Introduction: increasing evidence suggests a role of intestinal dysbiosis in obesity and non-alcoholic fatty liver disease (NAFLD). The advances in recent years with regard to the role of the gut microbiota raise the potential utility of new therapeutic approaches based on the modification of the microbiome. Objective: the aim of this study was to compare the bacterial communities in obese patients with or without NAFLD to those of healthy controls. Patients and methods: the fecal microbiota composition of 20 healthy adults, 36 obese patients with NAFLD and 17 obese patients without NAFLD was determined by 16S ribosomal RNA sequencing using the Illumina MiSeq system. Results: the results highlighted significant differences in the phylum Firmicutes between patients with and without NAFLD, which was a determining factor of the disease and supported its possible role as a marker of NAFLD. At the genus level, the relative abundance of Blautia, Alkaliphilus, Flavobacterium and Akkermansia was reduced in obese patients, both with or without NAFLD, compared to healthy controls. Furthermore, the number of sequences from the genus Streptococcus was significantly higher in patients with NAFLD in comparison with individuals without the disease, constituting another possible marker. Comparison of bacterial communities at the genus level by a principal coordinate analysis indicated that the bacterial communities of patients with NAFLD were dispersed and did not form a group. Conclusion: in conclusion, these results indicate the role of intestinal dysbiosis in the development of NAFLD associated with obesity. There was a differential microbiota profile between obese patients, with and without NAFLD. Thus, supporting gut microbiota modulation as a therapeutic alternative for the prevention and treatment of NAFLD.
Obesity is one of the main worldwide public health concerns whose clinical management demands new therapeutic approaches. Bariatric surgery is the most efficient treatment when other therapies have previously failed. Due to the role of gut microbiota in obesity development, the knowledge of the link between bariatric surgery and gut microbiota could elucidate new mechanistic approaches. This study aims to evaluate the long-term effects of bariatric surgery in the faecal metagenome and metabolome of patients with severe obesity. Faecal and blood samples were collected before and four years after the intervention from patients with severe obesity. Biochemical, metagenomic and metabolomic analyses were performed and faecal short-chain fatty acids were measured. Bariatric surgery improved the obesity-related status of patients and significantly reshaped gut microbiota composition. Moreover, this procedure was associated with a specific metabolome profile characterized by a reduction in energetic and amino acid metabolism. Acetate, butyrate and propionate showed a significant reduction with bariatric surgery. Finally, correlation analysis suggested the existence of a long-term compositional and functional gut microbiota profile associated with the intervention. In conclusion, bariatric surgery triggered long-lasting effects on gut microbiota composition and faecal metabolome that could be associated with the remission of obesity.
A safe and effective colorectal cancer (CRC) chemoprevention agent remains to be discovered. We aim to evaluate the association between the use of glucosamine and/or chondroitin sulphate and risk of colorectal cancer (CRC) in the MCC-Spain study, a case-control study performed in Spain that included 2140 cases of CRC and 3950 population controls. Subjects were interviewed on sociodemographic factors, lifestyle, family and medical history and regular drug use. Adjusted odds ratios and their 95% confidence intervals were estimated. The reported frequency of chondroitin and/or glucosamine use was 2.03% in controls and 0.89% in cases. Users had a reduced risk of CRC (OR: 0.47; 95% CI: 0.28–0.79), but it was no longer significant when adjusted for NSAID (nonsteroidal anti-inflammatory drugs) use (OR: 0.82; 95% CI: 0.47–1.40). A meta-analysis with previous studies suggested a protective effect, overall and stratified by NSAID use (OR: 0.77; 95% CI: 0.62–0.97). We have not found strong evidence of an independent preventive effect of CG on CRC in our population because the observed effects of our study could be attributed to NSAIDs concurrent use. These results merit further research due to the safety profile of these drugs.
