoses.
246 citations
TL;DR: SPT of the pancreas is a rare indolent neoplasm that typically occurs in young females and can be cured with extended resection, and the prognosis of such patients is good although the tumor may recur and metastasize.
Abstract: AIM: To sum up the clinical and pathological characteristics of solid pseudopapillary tumor (SPT) and the experience with it.
244 citations
TL;DR: Until more data are available, it is believed the use of probiotics for the treatment of constipation condition should be considered investigational.
Abstract: AIM: To systematically evaluate and update evidence on the efficacy and safety of probiotic supplementation for the treatment of constipation.
METHODS: The MEDLINE, EMBASE, CINAHL, and Cochrane Library databases were searched in May 2009 for randomised controlled trials (RCTs) performed in paediatric or adult populations related to the study aim.
RESULTS: We included five RCTs with a total of 377 subjects (194 in the experimental group and 183 in the control group). The participants were adults (three RCTs, n = 266) and children (two RCTs, n = 111) with constipation. In adults, data suggests a favourable effect of treatment with Bifidobacterium lactis DN-173 010, Lactobacillus casei Shirota, and Escherichia coli Nissle 1917 on defecation frequency and stool consistency. In children, L. casei rhamnosus Lcr35, but not L. rhamnosus GG, showed a beneficial effect.
CONCLUSION: Until more data are available, we believe the use of probiotics for the treatment of constipation condition should be considered investigational.
238 citations
TL;DR: Treatment is directed at correcting coexisting clinical conditions, restoring hemodynamic stability, nil-per-os restriction, supportive red blood cell transfusion, and intravenous acid suppression with proton pump inhibitors.
Abstract: Acute esophageal necrosis (AEN), commonly referred to as “black esophagus”, is a rare clinical entity arising from a combination of ischemic insult seen in hemodynamic compromise and low-flow states, corrosive injury from gastric contents in the setting of esophago-gastroparesis and gastric outlet obstruction, and decreased function of mucosal barrier systems and reparative mechanisms present in malnourished and debilitated physical states. AEN may arise in the setting of multiorgan dysfunction, hypoperfusion, vasculopathy, sepsis, diabetic ketoacidosis, alcohol intoxication, gastric volvulus, traumatic transection of the thoracic aorta, thromboembolic phenomena, and malignancy. Clinical presentation is remarkable for upper gastrointestinal bleeding. Notable symptoms may include epigastric/abdominal pain, vomiting, dysphagia, fever, nausea, and syncope. Associated laboratory findings may reflect anemia and leukocytosis. The hallmark of this syndrome is the development of diffuse circumferential black mucosal discoloration in the distal esophagus that may extend proximally to involve variable length of the organ. Classic “black esophagus” abruptly stops at the gastroesophageal junction. Biopsy is recommended but not required for the diagnosis. Histologically, necrotic debris, absence of viable squamous epithelium, and necrosis of esophageal mucosa, with possible involvement of submucosa and muscularis propria, are present. Classification of the disease spectrum is best described by a staging system. Treatment is directed at correcting coexisting clinical conditions, restoring hemodynamic stability, nil-per-os restriction, supportive red blood cell transfusion, and intravenous acid suppression with proton pump inhibitors. Complications include perforation with mediastinal infection/abscess, esophageal stricture and stenosis, superinfection, and death. A high mortality of 32% seen in the setting of AEN syndrome is usually related to the underlying medical co-morbidities and diseases.
TL;DR: Supportive measures such as bowel rest, nutritional support, antibiotics and prokinetic medications are helpful in facilitating functional recovery and improving the outcome.
