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Background: Colorectal neoplasia and diverticulosis are common findings on colonoscopies. While adenomas are precursors to colorectal cancer, diverticulosis is usually asymptomatic but can lead to diverticulitis. Despite their prevalence and coexistence, the relationship between these conditions remains unclear. This study investigates whether diverticulosis is associated with adenomas, considering shared risk factors and potential inflammation-driven mechanisms. Methods: We examined 6154 asymptomatic individuals undergoing colorectal cancer screening in Austria. Diverticulosis and colorectal neoplasia were documented during screenings based on macroscopic definitions. Advanced neoplasia was defined as polyps >1 cm or high-grade dysplasia. Associations between diverticulosis and neoplastic findings were assessed using univariate and multivariable logistic regression models. Results: Although the overall incidence of any polypoid lesion was higher in the diverticulosis group (37% vs. 30%), statistical analysis revealed a comparable rate of advanced neoplasms in both groups. Importantly, no significant link between diverticulosis and advanced neoplasms was found (OR 1.125; 95% CI: 0.933 to 1.357, p = 0.218) even after adjusting for confounding factors. In a univariate analysis, a statistically significant association between diverticulosis and the presence of any colorectal polyps was identified (OR 1.388; 95% CI: 1.244-1.549, p < 0.0001). However, after adjusting for confounding factors in model 2 (OR 1.065, 95% CI: 0.942 to 1.204, p = 0.314) and model 3 (OR 1.071, 95% CI: 0.925 to 1.239, p = 0.360), this effect was also not statistically significant. Conclusions: Patients with diverticulosis share demographic and clinical features with those at risk of colorectal neoplasia, such as older age, male gender, and higher cardiometabolic risk. However, diverticulosis does not independently increase the risk of advanced colorectal neoplasia or unspecified polypoid lesions.

Background: The aim of this retrospective observational study was to examine the relationship between SCORE2 and the occurrence of colonic diverticula in a screening population without cardiovascular or gastrointestinal symptoms. SCORE2, recognized and supported by the European Society of Cardiology for cardiovascular risk assessment, served as the primary metric for the analysis in this investigation., Methods: We studied 3935 asymptomatic individuals undergoing screening colonoscopy. SCORE2 was calculated for each participant and categorized into three groups based on the following projected 10-year cardiovascular disease risk: SCORE2 0-4.9%, SCORE2 5-9.9%, and SCORE2 ≥ 10%. Logistic regression was used to assess the relationship between SCORE2 and diverticulosis., Results: SCORE2 was associated with the presence of diverticulosis (OR 1.09, 95%CI 1.07-1.10; p < 0.001) in univariable logistic regression, translating into an RR of 1.07 per unit increase. The association persisted after multivariable adjusting for metabolic syndrome (aOR 1.08; 95%CI 1.06-1.10; p < 0.001). Patients with high cardiovascular risk had higher rates of diverticulosis compared to those with lower risk: high risk (OR 2.00, 95%CI 1.71-2.33; p < 0.001); very high risk (OR 2.53, 95%CI 2.10-3.05; p < 0.001). This association remained after adjusting for metabolic syndrome: high risk (aOR 1.86, 95%CI 1.59-2.18; p < 0.001); very high risk (aOR 2.27, 95%CI 1.88-2.75; p < 0.001)., Conclusions: A higher SCORE2 was found to be a suitable screening parameter for diverticular disease. This suggests a potential link between cardiovascular risk factors and colon diverticula development, warranting further research on whether optimizing cardiovascular risk factors could positively influence diverticular disease.

