Objective: Gut microbes and microbe-dependent metabolites (eg, tryptophan-kynurenine-serotonin pathway metabolites) have been linked to systemic inflammation, but the microbiota-metabolite-inflammation axis remains uncharacterised in children. Here we investigated whether gut microbiota features and circulating metabolites (both microbe-dependent and non-microbe-dependent metabolites) associated with circulating inflammation markers in children.
Methods: We studied children from the prospective Gen3G birth cohort who had data on untargeted plasma metabolome (n=321 children; Metabolon platform), gut microbiota (n=147; 16S rRNA sequencing), and inflammation markers (plasminogen activator inhibitor-1 (PAI-1), monocyte chemoattractant protein-1, and tumour necrosis factor-α) measured at 5-7 years. We examined associations of microbial taxa and metabolites-examining microbe-dependent and non-microbe-dependent metabolites separately-with each inflammatory marker and with an overall inflammation score (InfSc), adjusting for key confounders and correcting for multiple comparisons. We also compared the proportion of significantly associated microbe-dependent versus non-microbe-dependent metabolites, identified a priori (Human Microbial Metabolome Database), with each inflammation marker.
Results: Of 335 taxa tested, 149 were associated (qFDR<0.05) with at least one inflammatory marker; 10 of these were robust to pseudocount choice. Several bacterial taxa involved in tryptophan metabolism were associated with inflammation, including kynurenine-degrading Ruminococcus, which was inversely associated with all inflammation markers. Of 1037 metabolites tested, 315 were previously identified as microbe dependent and were more frequently associated with PAI-1 and the InfSc than non-microbe dependent metabolites. In total, 87 metabolites were associated (qFDR<0.05) with at least one inflammation marker, including kynurenine (positively), serotonin (positively), and tryptophan (inversely).
Conclusion: A distinct set of gut microbes and microbe-dependent metabolites, including those involved in the tryptophan-kynurenine-serotonin pathway, may be implicated in inflammatory pathways in childhood.
Introduction: Supporting patient self-care and the contribution of their caregivers is crucial in chronic illness care. Inflammatory bowel disease (IBD) is a chronic condition whose prevalence is expected to double, especially in Western countries. IBD symptoms can negatively impact patients' well-being, causing high anxiety, depression, stress and reduced quality of life. These symptoms also affect the health of family members and friends, who often take on caregiving roles during exacerbations. Knowledge about self-care in IBD (IBD-SELF) is limited, and few studies have explored this context. This paper outlines a research protocol for a multicentre longitudinal study to investigate patient self-care and caregiver contributions to IBD-SELF.
Methods and analysis: A sample of 250 consecutive patients diagnosed with IBD and their caregivers will be recruited from 9 dedicated IBD units in northern, central and southern Italy during outpatient visits. Data collection will occur at baseline, 6 and 12 months after enrolment. Multivariable regressions, path analyses and structural equation models will identify predictors (eg, health literacy, caregiver burden and depression) and outcomes (use of healthcare services, disease severity and quality of life) of self-care and caregiver contributions. Dyadic analyses will control for the interdependence of dyad members.
Ethics and dissemination: Ethical approval was obtained from the Territorial Ethics Committee (Lazio 3) N. 0023486/23 and registered on ClinicalTrials.gov (Identifier number: NCT06015789). This study will enhance our understanding of the self-care process in the patient-caregiver dyad in IBD, aiding the design of future educational interventions and promoting greater patient and caregiver involvement in the care pathway.
Trial registration number: ClinicalTrials.gov: NCT06015789.
Objective: Considerable disparities exist in access to gastrointestinal (GI) care and digestive outcomes across gender, racial, and socioeconomic groups. We evaluated (1) whether adults with chronic GI symptoms from diverse demographic groups would use a digital digestive care programme and (2) the effects of participation on GI symptom severity and other patient-reported outcomes.
Methods: Access to a digital digestive chronic care programme was provided to participants regardless of prior digestive diagnoses or symptoms for 90 days. The intervention included GI symptom tracking, personalised medical nutrition therapy, GI-specific health coaching, and targeted education on common GI symptoms. We assigned a Social Vulnerability Index (SVI) score to each participant according to their home address and compared baseline and end-intervention symptoms and other patient-reported outcomes by gender, race/ethnicity, and SVI.
Results: Of the 1936 participants, mean age was 43.1 years; 67% identified as white/Caucasian, 11% Asian/Pacific Islander, 6% Hispanic/Latinx, 7% black/African American, and 7% of multiple races. Participants of all demographic groups used the app symptom logging, reviewed educational materials, and interacted with their care team and reported similar statistically significant improvements in GI symptoms (by the end of the intervention, 85% improved, p<0.05). Participants reported feeling greater control of their health (83%), better able to manage their digestive symptoms (83%), increased happiness (76%), and greater productivity at work (54%), with black/African Americans and Native Americans most likely to report these changes.
Conclusion: We conclude that a digital GI disease management programme may be of value in reducing disparities in access to GI care.
Background: Oesophageal squamous cell carcinoma (OSCC) poses a considerable health burden, particularly in regions such as East Asia. This study aims to investigate the long-term outcomes of OSCC patients who are smokers and drinkers.
Materials and methods: In this retrospective analysis, data from Sichuan Cancer Hospital and Institute Esophageal Cancer Case Management Database between January 2010 and December 2017 were examined. Patients were categorised into different groups based on their smoking and alcohol consumption history: None, Smoker, Non-Smoker, Smoke-Only, Drinker, Non-Drinker, Drinker-Only, and Both. Survival outcomes were compared between the groups using Kaplan-Meier analysis and propensity score matching (PSM). The primary outcome was overall survival (OS), measured from surgery to death or last follow-up in April 2022.
