How IBD patients cope with IBD: A systematic review

AbstractObjectiveInflammatory bowel disease (IBD) can have a significant impact on psychological wellbeing and quality of life. How one responds to and copes with IBD may be an important determinant of psychological wellbeing. We aimed to systematically review all published literature regarding coping strategies of IBD patients.MethodsOvid and Pubmed databases were searched over 6months. All articles about coping strategies of IBD patients were included.ResultsThirty-nine articles using twenty-two survey instruments were found, of which twenty-six were adult exclusive, eleven were children exclusive, and two had both adults and children. Two were interventional, four were longitudinal, and the rest were cross-sectional studies. Four studies were qualitative while the rest used quantitative measures. Variance in research designs and coping instruments led to inconsistent results. The most common theme was that emotion-focused coping was associated with worse psychological outcomes, while the effect of problem-focused coping was less consistently associated with better psychological outcomes.ConclusionsMore longitudinal and interventional studies are needed to causally link coping strategies with psychological outcomes in IBD patient

Habitual Green Kiwifruit Consumption Is Associated with a Reduction in Upper Gastrointestinal Symptoms: A Systematic Scoping Review

Kiwifruit have known positive effects on digestion. During clinical intervention trials using kiwifruit to improve constipation, upper gastrointestinal (GI) symptoms such as abdominal discomfort and pain, indigestion, and reflux were also alleviated. We aimed to evaluate the evidence for upper GI symptom relief by kiwifruit in clinical trials on participants with functional constipation (FC), irritable bowel syndrome with constipation (IBS-C), and healthy participants, and to elucidate which symptoms may be relieved and whether a difference exists between the effects of gold and green kiwifruit. We executed a systematic scoping review of 3 electronic databases from 1947 through January 2021 to identify clinical trials that reported effects of green or gold kiwifruit or kiwifruit compounds on upper GI symptoms as secondary outcomes in healthy participants or participants with FC or IBS-C. Studies were divided into those using the Gastrointestinal Symptom Rating Scale (GSRS) and those using alternative measurement tools. GSRS outcomes were pooled and statistically analyzed; non-GSRS outcomes were summarized. We identified 12 clinical trials with a total of 661 participants (124 controls, 537 receiving intervention) providing evidence for symptom relief of upper GI symptoms by kiwifruit intake. Only 5 of the 12 clinical trials used the GSRS to assess upper GI symptom relief. We found good evidence that green kiwifruit may reduce abdominal discomfort and pain, and some evidence that kiwifruit consumption may attenuate indigestion. Pooled GSRS outcome analysis indicates an average reduction of -0.85 (95% CI: -1.1, -0.57; Z = 6.1) in abdominal pain scores and -0.33 (95% CI: -0.52, -0.15; Z = -3.5) in indigestion scores with habitual kiwifruit consumption. While the number of studies reporting on upper GI symptom relief with a comparable measurement is limited, there is consistent evidence for the efficacy of kiwifruit on upper GI symptom relief. More research to strengthen the evidence is recommended.Statement of Significance: This is the first review showing evidence that habitual consumption of kiwifruit may improve upper gastrointestinal symptoms such as abdominal pain and dyspepsia

Does Computerized Cognitive Behavioral Therapy Help People with Inflammatory Bowel Disease? : A Randomized Controlled Trial