Background: With the implementation of the 11th edition of the International Classification of Diseases (ICD-11) and the publication of the metabolic dysfunction-associated fatty liver disease (MAFLD) nomenclature in 2020, it is important to establish consensus for the coding of MAFLD in ICD-11. This will inform subsequent revisions of ICD-11., Methods: Using the Qualtrics XM and WJX platforms, questionnaires were sent online to MAFLD-ICD-11 coding collaborators, authors of papers, and relevant association members., Results: A total of 890 international experts in various fields from 61 countries responded to the survey. We also achieved full coverage of provincial-level administrative regions in China. 77.1% of respondents agreed that MAFLD should be represented in ICD-11 by updating NAFLD, with no significant regional differences (77.3% in Asia and 76.6% in non-Asia, p = 0.819). Over 80% of respondents agreed or somewhat agreed with the need to assign specific codes for progressive stages of MAFLD (i.e. steatohepatitis) (92.2%), MAFLD combined with comorbidities (84.1%), or MAFLD subtypes (i.e., lean, overweight/obese, and diabetic) (86.1%)., Conclusions: This global survey by a collaborative panel of clinical, coding, health management and policy experts, indicates agreement that MAFLD should be coded in ICD-11. The data serves as a foundation for corresponding adjustments in the ICD-11 revision., (© 2024. Asian Pacific Association for the Study of the Liver.)

Objective: Rheumatoid arthritis (RA) is recognized as a chronic autoimmune disorder with systemic inflammation and joint damage. Its potential role as a risk factor for cardiovascular diseases (CVD) is increasingly noted. This review delves into the causal relationship between RA and CVD, with Mendelian randomization (MR) offering a genetic perspective., Methods: An extensive search was conducted in PubMed, Cochrane and Web of Science to identify MR studies addressing the RA-CVD link. Out of 530 studies, 9 met the inclusion criteria, which were rigorously assessed using a critical appraisal checklist. These were further stratified by a sensitivity analysis into categories reflecting the strength of their evidence, from not evaluable to robust., Results: From the nine included studies, eight supported a causal association between RA and an increased risk of CVD, specifically coronary artery disease (CAD) and one did not support a link between RA and heart failure. The results suggest that genetic factors associated with RA may contribute to an elevated risk for CVD. Chronic inflammation, prevalent in RA, emerges as a key mediator in this connection., Conclusion: The systematic review corroborates a genetic causal link between RA and CVD, as evidenced by eight of the nine MR studies reviewed. This suggests a need for integrated cardiovascular risk management in the treatment of RA patients. The findings advocate considering anti-inflammatory treatment that can reduce cardiovascular risk. The overarching evidence signifies a potential direction for new therapeutic strategies aimed at enhancing cardiovascular health in RA patients., (© 2024. The Author(s).)

Background and Aims: Experimental studies linked dysfunctional Farnesoid X receptor (FXR)-fibroblast growth factor 19 (FGF19) signaling to liver disease. This study investigated key intersections of the FXR-FGF19 pathway along the gut-liver axis and their link to disease severity in patients with cirrhosis., Methods: Patients with cirrhosis undergoing hepatic venous pressure gradient measurement (cohort-I n = 107, including n = 53 with concomitant liver biopsy; n = 5 healthy controls) or colonoscopy with ileum biopsy (cohort-II n = 37; n = 6 controls) were included. Hepatic and intestinal gene expression reflecting FXR activation and intestinal barrier integrity was assessed. Systemic bile acid (BA) and FGF19 levels were measured., Results: Systemic BA and FGF19 levels correlated significantly (r = 0.461; p < 0.001) and increased with cirrhosis severity. Hepatic SHP expression decreased in patients with cirrhosis (vs. controls; p < 0.001), indicating reduced FXR activation in the liver. Systemic FGF19 (r = -0.512, p < 0.001) and BA (r = -0.487, p < 0.001) levels correlated negatively with hepatic CYP7A1, but not SHP or CYP8B1 expression, suggesting impaired feedback signaling in the liver. In the ileum, expression of FXR, SHP and FGF19 decreased in patients with cirrhosis, and interestingly, intestinal FGF19 expression was not linked to systemic FGF19 levels. Intestinal zonula occludens-1, occludin, and alpha-5-defensin expression in the ileum correlated with SHP and decreased in patients with decompensated cirrhosis as compared to controls., Conclusions: FXR-FGF19 signaling is dysregulated at essential molecular intersections along the gut-liver axis in patients with cirrhosis. Decreased FXR activation in the ileum mucosa was linked to reduced expression of intestinal barrier proteins. These human data call for further mechanistic research on interventions targeting the FXR-FGF19 pathway in patients with cirrhosis., Clinical Trial Number: NCT03267615., (© 2024. The Author(s).)

