Intraduodenal lipids increase visceral sensitivity in both IBS-C and IBS-D; symptoms specificity in response to rectal distension is maintained in the postprandial period. Lipids may be responsible for the postprandial symptoms exacerbation in IBS.

No abstract

SUMMARYBackground: The resistance of Helicobacter pylori to antibiotics has been advocated as a major cause of treatment failure, and antimicrobial sensitivity testing has been proposed to improve efficacy; however, its role before firstline therapy has not been investigated in detail. Aim: To assess whether antimicrobial sensitivity testing improves the eradication rate of first-line anti-Helicobacter treatments and to compare the effectiveness of ranitidine bismuth citrate and omeprazole in the presence of H. pylori resistance to antibiotics. Methods: Two hundred and forty-two patients were assigned to either empirical or antimicrobial sensitivity testing-based treatment; within each group, subjects were further randomized to receive ranitidine bismuth citrate, 400 mg b.d., tinidazole, 500 mg b.d., and

Our observations seem to indicate that, although sharing a common hypersensitivity background, multiple mechanisms may modulate perceptual somatic and visceral responses in patients with IBS and FM.

In adult symptomatic patients showing EMA-positivity and genetic susceptibility, anti-tTG titers correlated with histology. ESPGHAN criteria performed similarly to previous studies. However, a calculated 16 × ULN cutoff showed an improved PPV. Among prevalent assays, PPV peaked differently both after normalization and standardization, indicating intrinsic differences in performance, thus preventing uniform prediction of disease in a real-life setting. Assay-specific optimal cutoffs seem possible, but would complicate diagnostic criteria. However, biopsy-sparing strategies in adults could prove useful in challenging patients.