BACKGROUND: Cognitive behavioral therapy may be useful for improving health-related quality of life (HRQOL) of at least some patients with inflammatory bowel disease (IBD), especially those with psychiatric comorbidities. However, cognitive behavioral therapy can be difficult to access. These difficulties can be overcome by computerized cognitive behavioral therapy (CCBT). This is a randomized controlled trial of a self-administered CCBT intervention for patients with IBD focused on improving HRQOL. It is hypothesized that CCBT completers will have an improved HRQOL relative to people not allocated to CCBT. METHODS: Patients with IBD were randomly allocated to CCBT (n = 113) versus treatment as usual (n = 86). The IBD Questionnaire at 12 weeks after baseline was the primary outcome, while generic HRQOL, anxiety, depression, coping strategies, perceived stress, and IBD symptoms were secondary outcomes. Outcomes were also measured at 6 months after baseline. Predictors of dropout were also determined. RESULTS: Twenty-nine CCBT participants (25.7%) completed the CCBT. The IBD Questionnaire was significantly increased at 12 weeks in CCBT completers compared with treatment-as-usual patients (F = 6.38, P = 0.01). Short Form-12 mental score (F = 5.00, P = 0.03) was also significantly better in CCBT compared with treatment-as-usual patients at 12 weeks. These outcomes were not maintained at 6 months. The predictors of dropout were baseline depression, biological use, lower IBD Questionnaire scores, and not having steroids. CONCLUSIONS: Improvements at 12 weeks after baseline were not maintained at 6 months. Future research should aim to improve adherence rates. Moreover, CCBT may not work for patients with IBD with comorbid depression

Consumption of kiwifruit capsules increases Faecalibacterium prausnitzii abundance in functionally constipated individuals: a randomised controlled human trial

This study investigated the impact of ACTAZIN™ green (2400 and 600 mg) and Livaux™ (2400 mg) gold kiwifruit supplements on faecal microbial composition and metabolites in healthy and functionally constipated (FC) participants. The participants were recruited into the healthy group (n 20; one of whom did not complete the study) and the FC group (n 9), each of whom consumed all the treatments and a placebo (isomalt) for 4 weeks in a randomised cross-over design interspersed with 2-week washout periods. Modification of faecal microbiota composition and metabolism was determined by 16S rRNA gene sequencing and GC, and colonic pH was calculated using SmartPill® wireless motility capsules. A total of thirty-two taxa were measured at greater than 1 % abundance in at least one sample, ten of which differed significantly between the baseline healthy and FC groups. Specifically, Bacteroidales and Roseburia spp. were significantly more abundant (P < 0·05) in the healthy group and taxa including Ruminococcaceae, Dorea spp. and Akkermansia spp. were significantly more abundant (P < 0·05) in the FC group. In the FC group, Faecalibacterium prausnitzii abundance significantly increased (P = 0·024) from 3·4 to 7·0 % following Livaux™ supplementation, with eight of the nine participants showing a net increase. Lower proportions of F. prausnitzii are often associated with gastrointestinal disorders. The discovery that Livaux™ supplementation increased F. prausnitzii abundance offers a potential strategy for improving gut microbiota composition, as F. prausnitzii is a butyrate producer and has also been shown to exert anti-inflammatory effects in many studies

Association of the HLA locus and TNF with type I autoimmune hepatitis susceptibility in New Zealand Caucasians

PURPOSE: The precise etiology of autoimmune hepatitis (AIH) remains unknown, although a number of genetic loci have been implicated in the susceptibility of type 1 AIH. The purpose of this study was to test for association of these loci with type 1 AIH in New Zealand Caucasians. METHODS: 77 AIH patients and 485 healthy controls were genotyped for the SNPs rs2187668 (HLA-DRB*03:01), rs660895 (HLA-DRB*04:01), rs3749971 (HLA-A1-B8-DR3), rs231775 (CLTLA4), rs1800629 (TNF), and rs1800682 (FAS) using predesigned TaqMan SNP genotyping assays. Chi square analysis was used to test for association of allele and genotype with overall AIH, and with severe fibrosis and ALT levels at 6 months. RESULTS: Significant risk of AIH was conferred by the minor alleles of rs2187668 (OR = 2.45, 95% CI 1.65-3.61, p < 0.0001), rs3749971 (OR = 1.89, 95% CI 1.21-2.94, p = 0.004) and rs1800629 (OR = 2.06, 95% CI 1.41-3.01, p = 0.0001). Multivariate analysis showed that rs2187668 was independently associated with type 1 AIH susceptibility (OR = 2.40, 95% CI 1.46-3.93, p = 0.001). The C allele of FAS SNP rs1800682 was associated with increased risk of severe fibrosis at diagnosis (OR = 2.03, 95% CI 1.05-3.93, p = 0.035) and with incomplete normalization of ALT levels at 6 months post-diagnosis (OR = 3.94, 95% CI 1.62-9.54, p = 0.0015). CONCLUSIONS: This is the first population-based study to investigate genetic risk loci for type 1 AIH in New Zealand Caucasians. We report significant independent association of HLA-DRB1*03:01 with overall susceptibility to type 1 AIH, as well as FAS with a more aggressive disease phenotype