Abstract: Systemic lupus erythematosus (SLE) is an autoimmune inflammatory disease characterized by the presence of a plethora of autoantibodies and immune complex formation. Virtually every system and organ can be affected by SLE. Gastrointestinal symptoms are common in SLE patients, and more than half of them are caused by adverse reactions to medications and viral or bacterial infections. Though not as common as lupus nephritis, SLE-related gastrointestinal involvement is clinically important because most cases can be life-threatening if not treated promptly. Lupus mesenteric vasculitis is the most common cause, followed by protein-losing enteropathy, intestinal pseudo-obstruction, acute pancreatitis and other rare complications such as celiac disease, inflammatory bowel diseases, etc. No specific autoantibody is identified as being associated with SLE-related gastroenteropathy. Imaging studies, particularly abdominal computed tomography scans, are helpful in diagnosing some SLE-related gastroenteropathies. Most of these complications have good therapeutic responses to corticosteroids and immunosuppressive agents. Supportive measures such as bowel rest, nutritional support, antibiotics and prokinetic medications are helpful in facilitating functional recovery and improving the outcome.
TL;DR: A critical analysis of the dissimilar results currently available in the literature concerning the epidemiology of NSAIDS hepatotoxicity is provided to review the risk of hepatot toxicity for each one of the most commonly employed compounds of the NSAIDs family, based on past and recently published data.
Abstract: Non-steroidal anti-inflammatory drugs (NSAIDs) constitute a family of drugs, which taken as a group, represents one of the most frequently prescribed around the world. Thus, not surprisingly NSAIDs, along with anti-infectious agents, list on the top for causes of Drug-Induced Liver Injury (DILI). The incidence of liver disease induced by NSAIDs reported in clinical studies is fairly uniform ranging from 0.29/100 000 [95% confidence interval (CI): 0.17-051] to 9/100 000 (95% CI: 6-15). However, compared with these results, a higher risk of liver-related hospitalizations was reported (3-23 per 100 000 patients). NSAIDs exhibit a broad spectrum of liver damage ranging from asymptomatic, transient, hyper-transaminasemia to fulminant hepatic failure. However, under-reporting of asymptomatic, mild cases, as well as of those with transient liver-tests alteration, in conjunction with reports non-compliant with pharmacovigilance criteria to ascertain DILI and flawed epidemiological studies, jeopardize the chance to ascertain the actual risk of NSAIDs hepatotoxicity. Several NSAIDs, namely bromfenac, ibufenac and benoxaprofen, have been withdrawn from the market due to hepatotoxicity; others like nimesulide were never marketed in some countries and withdrawn in others. Indeed, the controversy concerning the actual risk of severe liver disease persists within NSAIDs research. The present work intends (1) to provide a critical analysis of the dissimilar results currently available in the literature concerning the epidemiology of NSAIDS hepatotoxicity; and (2) to review the risk of hepatotoxicity for each one of the most commonly employed compounds of the NSAIDs family, based on past and recently published data.
TL;DR: A review summarizes some of the relationships between oxidative stress and liver pathogenesis, focusing upon HBV and alcohol, and suggests antioxidant therapeutic approaches.
Abstract: Long term hepatitis B virus (HBV) infection is a major risk factor in pathogenesis of chronic liver diseases, including hepatocellular carcinoma (HCC). The HBV encoded proteins, hepatitis B virus X protein and preS, appear to contribute importantly to the pathogenesis of HCC. Both are associated with oxidative stress, which can damage cellular molecules like lipids, proteins, and DNA during chronic infection. Chronic alcohol use is another important factor that contributes to oxidative stress in the liver. Previous studies reported that treatment with antioxidants, such as curcumin, silymarin, green tea, and vitamins C and E, can protect DNA from damage and regulate liver pathogenesis-related cascades by reducing reactive oxygen species. This review summarizes some of the relationships between oxidative stress and liver pathogenesis, focusing upon HBV and alcohol, and suggests antioxidant therapeutic approaches.
TL;DR: Oral supplementation with probiotic for 8 wk significantly ameliorated the inflammation by decreasing the colonic concentration of IL-6, expression of TNF-alpha and NF-kappaB p65, leukocyte recruitment, as demonstrated by a decrease in colonic MPO activity, and the level of fecal calprotectin compared to sulfasalazine group and the control group.