Background: In Europe, acute hepatitis caused by the hepatitis E virus (HEV) traditionally was an infection found in people who had travelled to endemic zones, mainly Asia and Africa. However, a growing number of sporadic autochthonous cases are now being diagnosed in the Western world.Objective: To analyze the cases of acute HEV hepatitis diagnosed in our setting, with the identification of the clinicalepidemiological characteristics. Material and methods:We included the cases of acute HEV hepatitis diagnosed (positive anti-HEV IgM and/or HEV RNA present in serum) between January 2008 and December 2014. Different clinical, epidemiological and evolutive parameters were analyzed.Results: A total of 23 patients were identified, all originating from Spain. Fourteen cases (60.87%) presented jaundice and marked cytolysis at the time of diagnosis (aspartate aminotransferase [AST] 1,106.91 U/l and alanine aminotransferase [ALT] 1,407.04 U/l). Twenty-two cases were regarded as autochthonous, and one patient had travelled to China three months before. The mean time to resolution was 11.2 weeks. Some autoimmune markers were positive in 43.5% of the patients. Two subjects were diagnosed with previous chronic liver disease and were classified as "acuteon-chronic liver failure" (ACLF), one died and the other underwent liver transplantation.Conclusion: Acute HEV hepatitis in our setting is an autochthonous condition that is probably underdiagnosed, manifesting with jaundice and cytolysis. Autoimmune marker positivity is an epiphenomenon, which in some cases complicates the diagnosis.
Introduction: The only available effective treatment for celiac disease is strict and long-term compliance with a gluten-free diet. Dietary gluten restriction must be strict and long term, but is difficult to achieve in many cases and alternative dietary strategies have been investigated in the past few years.Areas covered: This review highlights the progress that has been made in the development of new therapeutics for CD. Detailed information of the evidence about the targets of the drugs related to their mechanisms of action is covered. The therapies are classified in five mechanisms: modification of gluten, intraluminal therapies, immunomodulation, intestinal permeability and modulation of adaptative response. The actual development phase and future approach are also described and discussed.Expert opinion: There are several limitations in each of the treatment targets related to their complications or the lack of complete response to normal gluten containing diet. The most desired therapy for celiac patients is the induction of gluten tolerance that would be curative.Therefore, it is expected that shortly, alternative or complementary tools for the treatment of gluten-free diet will be available to patients with celiac disease and will improve their quality of life.Gluten is a protein that is insoluble in both water and diluted salt solutions [9]. This protein triggers intestinal inflammation mediated by the human leucocyte antigen (HLA) system via HLA-DQ2 or DQ8 molecules. Intestinal inflammation may lead to the malabsorption of nutrients, as well as secondary iron deficiency (anemia) and osteoporosis.The only available effective treatment for CD is strict and long-term compliance with a glutenfree diet (GFD). Nonetheless, it has been shown that mucosal recovery can be lengthy.Moreover, 30%-50% of patients have persistent lesions in the intestinal mucosa and recurrent symptoms despite dietary gluten restriction (GFD-resistant CD or non-responsive CD) [10, 11].Gluten restriction requires extensive personal effort, which has psychological and social consequences and may limit full compliance [12,13]. Unintentional or deliberate noncompliance with GFD occurs in up to 50% of cases [14, 15]. In addition, approximately 1% of patients with celiac disease do not respond to GFD (refractory CD [RCD]). These patients are diagnosed mainly in adulthood after long-term exposure to gluten and are at risk of developing complications such as RCD type II (an intestinal lymphoma) or its more severe complication, enteropathy-associated T-cell lymphoma (EATL) [16, 17]. PATHOGENESIS OF CDCD develops in genetically predisposed individuals as an immune response to gluten present in certain grains (wheat, barley, and rye [18]). Although oats are considered safe for patients with CD, different oat varieties have distinct immunogenic potentials in patients with celiac disease based on the presence of toxic prolamines [19]. The immune system involves innate responses (caused by the direct toxic effects of gluten on the epithelium) and ...
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