Tumor Necrosis Factor Receptor Superfamily, Member 1B Haplotypes Increase or Decrease the Risk of Inflammatory Bowel Diseases in a New Zealand Caucasian Population

Inflammatory bowel diseases (IBDs) comprising Crohn disease (CD) and ulcerative colitis (UC) are chronic inflammatory conditions with polygenic susceptibility. Interactions between TNF-alpha and TNF-alpha receptor play a fundamental role in inflammatory response. This study investigates the role that selected single nucleotide polymorphisms (SNPs) and haplotypes in the TNF-alpha receptor (TNSFRSF1B) gene play in the risk of IBD in a New Zealand Caucasian population. DNA samples from 388 CD, 405 UC, 27 indeterminate colitis patients, and 293 randomly selected controls, from Canterbury, New Zealand were screened for 3 common SNPs in TNSFRSF1B: rs1061622 (c.676T > C), rs1061624 (c.*1663A > G), and rs3397 (c.*1690T > C), using TaqMan technologies. Carrying the rs1061624 variant decreased the risk of UC in the left colon (OR 0.73, 95% CI = 0.54–1.00) and of being a smoker at diagnosis (OR 0.62; 95% CI = 0.40–0.96). Carrying the rs3397 variant decreased the risk of penetrating CD (OR 0.62, 95% CI = 0.40–0.95). Three marker haplotype analyses revealed highly significant differences between CD patients and control subjects (χ2 = 29.9, df = 7, P = .0001) and UC cases and controls (χ2 = 46.3, df = 7, P < .0001). We conclude that carrying a 3-marker haplotype in the TNSFRSF1B gene may increase (e.g., haplotype of GGC was 2.9-fold more in the CD or UCpatients) or decrease (e.g., TGT was 0.47-fold less in UC patients) the risk of IBD in a New Zealand Caucasian population

Tumor Necrosis Factor Receptor Superfamily, Member 1B Haplotypes Increase or Decrease the Risk of Inflammatory Bowel Diseases in a New Zealand Caucasian Population

Inflammatory bowel diseases (IBDs) comprising Crohn disease (CD) and ulcerative colitis (UC) are chronic inflammatory conditions with polygenic susceptibility. Interactions between TNF-alpha and TNF-alpha receptor play a fundamental role in inflammatory response. This study investigates the role that selected single nucleotide polymorphisms (SNPs) and haplotypes in the TNF-alpha receptor (TNSFRSF1B) gene play in the risk of IBD in a New Zealand Caucasian population. DNA samples from 388 CD, 405 UC, 27 indeterminate colitis patients, and 293 randomly selected controls, from Canterbury, New Zealand were screened for 3 common SNPs in TNSFRSF1B: rs1061622 (c.676T > C), rs1061624 (c.*1663A > G), and rs3397 (c.*1690T > C), using TaqMan technologies. Carrying the rs1061624 variant decreased the risk of UC in the left colon (OR 0.73, 95% CI = 0.54–1.00) and of being a smoker at diagnosis (OR 0.62; 95% CI = 0.40–0.96). Carrying the rs3397 variant decreased the risk of penetrating CD (OR 0.62, 95% CI = 0.40–0.95). Three marker haplotype analyses revealed highly significant differences between CD patients and control subjects (χ2 = 29.9, df = 7, P = .0001) and UC cases and controls (χ2 = 46.3, df = 7, P < .0001). We conclude that carrying a 3-marker haplotype in the TNSFRSF1B gene may increase (e.g., haplotype of GGC was 2.9-fold more in the CD or UCpatients) or decrease (e.g., TGT was 0.47-fold less in UC patients) the risk of IBD in a New Zealand Caucasian population

