RESUMEN
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.
Asunto(s)
Colonoscopía , Escolaridad , Humanos , Masculino , Femenino , Austria/epidemiología , Persona de Mediana Edad , Anciano , Colonoscopía/estadística & datos numéricos , Estudios de Cohortes , Adulto , Factores de Riesgo , Modelos Logísticos , Diverticulosis del Colon/epidemiología , Divertículo del Colon/epidemiología , Síndrome Metabólico/epidemiología , Factores SexualesRESUMEN
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 PNPLA3G and 278 (16%) TM6SF2-T-alleles. MAFLD (PNPLA3G-allele: 46% vs. 41%, pâ¯= 0.041; TM6SF2T-allele: 54% vs. 42%, pâ¯< 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 PNPLA3G-allele carriers (10 vs. 8, pâ¯= 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 PNPLA3G-allele nor TM6SF2T-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.
RESUMEN
Objectives: The European Society of Cardiology endorsed SCORE2 to assess cardiovascular risk. The aim of this observational, retrospective study was to assess whether SCORE2 is associated with colorectal neoplasia in an asymptomatic screening population. Further, we evaluated if SCORE2 predicts tumor-related mortality. Methods: We included 3408 asymptomatic patients who underwent a screening colonoscopy. We calculated SCORE2 for each participant and stratified patients according to their predicted 10-year risk of cardiovascular disease: SCORE2 0−4.9%, SCORE2 5−9.9%, and SCORE2 ≥ 10%. We assessed the association between SCORE2 as a continuous variable, the presence of colorectal neoplasia using multilevel logistic regression, and SCORE2 and mortality using Cox regression. Results: In total, 1537 patients had a SCORE2 of 0−4.9%, 1235 a SCORE2 of 5−9.9%, and 636 a SCORE2 ≥ 10%. The respective rates of colorectal neoplasia were 20%, 37%, and 44%. SCORE2 was associated with the presence of any (OR 1.11 95%CI 1.09−1.12; p < 0.001) and advanced colorectal neoplasia (OR 1.06 95%CI 1.08−1.13; p < 0.001) in univariate analysis. After multivariable adjustment (age, sex, family history, and metabolic syndrome) a higher SCORE2 remained associated with higher odds for any (aOR 1.04 95%CI 1.02−1.06; p = 0.001) and advanced (aOR 1.06 95%CI 1.03−1.10; p < 0.001) colorectal neoplasia. SCORE2 was associated with both all-cause (HR 1.11 95%CI 1.09−1.14; p < 0.001) and tumor-related mortality (HR 1.10 95%CI 1.05−1.14; p < 0.001). Conclusions: We found that SCORE2 is associated with the presence of colorectal neoplasia. Clinicians could kill two birds with one stone calculating SCORE2. In patients with a high SCORE2, screening colonoscopy aside from cardiovascular risk mitigation could improve outcomes.
RESUMEN
BACKGROUND: Single nucleotide polymorphisms (SNPs) in genes including PNPLA3, TM6SF2, HSD17B13 and SERPINA1 have been identified as risk modifiers of progression in chronic liver disease (CLD). However, it is unclear whether genotyping for these risk variants is useful in clinical routine. METHODS: Liver disease severity was assessed by liver stiffness measurement (LSM) and by presence of clinical manifestations of advanced-chronic liver disease (ACLD) in 779 consecutive CLD patients at the time of referral to a tertiary center. The associations of risk variants with CLD severity were calculated individually and in a combined model using a polygenic risk-score. RESULTS: Non-alcoholic fatty liver disease (NAFLD) was the most common etiology (n = 511, 65.6%), and ACLD was present in 217 (27.9%) patients. The PNPLA3-G-allele remained independently associated with higher LSM (adjusted-B: 2.508 [95%CI: 0.887-4.130], P = 0.002) or the presence of ACLD (aOR: 1.562 [95%CI: 1.097-2.226], P = 0.013). SERPINA1-Z-allele was also independently associated with LSM (adjusted-B: 4.558 [95%CI: 1.182-7.934], P = 0.008), while the other risk alleles did not attain statistical significance. Combining these risk alleles into a polygenic risk-score was significantly associated with LSM (adjusted-B: 0.948 [95%CI: 0.153-1.743], P = 0.020). CONCLUSION: PNPLA3 risk-variants are linked to liver disease severity at the time of first referral to an outpatient hepatology clinic.
Asunto(s)
Aciltransferasas/genética , Hepatopatías/genética , Fosfolipasas A2 Calcio-Independiente/genética , Polimorfismo de Nucleótido Simple/genética , Índice de Severidad de la Enfermedad , 17-Hidroxiesteroide Deshidrogenasas/genética , Alelos , Enfermedad Crónica , Estudios Transversales , Femenino , Marcadores Genéticos/genética , Genotipo , Humanos , Hígado/patología , Masculino , Proteínas de la Membrana/genética , Persona de Mediana Edad , Enfermedad del Hígado Graso no Alcohólico/genética , Derivación y Consulta , Estudios Retrospectivos , Factores de Riesgo , alfa 1-Antitripsina/genéticaRESUMEN
CONTEXT: Recently, the novel metabolic dysfunction-associated fatty liver disease (MAFLD) definition has been introduced. OBJECTIVE: To assess the relevance of MAFLD for mortality. METHODS: Single-center cohort-study using colorectal cancer screening program involving 4718 subjects aged 45 to 80 who were grouped according to their body mass index (BMI) and the presence or absence of MAFLD. Mortality was compared among these groups by performing a systematic read-out of the national health insurance system, fatty liver (FL) was diagnosed using ultrasound. RESULTS: Overall prevalence of FL was 47.9%: 1200 (25.4%) patients were lean (BMIâ <â 25 kg/m2) and did not have MAFLD, 73 (1.5%) patients were lean and had nonalcoholic fatty liver disease but did not fulfill criteria for MAFLD, and 221 (4.7%) patients were lean and fulfilled criteria for MAFLD. Additionally, 1043 (22.1%) and 925 (19.6%) subjects had MAFLD with overweight (BMI 25-30 kg/m2) and obesity (BMIâ ≥â 30 kg/m2), respectively, while 1041 (22.1%) and 215 (4.6%) had overweight and obesity, respectively, without FL. During a median follow-up of 7.5 (interquartile range: 4.0-9.6) years, 278 deaths (5.9%) occurred. Of these, 98 (2.1%) were cancer-related, 65 (1.4%) were cardiovascular, and 17 (0.4%) were liver-related. Overall survival was similar between patient strata (after 5 years: 93.9%-98.2%) with lean MAFLD having the numerically worst survival. Although lean and overweight patients with MAFLD had a numerically worse outcome compared to their non-MAFLD counterparts, this association was driven by age and metabolic comorbidities (predominantly diabetes) rather than the presence of MAFLD. CONCLUSION: Presence of MAFLD does not increase mortality in a cohort of individuals aged 45 to 80 years.