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Background and Objectives: Inflammatory bowel diseases are a main focus in current research, with diet being an emerging therapeutic line due to its links in both onset and progression. A Western-style diet high in processed foods, food additives, red meat, and animal fat has been linked to a higher risk of developing IBD. The aim of this study was to establish an association between an anti-inflammatory exclusion diet and maintenance of remission in IBD. Also, we assessed the efficacy and safety of this diet compared to a non-dietary group and the possible therapeutic effect of this diet in the maintenance of IBD remission. Materials and Methods: A total of 160 patients with IBD were screened for inclusion, but 21 did not met the inclusion criteria. Thus, 139 patients were assigned to either an exclusion diet or a regular diet according to their choice. Results: Clinical remission after six months was maintained in the exclusion diet arm (100%). In the control arm, four patients had clinically active disease (one patient with UC and three with CD), and 90 patients maintained the clinical remission state (95.7%) (p-value = 0.157). Regarding biochemical markers, ESR at baseline was higher in the exclusion diet arm: 29 (5–62) versus in the control arm 16 (4–48) (p-value = 0.019), but six months after, the groups were similar (p-value = 0.440). Conclusions: Patients who followed an exclusion diet maintained clinical remission more frequently. However, the threshold for statistical significance was not achieved. There was also a trend of improvement in inflammation tests in the intervention group. [ABSTRACT FROM AUTHOR]

Background & Aims: Celiac disease (CD) is characterized by an inappropriate T-cell-mediated response to gluten in small bowel in genetically predisposed individuals, carriers of the DQ2 and/or DQ8 haplotypes of the human leukocyte antigen (HLA). Our aim was to assess HLA typing in adult patients with CD, in their first-degree relatives and in a healthy control group. Methods: Our prospective observational study included three cohorts: 117 patients diagnosed with CD, 41 first-degree relatives of CD patients and 57 asymptomatic healthy volunteers. Low resolution HLA typing for DQ alleles was performed in all subjects with DNA extracted from peripheral blood, using SSP HLA-DQB1 kit (InnotrainDiagnostik GmbH, Germany). Next generation sequencing was used only in 18 patients for typing confirmation of DQB1 and DQA1 loci and whole gene sequencing. Results: Prevalence of HLA-DQ2 was significantly higher in the CD group compared to the healthy subjects group (95.6% vs 29.8%, p<0.001), with no statistically significant differences in HLA-DQ8 and combined HLA-DQ2/DQ8 prevalences. Several HLA DQA1 and DQB1 alleles (HLA-DQA1*05:01, HLA-DQB1*02:01, HLA-DQB1*02:02) and haplotypes (DQA1*02:01-DQB1*02:02,DQA1*05:01-DQB1*02:01) were strongly associated with CD in our group (OR 4.28, 4.28, 4.67 and 5.43 and 4.28 respectively). Screening adherence for first-degree relatives was very low: 16%. Familial screening diagnosed 4 cases of asymptomatic CD. 32 relatives (78%) had HLA-DQ2 haplotype, 5 carried HLA-DQ8, 4 did not carry any risk of a haplotype. Conclusions: This study demonstrated a higher prevalence of the HLA-DQ2 genotype in patients with CD compared to the healthy population but not of HLA-DQ8 or combined HLA-DQ2/DQ8. Alleles HLA-DQA1* 05:01, HLA-DQB1*02:01, HLA-DQB1*02:02 and haplotypes (DQA1*02:01-DQB1*02:02,DQA1*05:01-DQB1*02:01) were strongly associated with CD in our cohort. [ABSTRACT FROM AUTHOR]