BackgroundInflammatory bowel disease (IBD) is being increasingly diagnosed in Asia. However there are few epidemiological data from the region.MethodsTo determine prevalence and clinical characteristics of IBD, a hospital-based survey was performed in the Colombo and Gampaha districts (combined population 4.5 million) in Sri Lanka. Patients with established ulcerative colitis (UC) and Crohn's disease (CD), who were permanent residents of these adjoining districts, were recruited from hospital registries and out-patient clinics. Clinical information was obtained from medical records and patient interviews.ResultsThere were 295 cases of IBD (UC = 240, CD = 55), of which 34 (UC = 30, CD = 4) were newly diagnosed during the study year. The prevalence rate for UC was 5.3/100,000 (95% CI 5.0-5.6/100,000), and CD was 1.2/100,000 (95% CI 1.0-1.4/100,000). The incidence rates were 0.69/100,000 (95% CI 0.44-0.94/100,000) for UC and 0.09/100,000 (95% CI 0.002-0.18/100,000) for CD. Female:male ratios were 1.5 for UC and 1.0 for CD. Mean age at diagnosis was (males and females) 36.6 and 38.1y for UC and 33.4 and 36.2y for CD. Among UC patients, 51.1% had proctitis and at presentation 58.4% had mild disease. 80% of CD patients had only large bowel involvement. Few patients had undergone surgery.ConclusionsThe prevalence of IBD in this population was low compared to Western populations, but similar to some in Asia. There was a female preponderance for UC. UC was mainly mild, distal or left-sided, while CD mainly involved the large bowel.

Nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases and may progress to advanced hepatic fibrosis and cirrhosis in some patients. Cirrhosis due to NAFLD is considered extremely rare in children in the Asia-Pacific region. We report the characteristics of 5 children with advanced hepatic fibrosis and cirrhosis due to NAFLD. Four of them were obese, and all of them had high alanine transaminase levels and ultrasonographic evidence of fatty liver. None had diabetes mellitus or hyperlipidemia. The calculated HOMA-IR was more than two in all five cases. Liver biopsy showed stage III fibrosis in 2 patients and stage IV fibrosis (cirrhosis) in 3.

Background: Impaired gut barrier function has been reported in some functional gastrointestinal (GI) disorders. Evidences suggest that gut microbiota affects GI motility in particular Lactobacillus species elicits anti-inflammatory activity and exerts protective effects on damage induced by pathogen Gram negative-derived lipopolysaccharide (LPS). LPS produced an oxidative imbalance in human colonic smooth muscle cells (SMC) that persists after LPS-washout and contributes to SMC morphofunctional alterations. The aim was to evaluate if supernatants harvested from LGG cultures protect SMC from LPS-induced myogenic damage. Methods: L. rhamnosus GG (ATCC 53103 strain) was grown in MRS medium and samples were collected from bacterial cultures in middle exponential phase, in early, in middle and late stationary phase (overnight). Supernatants were recovered, filtered and stored at -20 8C. Highly pure human SMC culture was then exposed for 24 h to highly purified LPS (1 mg/ml) of E. coli (O111:B4) in the absence and presence of the supernatants. Their effects were evaluated on LPS-induced SMC morphofunctional alterations and pro-inflammatory IL-6 production. Data are expressed as mean AE SE (P < 0.05 significant). Results: LPS induced persistent significant 20.7% AE 1.2 cell shortening and 35.2% AE 2.6 decrease in contraction of human colonic SMC. These alterations were paralleled to a 238.5% AE 82.5% increase in IL-6 production. These effects disappeared in the presence of LGG-supernatants, following a progression related to LGG growth curve phases. Supernatants collected in the middle exponential phase already significantly partially restored LPS-induced cell shortening by 43.4% AE 10.2% and IL-6 increase by 47.6% AE 13.1%, but had no effect on LPS-induced inhibition of contraction. Supernatants collected later, in the early and middle stationary phase, further counteract LPS-induced damage, including inhibition of contraction. Maximal protective effects were observed with supernatants of the late stationary phase where LPS-induced cell shortening was reversed by 86% AE 4.7%, inhibition of contraction by 98.2% AE 1.8%, and IL-6 basal production by 91.3% AE 0.6%. Conclusions: LGG-secreted products are substances/byproducts able to directly protect human SMC from LPS-induced myogenic damage. Novel insights are then provided about the possibility that LGG-derived products could reduce the risk of progression to a post-infective motor disorder.

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