Abstract: Effect of probiotics on pro-inflammatory cytokines and NF-κB activation in ulcerative colitis
TL;DR: The response of energy metabolism to administration of Bifidobacteria is strain dependent, which might drive different directions of fat distribution in an obese murine model induced by high-fat diet.
Abstract: AIM: To compare the effects of four Bifidobacteria strains (Bifidobacteria L66-5, L75-4, M13-4 and FS31-12, originated from normal human intestines) on weight gain, lipid metabolism, glucose metabolism in an obese murine model induced by high-fat diet.
METHODS: Forty-eight Sprague-Dawley rats were randomly divided into six groups. Control group received standard chow, model group received high-fat diet, and intervention groups received high-fat diet added with different Bifidobacteria strains isolated from healthy volunteers’ fresh feces. All rats were executed at the 6th weekend. Body weight (BW), obese indexes, oral glucose tolerance test, serum and liver lipid and serum insulin (INS) were tested. Liver lipid deposition was classified pathologically.
RESULTS: Compared with the model group, B. M13-4 improved BW gains (264.27 ± 26.91 vs 212.55 ± 18.54, P = 0.001) while B. L66-5 induced a decrease in BW (188.47 ± 11.96 vs 212.55 ± 18.54, P = 0.043). The rest two strains had no significant change in BW. All the four strains can reduce serum and liver triglyceride and significantly alleviate the lipid deposition in liver. All strains showed a trend of lowing serum and liver total cholesterol while B. L66-5 and B. FS31-12 did so more significantly. In addition, all the four strains showed no significant differences in serum INS and glucose level.
CONCLUSION: The response of energy metabolism to administration of Bifidobacteria is strain dependent. Different strains of Bifidobacteria might drive different directions of fat distribution.
TL;DR: This meta-analysis on observational studies suggests an association between H. pylori and IDA, and in RCTs, eradication of H.pylori can improve HB and SF levels but not significantly.
Abstract: AIM: To perform a meta-analysis of observational studies and randomized controlled trials (RCTs) on the association between Helicobacter pylori (H. pylori) and iron deficiency anemia (IDA).
METHODS: A defined search strategy was used to search Medline, Embase, the Cochrane Library, Clinical Trials, Cochrane Central Register of Controlled Trials, Premedline and Healthstar. Odds ratio (OR) was used to evaluate observational epidemiology studies, and weighted mean difference (WMD) was used to demonstrate the difference between control and intervention groups.
RESULTS: Fifteen observational studies and 5 RCTs were identified and used for calculation. The pooled OR for observational studies was 2.22 (95% CI: 1.52-3.24, P < 0.0001). The WMD for hemoglobin (HB) was 4.06 g/L (95% CI: -2.57-10.69, P = 0.01), and the WMD for serum ferritin (SF) was 9.47 μg/L (95% CI: -0.50-19.43, P < 0.0001). Results were heterogeneous for all comparisons.
CONCLUSION: This meta-analysis on observational studies suggests an association between H. pylori and IDA. In RCTs, eradication of H. pylori can improve HB and SF levels but not significantly.
TL;DR: Current therapeutic approaches include conservative management, endoscopic management, and operative management (open or laparoscopic approach), which are mainly based on patients' clinical grounds and their underlying colorectal diseases.
Abstract: This review discusses the incidence, risk factors, management and outcome of colonoscopic perforation (CP). The incidence of CP ranges from 0.016% to 0.2% following diagnostic colonoscopies and could be up to 5% following some colonoscopic interventions. The perforations are frequently related to therapeutic colonoscopies and are associated with patients of advanced age or with multiple comorbidities. Management of CP is mainly based on patients' clinical grounds and their underlying colorectal diseases. Current therapeutic approaches include conservative management (bowel rest plus the administration of broad-spectrum antibiotics), endoscopic management, and operative management (open or laparoscopic approach). The applications of each treatment are discussed. Overall outcomes of patients with CP are also addressed.
TL;DR: Local excision (polypectomy or endoscopic submucosal dissection or conventional endoscopic mucosal resection) is considered the definitive treatment for malignant colorectal polyps.