Background: H. pylori is a common bacterial infection that can cause gastritis, peptic ulcers, and cancer. The distribution of H. pylori infection is not uniform and can vary based on socio-economic factors. The aim of this study was to investigate the relationship between H. pylori infection and educational status in Central Europe. If the prevalence of H. pylori infection was found to be exceptionally high in one particular educational stratum, then systematic screening in this population group could be a sensible strategy., Methods: Participants were included from the Salzburg Colon Cancer Prevention Initiative (Sakkopi) cohort, consisting of 5313 asymptomatic Austrian patients. Clinical and laboratory parameters and the biopsy proven presence of H. pylori during an esophagoduodenoscopy were obtained, and patients' educational status was categorized into lower (38%), medium (54%), and higher (9%) education. Logistic regression models were fitted to evaluate the relationship between H. pylori infection and educational status., Results: Compared to patients with lower educational status (21%), patients with medium (17%) and higher (15%) educational status were less often infected with H. pylori (P<0.001). This association remained after adjustment for age, sex, and concomitant diagnosis of metabolic syndrome in multivariable logistic regression models. Sensitivity analysis showed lower odds for H. pylori infection with both medium and higher education in most strata., Conclusions: We discovered a statistically significant association between low educational status and an elevated risk for H. pylori infection. Nonetheless, the absolute difference is not enough to advocate for partially population-based screening in a specific education status group. As a result, we believe that the information linking low educational attainment to higher H. pylori prevalence should primarily be taken into account in clinical decision-making, but should not replace the existing testing approach for H. pylori, which is based on clinical reasoning and symptoms.

Background and Aims: Single-nucleotide-polymorphisms in PNPLA3-rs738409 and the TM6SF2-rs58542926, associated with metabolic-dysfunction-associated fatty liver disease (MAFLD), have been discussed as potentially protective for cardiovascular diseases. Therefore, we aimed to study the associations of PNPLA3/TM6SF2 variants with MAFLD and cardiovascular risk in a population-based sample of asymptomatic patients., Methods: The study cohort comprised 1742 patients of European decent aged 45-80 years from a registry study undergoing screening colonoscopy for colorectal cancer between 2010 and 2014. SCORE2 and Framingham risk score calculated to assess cardiovascular risk. Data on survival were obtained from the national death registry RESULTS: Half of included patients were male (52%, 59 ± 10 years), 819 (47%) carried PNPLA3‑G and 278 (16%) TM6SF2-T-alleles. MAFLD (PNPLA3‑G-allele: 46% vs. 41%, p = 0.041; TM6SF2‑T-allele: 54% vs. 42%, p < 0.001) was more frequent in patients harbouring risk alleles with both showing independent associations with MAFLD on multivariable binary logistic regression analysis. While median Framingham risk score was lower in PNPLA3‑G-allele carriers (10 vs. 8, p = 0.011), SCORE2 and established cardiovascular diseases were similar across carriers vs. non-carriers of the respective risk-alleles. During a median follow-up of 9.1 years, neither PNPLA3‑G-allele nor TM6SF2‑T-allele was associated with overall nor with cardiovascular mortality., Conclusion: Carriage of PNPLA3/TM6SF2 risk alleles could not be identified as significant factor for all-cause or cardiovascular mortality in asymptomatic middle-aged individuals undergoing screening colonoscopy., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Austria, part of Springer Nature.)