Nucleotide-binding oligomerization domain containing 1 (NOD1) haplotypes and single nucleotide polymorphisms modify susceptibility to inflammatory bowel diseases in a New Zealand caucasian population: a case-control study

<p>Abstract</p> <p>Background</p> <p>The nucleotide-binding oligomerization domain containing 1 (<it>NOD1</it>) gene encodes a pattern recognition receptor that senses pathogens, leading to downstream responses characteristic of innate immunity. We investigated the role of <it>NOD1 </it>single nucleotide polymorphisms (SNPs) on IBD risk in a New Zealand Caucasian population, and studied Nod1 expression in response to bacterial invasion in the Caco2 cell line.</p> <p>Findings</p> <p>DNA samples from 388 Crohn's disease (CD), 405 ulcerative colitis (UC), 27 indeterminate colitis patients and 201 randomly selected controls, from Canterbury, New Zealand were screened for 3 common SNPs in <it>NOD1</it>, using the MassARRAY^®iPLEX Gold assay. Transcriptional activation of the protein produced by <it>NOD1 </it>(Nod1) was studied after infection of Caco2 cells with <it>Escherichia coli </it>LF82. Carrying the rs2075818 G allele decreased the risk of CD (OR = 0.66, 95% CI = 0.50–0.88, p < 0.002) but not UC. There was an increased frequency of the three SNP (rs2075818, rs2075822, rs2907748) haplotype, CTG (p = 0.004) and a decreased frequency of the GTG haplotype (p = 0.02).in CD. The rs2075822 CT or TT genotypes were at an increased frequency (genotype p value = 0.02), while the rs2907748 AA or AG genotypes showed decreased frequencies in UC (p = 0.04), but not in CD. Functional assays showed that Nod1 is produced 6 hours after bacterial invasion of the Caco2 cell line.</p> <p>Conclusion</p> <p>The <it>NOD1 </it>gene is important in signalling invasion of colonic cells by pathogenic bacteria, indicative of its' key role in innate immunity. Carrying specific SNPs in this gene significantly modifies the risk of CD and/or UC in a New Zealand Caucasian population.</p

Randomized, placebo controlled trial of experimental hookworm infection for improving gluten tolerance in Celiac disease

INTRODUCTION: Celiac disease is an autoimmune disorder where intestinal immunopathology arises after gluten consumption. Previous studies suggested that hookworm infection restores gluten tolerance; however, these studies were small (n = 12) and not placebo controlled. METHODS: We undertook a randomized, placebo-controlled trial of hookworm infection in 54 people with celiac disease. The 94-week study involved treatment with either 20 or 40 Necator americanus third-stage larvae (L3-20 or L3-40) or placebo, followed by escalating gluten consumption (50 mg/d for 12 weeks, 1 g intermittent twice weekly for 12 weeks, 2 g/d sustained for 6 weeks, liberal diet for 1 year). RESULTS: Successful study completion rates at week 42 (primary outcome) were similar in each group (placebo: 57%, L3-20: 37%, and L3-40: 44%; P = 0.61), however gluten-related adverse events were significantly reduced in hookworm-treated participants: Median (range) adverse events/participant were as follows: placebo, 4 (1–9); L3-20, 1 (0–9); and L3-40, 0 (0–3) (P = 0.019). Duodenal villous height:crypt depth deteriorated similarly compared with their enrolment values in each group (mean change [95% confidence interval]: placebo, −0.6 [−1.3 to 0.2]; L3-20, −0.5 [−0.8 to 0.2]; and L3-40, −1.1 [−1.8 to 0.4]; P = 0.12). A retrospective analysis revealed that 9 of the 40 L3-treated participants failed to establish hookworm infections. Although week 42 completion rates were similar in hookworm-positive vs hookworm-negative participants (48% vs 44%, P = 0.43), quality of life symptom scores were lower in hookworm-positive participants after intermittent gluten challenge (mean [95% confidence interval]: 38.9 [33.9–44] vs 45.9 [39.2–52.6]). DISCUSSION: Hookworm infection does not restore tolerance to sustained moderate consumption of gluten (2 g/d) but was associated with improved symptom scores after intermittent consumption of lower, intermittent gluten doses