Abstract: Nowadays, the number of cases in which malignant colorectal polyps are removed is increasing due to colorectal cancer screening programmes. Cancerous polyps are classified into non-invasive high grade neoplasia (NHGN), when the cancer has not reached the muscularis mucosa, and malignant polyps, classed as T1, when they have invaded the submucosa. NHGN is considered cured with polypectomy, while the prognosis for malignant polyps depends on various morphological and histological factors. The prognostic factors include, sessile or pedunculated morphology of the polyp, whether partial or en bloc resection is carried out, the degree of differentiation of the carcinoma, vascular or lymphatic involvement, and whether the polypectomy resection margin is tumor free. A malignant polyp at T1 is considered cured with polypectomy if it is a pedunculated polyp (Ip of the Paris classification), it has been completely resected, it is not poorly differentiated, the resection edge is not affected by the tumor and there is no vascular or lymphatic involvement. The sessile malignant polyp (Is of the Paris classification) at T1 is considered not cured with polypectomy. Only in some cases (e.g. older people with high surgical risk) local excision (polypectomy or endoscopic submucosal dissection or conventional endoscopic mucosal resection) is considered the definitive treatment.
TL;DR: Coexisting steatohepatitis markedly increases LS in patients with ALD independent of fibrosis stage, and postponing cirrhosis assessment by FS during alcohol withdrawal until GOT decreases to < 100 U/mL significantly improves the diagnostic accuracy.
Abstract: AIM: To test if inflammation also interferes with liver stiffness (LS) assessment in alcoholic liver disease (ALD) and to provide a clinical algorithm for reliable fibrosis assessment in ALD by FibroScan® (FS).
METHODS: We first performed sequential LS analysis before and after normalization of serum transaminases in a learning cohort of 50 patients with ALD admitted for alcohol detoxification. LS decreased in almost all patients within a mean observation interval of 5.3 d. Six patients (12%) would have been misdiagnosed with F3 and F4 fibrosis but LS decreased below critical cut-off values of 8 and 12.5 kPa after normalization of transaminases.
RESULTS: Of the serum transaminases, the decrease in LS correlated best with the decrease in glutamic oxaloacetic transaminase (GOT). No significant changes in LS were observed below GOT levels of 100 U/L. After establishing the association between LS and GOT levels, we applied the rule of GOT 100 U/L at the time of LS assessment from this cohort, the area under the receiver operating characteristic (AUROC) for cirrhosis detection by FS improved from 0.921 to 0.945 while specificity increased from 80% to 90% at a sensitivity of 96%. A similar AUROC could be obtained for lower F3 fibrosis stage if LS measurements were restricted to patients with GOT < 50 U/L. Histological grading of inflammation did not further improve the diagnostic accuracy of LS.
CONCLUSION: Coexisting steatohepatitis markedly increases LS in patients with ALD independent of fibrosis stage. Postponing cirrhosis assessment by FS during alcohol withdrawal until GOT decreases to < 100 U/mL significantly improves the diagnostic accuracy.
TL;DR: Chronic alcohol use impairs not only gut and liver functions, but also multi-organ interactions, leading to persistent systemic inflammation and ultimately, to organ damage.
Abstract: Chronic inflammation is often associated with alcohol-related medical conditions. The key inducer of such inflammation, and also the best understood, is gut microflora-derived lipopolysaccharide (LPS). Alcohol can significantly increase the translocation of LPS from the gut. In healthy individuals, the adverse effects of LPS are kept in check by the actions and interactions of multiple organs. The liver plays a central role in detoxifying LPS and producing a balanced cytokine milieu. The central nervous system contributes to anti-inflammatory regulation through neuroimmunoendocrine actions. Chronic alcohol use impairs not only gut and liver functions, but also multi-organ interactions, leading to persistent systemic inflammation and ultimately, to organ damage. The study of these interactions may provide potential new targets for therapeutic intervention.
TL;DR: i-scan technology is the newly developed image-enhanced endoscopy technology from PENTAX, Japan that leads us to easier detection, diagnosis and treatment of gastrointestinal diseases.