Introduction: The global burden of chronic diseases, including cardiovascular disease, remains a significant public health challenge. The Life's Simple 7 (LS7) score was developed as a tool to evaluate cardiovascular health behaviours and habits and identify high-risk individuals. The present study aimed to assess the distribution of LS7 scores among educational strata., Methods: The study population consisted of 3,383 asymptomatic individuals screened for colorectal cancer at a single centre in Austria. We split patients into lower (n = 1,055), medium (n = 1,997), and higher (n = 331) education, based on the International Standard Classification of Education (ISCED). Cox regression models were utilized to determine the association between education and mortality over a median follow-up period of 7 years., Results: Individuals with higher educational status had a significantly higher prevalence of ideal cardiovascular health metrics, as defined by the LS7 score, compared to those with medium and lower educational status: n = 94 (28%) vs. n = 347 (17%) and n = 84 (8%), respectively, (p < 0.001). In the Cox regression analysis, both medium (HR = 0.61, 95% CI: 0.43-0.84, p < 0.001) and higher educational status (HR = 0.44, 95% CI: 0.19-1.01, p = 0.06) were associated with all-cause mortality, as was the LS7., Conclusion: Our findings highlight a significant association between lower educational status and poorer cardiovascular health, as assessed by LS7, which persisted even after multivariable adjustment. Additionally, both educational status and LS7 were associated with increased mortality, underscoring the significance of our results. These findings have important implications for public health, as screening and prevention strategies may need to be tailored to meet the diverse educational backgrounds of individuals, given the higher prevalence of unhealthy lifestyle behaviours among those with lower educational status.

Excess free iron is a substrate for the formation of reactive oxygen species (ROS), thereby augmenting oxidative stress. Oxidative stress is a well-established cause of organ damage in the liver, the main site of iron storage. Ferroptosis, an iron-dependent mechanism of regulated cell death, has recently been gaining attention in the development of organ damage and the progression of liver disease. We therefore summarize the main mechanisms of iron metabolism, its close connection to oxidative stress and ferroptosis, and its particular relevance to disease mechanisms in metabolic-dysfunction-associated fatty liver disease and potential targets for therapy from a clinical perspective.

Background: Hyperferritinemia (HF) is a common finding and can be considered as metabolic HF (MHF) in combination with metabolic diseases. The definition of MHF was heterogenous until a consensus statement was published recently. Our aim was to apply the definition of MHF to provide data on the prevalence and characteristics of MHF in a Central-European cohort., Methods: This study was a retrospective analysis of the Paracelsus 10,000 study, a population-based cohort study from the region of Salzburg, Austria. We included 8408 participants, aged 40-77. Participants with HF were divided into three categories according to their level of HF and evaluated for metabolic co-morbidities defined by the proposed criteria for MHF., Results: HF was present in 13% (n = 1111) with a clear male preponderance (n = 771, 69% of HF). Within the HF group, 81% (n = 901) of subjects fulfilled the metabolic criteria and were defined as MHF, of which 75% (n = 674) were characterized by a major criterion. In the remaining HF cohort, 52% (n = 227 of 437) of subjects were classified as MHF after application of the minor criteria., Conclusion: HF is a common finding in the general middle-aged population and the majority of cases are classified as MHF. The new classification provides useful criteria for defining MHF.

Objective: Education often reflects socioeconomic status. Research indicates that lower socioeconomic status may increase the risk of diverticulosis, and according to data from the USA, diverticular disease is a significant and costly health problem. Our study explores the link between educational level and colonic diverticula occurrence., Subject and Methods: We conducted a cohort study on 5,532 asymptomatic Austrian patients who underwent colonoscopy, categorizing them by education level using the updated Generalized International Standard Classification of Education (GISCED). Logistic regression models, adjusting for age, gender, metabolic syndrome, diet, and activity, were used to determine the association between education and diverticulosis., Results: Overall, 39% of the patients had low educational status, while 53% had medium, and 8% had high educational status. Colon diverticula were less frequent in patients with medium (OR 0.73) and high (aOR 0.62) educational status. Medium educational level remained associated with lower rates of diverticulosis after adjustment for age and sex (aOR 0.85) and further metabolic syndrome, dietary habits, and physical activity (aOR 0.84). In higher education status, this phenomenon was only seen by trend., Conclusion: Low education correlated with higher colon diverticula risk, while medium education showed lower rates even after adjustments. This trend persisted at higher education levels, highlighting the potential for strategies for cost reduction tailored to socioeconomic conditions., (© 2024 The Author(s). Published by S. Karger AG, Basel.)