Results: The OS median was 45.4 months for all patients after oesophagectomy. Smokers had a significantly lower median OS of 36.6 months compared with Non-Smokers with 66.2 months (p<0.001). Similarly, Drinkers had a lower median OS of 34.4 months compared with Non-Drinkers with 52.0 months (p<0.001). PSM analysis confirmed the significant differences in OS between Smokers and Non-Smokers (p=0.002) and between Drinkers and Non-Drinkers (p=0.002). Subgroup analyses showed no significant differences in OS between Group Another and Group Both, Group Smoker-Only and Group Drinker-Only, and Group Drinker-Only and Group Both. (figure 4) CONCLUSION: Smoking and drinking were associated with significantly reduced OS in patients. However, no significant differences were found between the subgroups of patients who only smoked, only drank, or engaged in both habits.
Background and aims: Gallstone disease affects ≥40 million people in the USA and accounts for health costs of ≥$4 billion a year. Risk factors such as obesity and metabolic syndrome are well established. However, data are limited on relevant metabolomic alterations that could offer mechanistic and predictive insights into gallstone disease. This study prospectively identifies and externally validates circulating prediagnostic metabolites associated with incident gallstone disease.
Methods: Female participants in Nurses' Health Study (NHS) and Nurses' Health Study II (NHS II) who were free of known gallstones (N=9960) were prospectively followed up after baseline metabolomic profiling with liquid chromatography-tandem mass spectrometry. Multivariable logistic regression and enrichment analysis were used to identify metabolites and metabolite groups associated with incident gallstone disease at PFDR<0.05. Findings were validated in 1866 female participants in the Women's Health Initiative and a comparative analysis was performed with 2178 male participants in the Health Professionals Follow-up Study.
Results: After multivariate adjustment for lifestyle and putative risk factors, we identified and externally validated 17 metabolites associated with incident gallstone disease in women-nine triacylglycerols (TAGs) and diacylglycerols (DAGs) were positively associated, while eight plasmalogens and cholesterol ester (CE) were negatively associated. Enrichment analysis in male and female cohorts revealed positive class associations with DAGs, TAGs (≤56 carbon atoms and ≤3 double bonds) and de novo TAG biosynthesis pathways, as well as inverse associations with CEs.
Conclusions: This study highlights several metabolites (TAGs, DAGs, plasmalogens and CE) that could be implicated in the aetiopathogenesis of gallstone disease and serve as clinically relevant markers.
Background and aims: The transition from compensated to decompensated cirrhosis is crucial, drastically reducing prognosis from a median survival of over 10 years to 2 years. There is currently an unmet need to accurately predict decompensation. We systematically reviewed and meta-analysed data regarding biomarker use to predict decompensation in individuals with compensated cirrhosis.
Methods: PubMed and EMBASE database searches were conducted for all studies from inception until February 2024. The study was carried out according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. The Quality of Prognosis Studies framework was used to assess the risk of bias. The meta-analysis was conducted with a random effects model using STATA software.
Results: Of the 652 studies initially identified, 63 studies (n=31 438 patients) were included in the final review, examining 49 biomarkers. 25 studies (40%) were prospective with the majority of studies looking at all-cause decompensation (90%). The most well-studied biomarkers were platelets (n=17), Model for End-Stage Liver Disease (n=17) and albumin (n=16). A meta-analysis revealed elevated international normalised ratio was the strongest predictor of decompensation, followed by decreased albumin. However, high statistical heterogeneity was noted (l2 result of 96.3%). Furthermore, 21 studies were assessed as having a low risk of bias (34%), 26 (41%) moderate risk and 16 (25%) high risk.
Conclusions: This review highlights key biomarkers that should potentially be incorporated into future scoring systems to predict decompensation. However, future biomarker studies should be conducted with rigorous and standardised methodology to ensure robust and comparable data.
Background: Helicobacter pylori (H. pylori) is a gram-negative gastrointestinal pathogen that colonises the human stomach and is considered a major risk factor for gastric cancer and mucosa-associated lymphoid tissue lymphoma. Furthermore, H. pylori is a potential trigger of a wide spectrum of extragastric cancer entities, extraintestinal chronic inflammatory processes and autoimmune diseases. In the present study, we evaluated the association between H. pylori infection and its eradication with the development of subsequent gastrointestinal and non-gastrointestinal cancer.
Methods: We identified 25 317 individuals with and 25 317 matched individuals without a diagnosis of H. pylori from the Disease Analyzer database (IQVIA). A subsequent cancer diagnosis was analysed using Kaplan-Meier and conditional Cox-regression analysis as a function of H. pylori and its eradication.
Results: After 10 years of follow-up, 12.8% of the H. pylori cohort and 11.8% of the non-H. pylori cohort were diagnosed with cancer (p=0.002). Results were confirmed in regression analysis (HR: 1.11; 95% CI 1.04 to 1.18). Moreover, a non-eradicated H. pylori status (HR: 1.18; 95% CI 1.07 to 1.30) but not an eradicated H. pylori status (HR: 1.06; 95% CI 0.97 to 1.15) was associated with a subsequent diagnosis of cancer. In subgroup analyses, H. pylori eradication was negatively associated with bronchus and lung cancer (HR: 0.60; 95% CI 0.44 to 0.83).
Conclusion: Our data from a large outpatient cohort in Germany reveal a distinct association between H. pylori infection and the subsequent development of cancer. These data might help to identify patients at risk and support eradication strategies in the future.
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