Abstract: i-scan technology is the newly developed image-enhanced endoscopy technology from PENTAX, Japan. This consists of three types of algorithms: surface enhancement (SE), contrast enhancement (CE), and tone enhancement (TE). SE enhances light-dark contrast by obtaining luminance intensity data for each pixel and applying an algorithm that allows detailed observation of a mucosal surface structure. CE digitally adds blue color in relatively dark areas, by obtaining luminance intensity data for each pixel and applying an algorithm that allows detailed observation of subtle irregularities around the surface. Both enhancement functions work in real time without impairing the original color of the organ, therefore, SE and CE are suitable for screening endoscopy to detect gastrointestinal tumors at an early stage. TE dissects and analyzes the individual RGB components of a normal image. The algorithm then alters the color frequencies of each component and recombines the components to a single, new color image. This is designed to enhance minute mucosal structures and subtle changes in color. TE works in real time and consists of three modes such as TE-g for gastric tumors, TE-c for colonic tumors, and TE-e for esophageal tumors. TE is suitable mainly for detailed examination of the lesions that are detected in a screening endoscopy. i-scan technology leads us to easier detection, diagnosis and treatment of gastrointestinal diseases.
TL;DR: Bacteria seemingly affecting the symptom scores are unlikely to be the underlying cause or cure of IBS, but they may serve as biomarkers of the condition.
Abstract: CONCLUSION: Bacteria seemingly affecting the symptom scores are unlikely to be the underlying cause or cure of IBS, but they may serve as biomarkers of the condition.
TL;DR: SVD was highly effective in preventing relapse in CD and showed significant prevention in the time to relapse compared to that in the omnivorous group.
Abstract: AIM: To investigate whether semi-vegetarian diet (SVD) has a preventive effect against relapse of Crohn’s disease (CD) in patients who have achieved remission, who are a high-risk group for relapse.
METHODS: A prospective, single center, 2-year clinical trial was conducted. Twenty-two adult CD patients who achieved clinical remission either medically (n = 17) or surgically (n = 5) and consumed an SVD during hospitalization were advised to continue with an SVD and avoid known high-risk foods for inflammatory bowel disease. The primary endpoint was clinical relapse defined as the appearance of active symptoms of CD. Kaplan-Meier survival analysis was used to calculate the cumulative proportion of patients who had a relapse. A 2-year analysis of relapse rates of patients who followed an SVD and those who did not (an omnivorous diet group) was undertaken.
RESULTS: SVD was continued by 16 patients (compliance 73%). Remission was maintained in 15 of 16 patients (94%) in the SVD group vs two of six (33%) in the omnivorous group. Remission rate with SVD was 100% at 1 year and 92% at 2 years. SVD showed significant prevention in the time to relapse compared to that in the omnivorous group (P = 0.0003, log rank test). The concentration of C-reactive protein was normal at the final visit in more than half of the patients in remission who were taking an SVD, who maintained remission during the study (9/15; 60%), who terminated follow-up (8/12; 67%), and who completed 2 years follow-up (7/10; 70%). There was no untoward effect of SVD.
CONCLUSION: SVD was highly effective in preventing relapse in CD.
TL;DR: This review will focus on other biomarkers that seem to improve HCC diagnosis, such as AFP-L3, des-gamma-carboxyprothrombin, alpha-l-fucosidase, gamma-glutamyl transferase, glypican-3, squamous cell carcinoma antigen, a new generation of immunoglobulin M-immunocomplexes, and very promising gene-expression profiling.
