Background:Although patients with active inflammatory bowel disease (IBD) change their dietary habits according to suggestions from their healthcare team, no restriction is required in the remission phase. Accordingly, we compared eating patterns in IBD patients with drug-induced clinical remission with those in healthy subjects.Methods:A total of 150 IBD patients, 84 with Crohn’s disease (CD) and 66 with ulcerative colitis (UC), in clinical remission, receiving immunomodulator/biologic therapy, and 100 healthy volunteers (controls) were enrolled. The IBD diagnosis had previously been established by a combined assessment of symptoms, endoscopy, histology and abdominal imaging. Clinical remission was defined as a Harvey Bradshaw index <5 for CD and a partial Mayo score <2 for UC. An experienced nutritionist guided the compilation of a food diary for 7 days according to current guidelines. Macronutrient and fiber intake was evaluated using dedicated software. Comparison between continuous variables was performed using Student’s t-test or analysis of variance plus Bonferroni post-hoc analysis. Categorical variables were tested with the χ2 test.Results:No difference in protein and carbohydrate intake was observed. IBD patients ate more calories (1970.7±348.4 vs. 1882.1±280.2 kcal/day, P=0.03), more lipids (68.9±15.2 vs. 59.4±19.0 g/day, P<0.001) and less fibers (11.9±4.7 vs. 15.5±8.3 g/day, P<0.001) than controls. No significant difference in total calories, proteins, lipids, carbohydrates or fibers was seen between CD and UC patients.Conclusion:IBD patients have a different macronutrient and fiber intake compared to healthy subjects, even when clinical remission and no symptoms do not dictate dietary restrictions. Therefore, psychological issues may be involved.

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A relevant percentage of non-erosive reflux disease (NERD) is refractory to proton pump inhibitors (PPIs) treatment. Multichannel intraluminal impedance pH (MII-pH) monitoring should give useful pathophysiological information about refractoriness. Therefore, our aim was to assess whether this technique could be useful to guide a 'tailored' therapy in refractory NERD. We retrospectively recruited NERD patients undergoing MII-pH monitoring for unsuccessful treatment. All patients had undergone upper endoscopy, and those with erosive esophagitis were excluded. No patient received PPI during MII-pH monitoring. Subjects were subgrouped into three categories: acid reflux, non-acid reflux and functional heartburn. MII-pH-guided therapy was performed for 4 weeks as follows: patients with acid reflux received PPI at double dose, patients with non-acid reflux PPI at full dose plus alginate four times a day and patients with functional heartburn levosulpiride 75 mg per day. A visual analog scale (VAS) ranging from 0 to 100 mm was administered before and after such tailored therapy to evaluate overall symptoms. Responders were defined by VAS improvement of at least 40%. Sixty-nine patients with refractory NERD were selected (female–male ratio 43 : 26, mean age 47.6±15.2 years). Overall effectiveness of tailored therapy was 84% without statistical difference among subgroups (88.5% acid reflux, 92% non-acid reflux, 66.6% functional heartburn; P=0.06). Univariate analysis showed that therapy failure directly correlated with functional heartburn diagnosis (OR=4.60) and suggested a trend toward a negative correlation with smoking and a positive one with nausea. However, at multivariate analysis, these parameters were not significant. Functional heartburn experienced a lower median percent VAS reduction than acid reflux (52.5% versus 66.6%, P<0.01) even if equal to non-acid reflux (66.6%). In conclusion, a tailored approach to refractory NERD, guided by MII-pH monitoring, demonstrated to be effective and should be promising to cure symptom persistence after conventional therapy failure. Nevertheless, standardized guidelines are advisable.

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Our experience suggests that gastric histology and close enquiry into any history of allergy may be useful diagnostic tools in cases of idiopathic gastroparesis.