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Background Quality of bowel cleansing in hospitalized patients undergoing colonoscopy is often unsatisfactory. No study has investigated the inpatient or outpatient setting as cause of inadequate cleansing. Aims To assess degree of bowel cleansing in inpatients and outpatients and to identify possible predictors of poor bowel preparation in the two populations. Methods Prospective multicentre study on consecutive colonoscopies in 25 regional endoscopy units. Univariate and multivariate analysis with odds ratio estimation were performed. Results Data from 3276 colonoscopies were analyzed (2178 outpatients, 1098 inpatients). Incomplete colonoscopy due to inadequate cleansing was recorded in 369 patients (11.2%). There was no significant difference in bowel cleansing rates between in- and outpatients in both colonic segments. In the overall population, independent predictors of inadequate cleansing both at the level of right and left colon were: male gender (odds ratio, 1.20 [1.02–1.43] and 1.27 [1.05–1.53]), diabetes mellitus (odds ratio, 2.35 [1.68–3.29] and 2.12 [1.47–3.05]), chronic constipation (odds ratio, 1.60 [1.30–1.97] and 1.55 [1.23–1.94]), incomplete purge intake (odds ratio, 2.36 [1.90–2.94] and 2.11 [1.68–2.65]) and a runway time >12 h (odds ratio, 3.36 [2.40–4.72] and 2.53 [1.74–3.67]). Conclusions We found no difference in the rate of inadequate bowel preparation between hospitalized patients and outpatients.

de Magistris, Alessio Fasano, Gabriele Riegler Background: Reaction to gluten can involve either an allergic (wheat allergy), or nonallergic [gluten sensitivity (GS)], or an autoimmune [celiac disease (CD)] mechanism. Recent evidences suggest that early changes in intestinal permeability (IP) may play a pivotal role in the pathogenesis of CD. Conversely, no data are available on the role of IP in the pathogenesis of GS. Aims: To investigate the changes in IP, TJ protein genes expression and TLRs in GS and to establish whether these changes are related to an over expression of inflammatory cytokines. Methods: After obtaining informed consent, biopsy samples were obtained from 17 GS patients (pts), 27 pts with active CD, 5 pts with CD in remission, and 11 healthy controls (age range: 5 years -50 years). Quantitative gene expression of TJ proteins Claudin (CL) 1, CL2, CL3, CL4, ZO-1 and of TLR1, TLR2 and TLR4 were performed by Real-time PCR. IP was evaluated by means of the lactulose/mannitol test (LA/MA). Cytofluorimetric analyses of IL6, IL8, TNFα, IFNγ were conducted on PBMC of all patients. Results: Expression of CL1, CL3 and CL4 were significantly increased in GS subjects compared to healthy controls, while no changes in CL2, ZO-1 and Occludin expression were detected. This up-regulation did not influence IP, since in GS patients IP (0.017±0.012) was similar to that detected in healthy controls (0.016±0.010). Conversely, in CD patients a significant over-expression of CL1 and CL2 was observed, while no significant changes in the other TJ proteins were detected. The increased expression of CL1/2 was associated to an increase in IP (0.202±0.55). In CD patients in remission both IP (0.014±0.004) and CL1/2 expression returned to normal levels. To evaluate if the innate immune system is involved in the pathogenesis of GS, TLRs expression was measured in a subgroup of patients. TLR1, but not TLR2 and TLR4, resulted significantly increased in CD (p=0,027) and in the GS (p=0,0039) respect to normal controls. Preliminary results showed that in GS patients up-regulation of CL was associated to increased expression of IL6 and IL8. Conclusions: Compared to CD patients, GS subjects showed normal IP and CL2 expression, while the other CL tested were up-regulated. These data suggest different pathogenic mechanisms in the two conditions, i.e., in GS loss of intestinal barrier function is not involved. The over expression of TLR 1 in CD and GS could suggest an important role of innate immune system in both conditions. Gluten Sensitivity appears to be a new chapter in the book of “Food intolerance” to be investigated.

Objectives: Intestinal permeability (IPT) was investigated in patients with autism as well as in their first-degree relatives to investigate leaky gut hypothesis. Faecal calprotectin (FC) was also measured in patients with autism, either with or without gastrointestinal symptoms, and in their firstdegree relatives. Patients and Methods: IPT results, assessed by means of the lactulose/ mannitol test, were compared with adult and child controls and with FC values. Results: A high percentage of abnormal IPT values were found among patients with autism (36.7%) and their relatives (21.2%) compared with normal subjects (4.8%). Patients with autism on a reported gluten-casein– free diet had significantly lower IPT values compared with those who were on an unrestricted diet and controls. Gastrointestinal symptoms were present in 46.7% of children with autism: constipation (45.5%), diarrhoea (34.1%), and others (alternating diarrhoea/constipation, abdominal pain, etc: 15.9%). FC was elevated in 24.4% of patients with autism and in 11.6% of their relatives; it was not, however, correlated with abnormal IPT values. Conclusions: The results obtained support the leaky gut hypothesis and indicate that measuring IPT could help to identify a subgroup of patients with autism who could benefit from a gluten-free diet. The IPT alterations found in first-degree relatives suggest the presence of an intestinal (tightjunction linked) hereditary factor in the families of subjects with autism.