Abstract: Hepatocellular carcinoma (HCC) represents the fifth most common cancer in the world, and the third most frequent oncological cause of death. The incidence of HCC is on the increase. HCC typically develops in patients with chronic liver diseases, and cirrhosis, usually with viral etiology, is the strongest predisposing factor. Nowadays HCC diagnosis is a multistage process including clinical, laboratory, imaging and pathological examinations. The prognosis of HCC is mostly poor, because of detection at an advanced, non-resectable stage. Potentially curative treatment (surgery) is limited and really possible only for cases with small HCC malignancies. For this reason, more effective surveillance strategies should be used to screen for early occurrence of HCC targeted to the population at risk. So far, the generally accepted serological marker is alpha-fetoprotein (AFP). Its diagnostic accuracy is unsatisfactory and questionable because of low sensitivity, therefore there is a strong demand by clinicians for new HCC-specific biomarkers. In this review, we will focus on other biomarkers that seem to improve HCC diagnosis, such as AFP-L3, des-gamma-carboxyprothrombin, alpha-l-fucosidase, gamma-glutamyl transferase, glypican-3, squamous cell carcinoma antigen, a new generation of immunoglobulin M-immunocomplexes, and very promising gene-expression profiling.
TL;DR: The etiology of inflammatory bowel disease (IBD) is not yet known, but many factors such as defects in the immune system, oxidative stress, microbial content in the gastrointestinal tract, nuclear factor (NF)-κB, nitric oxide (NO), cyclooxygenase-2 (Cox-2), and leukotriene B4 (LB4) are thought to play a role in its pathogenesis as discussed by the authors.
Abstract: The etiology of inflammatory bowel disease (IBD) is not yet known, but many factors such as defects in the immune system, oxidative stress, microbial content in the gastrointestinal tract, nuclear factor (NF)-κB, nitric oxide (NO), cyclooxygenase-2 (Cox-2), and leukotriene B4 (LB4) are thought to play a role in its pathogenesis. In traditional Iranian medicine (TIM), several medicinal plants are thought to be effective for the treatment of IBD. In this study, information on all of these remedies were derived from all available old sources such as documents or notes and books and were added to the information derived from modern medical databases covering all in vitro, in vivo and clinical trials. For some of these plants, only one or two mechanisms of action have been found such as in Cassia fistula, Lepidium sativum, and Bunium persicum. However, for some plants various mechanisms of action are known. For example, Commiphora mukul is effective in IBD due to its immunomodulatory, antioxidant, and antibacterial properties and it decreases NF-κB, NO and Cox-2. Another herb, Plantago ovata, has immunomodulatory, antioxidant, anti-inflammatory and wound healing activities and decreases NO and LB4. Considering the mechanisms of action of these plants, the combination of some of them may be useful because of their many mechanisms of action such as Pistacia lentiscus, Bunium persicum, Solanum nigrum, Plantago ovata, Boswellia, Solanum nigrum, Plantago ovata and Commiphora mukul. For some of the herbal products used in TIM such as oleogum resin from Commiphora myrrha, seeds of Ocimum basilicum, seeds of Linum usitatissimum, gum resin of Dracaena cinnabari, seeds of Plantago major, seeds of Lallementia royleana, and seeds of Allium porrum, there is no or not enough studies to confirm their benefits in IBD. It is suggested that an evaluation of the effects of these plants on different aspects of IBD should be performed.
TL;DR: In this article, a comparison of different nutritional assessments in detecting malnutrition among gastric cancer patients was made, and the results showed that the assessment was effective in detecting malignancy.
Abstract: Comparison of different nutritional assessments in detecting malnutrition among gastric cancer patients
TL;DR: This review emphasizes some hard facts about soft drinks, reviews fructose metabolism, and explains how fructose contributes to the development of obesity, diabetes, metabolic syndrome, and NAFLD.
Abstract: Nonalcoholic fatty liver disease (NAFLD) is a common clinical condition which is associated with metabolic syndrome in 70% of cases. Inappropriate dietary fat intake, excessive intake of soft drinks, insulin resistance and increased oxidative stress combine to increase free fatty acid delivery to the liver, and increased hepatic triglyceride accumulation contributes to fatty liver. Regular soft drinks have high fructose corn syrup which contains basic sugar building blocks, fructose 55% and glucose 45%. Soft drinks are the leading source of added sugar worldwide, and have been linked to obesity, diabetes, and metabolic syndrome. The consumption of soft drinks can increase the prevalence of NAFLD independently of metabolic syndrome. During regular soft drinks consumption, fat accumulates in the liver by the primary effect of fructose which increases lipogenesis, and in the case of diet soft drinks, by the additional contribution of aspartame sweetener and caramel colorant which are rich in advanced glycation end products that potentially increase insulin resistance and inflammation. This review emphasizes some hard facts about soft drinks, reviews fructose metabolism, and explains how fructose contributes to the development of obesity, diabetes, metabolic syndrome, and NAFLD.
