Nonalcoholic fatty liver disease is the most prevalent chronic liver disease in Western countries; it can progress to nonalcoholic steatohepatitis (NASH), cirrhosis and hepatocarcinoma. The importance of gut-liver-adipose tissue axis has become evident and treatments targeting gut microbiota may improve inflammatory and metabolic parameters in NASH patients. In a randomized, controlled clinical trial, involving 50 biopsy-proven NASH patients, we investigated the effects of synbiotic supplementation on metabolic parameters, hepatic steatosis, intestinal permeability, small intestinal bacterial overgrowth (SIBO) and lipopolysaccharide (LPS) serum levels. Patients were separated into two groups receiving Lactobacillus reuteri with guar gum and inulin for three months and healthy balanced nutritional counseling versus nutritional counseling alone. Before and after the intervention we assessed steatosis by magnetic resonance imaging, intestinal permeability by lactulose/mannitol urinary excretion and SIBO by glucose breath testing. NASH patients presented high gut permeability, but low prevalence of SIBO. After the intervention, only the synbiotic group presented a reduction in steatosis, lost weight, diminished BMI and waist circumference measurement. Synbiotic did not improve intestinal permeability or LPS levels. We concluded that synbiotic supplementation associated with nutritional counseling seems superior to nutritional counseling alone for NASH treatment as it attenuates steatosis and may help to achieve weight loss.

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This is a cross-sectional study that analyzed the pattern and frequency of articular and ophthalmologic manifestations in patients with Crohn's disease (CD) and ulcerative colitis (UC), with or without signs of active bowel inflammation. One hundred and thirty consecutive patients with CD (n = 71) and UC (n = 59) were examined. Simple X-rays of lumbar spine, sacroiliac joints, and calcaneal bone were performed and human leukocyte antigen (HLA)-B27 was typed. Joint manifestations occurred in 41 (31.5%) patients, 27 (38%) with CD and 14 (23.7%) with UC. Peripheral involvement occurred in 22 patients, axial involvement in five, and mixed involvement in 14. The most frequently involved joints were knees (56.1%), ankles (29.3%), and hips (29.3%), while the predominant pattern was oligoarticular (84.6%) and asymmetrical (65.6%). Enthesitis was identified in seven (5.4%) patients and inflammatory lumbar pain in 13 (10%). Eight of these patients fulfilled the diagnostic criteria for ankylosing spondylitis (6.2%). Radiographic sacroiliitis occurred in 12 patients (9.2%). Ocular abnormalities were present in six patients (6.2%), and HLA-B27 was positive in five (5.8%). In conclusion, the articular manifestations in the present study were predominantly oligoarticular and asymmetric, with a low frequency of ophthalmologic involvement and positive HLA-B27.

Although our results suggest an association between the presence of H. pylori in the intestine and ulcerative colitis-like phenotype of Crohn's disease, H. pylori infection in the actual causality of Crohn's disease is still to be determined.

In a search for Helicobacter species in the intestinal mucosae of 42 patients with ulcerative colitis (UC) and 74 without UC, only H. pylori was found. Although the bacterium was detected in UC patients by culture (7.1%) and nested PCR (19.0%), its presence was not associated with the disease (P ‫؍‬ 0.13).Ulcerative colitis (UC) is an inflammatory bowel disease (IBD) of unknown etiology that is confined to the large bowel mucosa. It seems to be a multifactorial disorder involving both genetic and environmental components, particularly the bacterial gut microbiota (13). However, no specific pathogenic or commensal bacterium has been convincingly implicated as the etiologic agent (4). Numerous studies have demonstrated that indigenous Helicobacter species of the gut of mice-Helicobacter hepaticus and Helicobacter bilis-are able to induce a persistent inflammation of the colon and cecum in some immunocompromised mouse models (1,5,8,15). Moreover, other Helicobacter species have been isolated from the gut of cottontop tamarins (14) and rhesus monkeys (7) with IBD-like disease. We hypothesize that species of the genus Helicobacter may also be associated with the pathogenesis of UC in human beings. Therefore, we investigated the presence of Helicobacter species in the intestinal mucosa of patients with UC and controls, by culture and PCR.We studied prospectively 42 patients with UC and 74 without IBD (controls) who were undergoing colonoscopy. Prior consent of all patients and approval of the institutional ethics committee were obtained. The UC diagnosis was established by standard clinic, radiologic, endoscopic, and histologic criteria. The extent of ulcerative colitis was determined by histology. The gastric H. pylori status was assessed by serology (Cobas-Core EIA; Roche Diagnostic Systems, Basel, Switzerland) (12) and 13 C urea breath test ( 13 C-UBT; NDIRIS; Wagner Analysen Technik, Bremen, Germany) (13). Patients' characteristics, including gastric H. pylori status, are shown in Table 1.Colonoscopic biopsy fragments were taken from the rectum, the sigmoid, descending, transverse, and ascending colon, the cecum, and the terminal ileum of each patient for culture and PCR. For culture, one fragment from each region was ground separately in a glass tissue grinder and plated onto Belo Horizonte medium (11) supplemented with polymyxin B plus bacitracin (Sigma Chemical Co., St. Louis, Mo.). The culture conditions and detailed characterization of the isolates were as previously described (10).DNA from bacteria and mucosal fragments was extracted with a QIAamp DNA minikit (Qiagen GmbH, Hilden, Germany).Primers C70 and B37 were used to amplify a product of ϳ1.5 kb from the 16S rRNA gene of the isolated strains (10). The amplicons were then purified and directly sequenced as described by Queiroz et al. (10). The sequences were aligned and compared with those in the GenBank database.For the detection of Helicobacter DNA in fragments of the intestinal mucosa, the 16S rRNA gene was amplified by nested PCR using an outer prime...