TL;DR: La1, but not BB536, adheres to the colonic mucosa, and affects intestinal microbiota by reducing the concentration of pathogens and modulates local immunity.
Abstract: AIM: To investigate whether probiotic bacteria, given perioperatively, might adhere to the colonic mucosa, reduce concentration of pathogens in stools, and modulate the local immune function
METHODS: A randomized, double-blind clinical trial was carried out in 31 subjects undergoing elective colorectal resection for cancer Patients were allocated to receive either a placebo (group A, n = 10), or a dose of 107 of a mixture of Bifidobacterium longum (BB536) and Lactobacillus johnsonii (La1) (group B, n = 11), or the same mixture at a concentration of 109 (group C, n = 10) Probiotics, or a placebo, were given orally 2 doses/d for 3 d before operation The same treatment continued postoperatively from day two to day four Stools were collected before treatment, during surgery (day 0) and 5 d after operation During the operation, colonic mucosa samples were harvested to evaluate bacterial adherence and to assess the phenotype of dendritic cells (DCs) and lymphocyte subsets by surface antigen expression (flow cytometry) The presence of BB536 and La1 was evaluated by the random amplified polymorphism DNA method with specific polymerase chain reaction probes
RESULTS: The three groups were balanced for baseline and surgical parameters BB536 was never found at any time-points studied At day 0, La1 was present in 6/10 (60%) patients in either stools or by biopsy in group C, in 3/11 (272%) in group B, and none in the placebo group (P = 002, C vs A) There was a linear correlation between dose given and number of adherent La1 (P = 001) The rate of mucosal colonization by enterobacteriacae was 30% (3/10) in C, 818% (9/11) in B and 70% (7/10) in A (P = 003, C vs B) The Enterobacteriacae count in stools was 24 (log10 scale) in C, 46 in B, and 45 in A (P = 007, C vs A and B) The same trend was observed for colonizing enterococci La1 was not found at day +5 We observed greater expression of CD3, CD4, CD8, and naive and memory lymphocyte subsets in group C than in group A with a dose response trend (C > B > A) Treatment didnot affect DC phenotype or activation, but after ex vivo stimulation with lipopolysaccharides, groups C and B had a lower proliferation rate compared to group A (P = 004) Moreover, dendritic phenotypes CD83-123, CD83-HLADR, and CD83-11c (markers of activation) were significantly less expressed in patients colonized with La1 (P = 003 vs not colonized)
CONCLUSION: La1, but not BB536, adheres to the colonic mucosa, and affects intestinal microbiota by reducing the concentration of pathogens and modulates local immunity
TL;DR: This review highlights the various pathways that contribute to the development of hepatic steatosis and Circulating concentrations of inflammatory cytokines are reckoned to be the most important factor in causing and maintaining IR.
Abstract: Non-alcoholic fatty liver disease (NAFLD), a further expression of metabolic syndrome, strictly linked to obesity and diabetes mellitus, is characterized by insulin resistance (IR), elevated serum levels of free fatty acids and fatty infiltration of the liver, which is known as hepatic steatosis. Hepatocyte apoptosis is a key feature of this disease and correlates with its severity. Free-fatty-acid-induced toxicity represents one of mechanisms for the pathogenesis of NAFLD and hormones, growth factors and adipokines influence also play a key role. This review highlights the various pathways that contribute to the development of hepatic steatosis. Circulating concentrations of inflammatory cytokines are reckoned to be the most important factor in causing and maintaining IR. Low-grade chronic inflammation is fundamental in the progression of NAFLD toward higher risk cirrhotic states.