Annals of hepatology最新文献

Introduction and objectives: This study aimed to explore the key genes involved in the pathophysiological process of liver fibrosis and develop a novel predictive model for noninvasive assessment of significant liver fibrosis patients.

Patients and methods: Differentially expressed genes (DEGs) were identified using the Limma package. The hub genes were explored using the CytoHubba plugin app and validated in GEO datasets and cell models. Furthermore, serum LTBP2 was measured in liver fibrosis (LF) patients with biopsy-proven by ELISA. All patients' clinical characteristics and laboratory results were analyzed. Finally, multivariate logistic regression analysis was used to construct the model for visualization by nomogram. Area under the receiver operating characteristic curve (AUROC) analysis, calibration curves, and decision curve analysis (DCA) certify the accuracy of the nomogram.

Results: RNA sequencing was performed on the liver tissues of 66 biopsy-proven HBV-LF patients. After multiple analyses and in vitro simulation of HSC activation, LTBP2 was found to be the most associated with HSC activation regardless of the causes. Serum LTBP2 expression was measured in 151 patients with biopsy, and LTBP2 was found to increase in parallel with the fibrosis stage. Multivariate logistic regression analysis showed that LTBP2, PLT and AST levels were demonstrated as the independent prediction factors. A nomogram that included the three factors was tabled to evaluate the probability of significant fibrosis occurrence. The AUROC of the nomogram model was 0.8690 in significant fibrosis diagnosis.

Conclusions: LTBP2 may be a new biomarker for liver fibrosis patients. The nomogram showed better diagnostic performance in patients.

Introduction and objectives: This study aimed to investigate the association between biological aging and liver fibrosis in patients with metabolic dysfunction-associated steatotic liver disease (MASLD).

Materials and methods: We analyzed NHANES 2017-2020 data to calculate phenotypic age. Hepatic steatosis and fibrosis were identified using controlled attenuation parameters (CAP), fatty liver index (FLI) and transient elastography (TE). The odds ratios (ORs) and 95 % confidence intervals (CI) for significant MASLD fibrosis were calculated using multivariate logistic regression, and subgroup analyses were performed. We explored the potential causal relationship between telomere length and liver fibrosis using Mendelian randomization (MR). Additionally, we used the expression quantitative trait loci (eQTL) method and GSE197112 data to identify genes related to liver fibrosis and senescence. Finally, the APOLD1 expression was validated using GSE89632.

Results: Phenotypic age was associated with liver fibrosis occurrence in MASLD (OR = 1.08, 95 % CI 1.05-1.12). Subgroup analyses by BMI and age revealed differences. For obese or young to middle-aged MASLD patients, phenotypic age is significantly associated with liver fibrosis. (OR = 1.14, 95 % CI 1.10-1.18; OR = 1.07, 95 % CI 1.01-1.14 and OR = 1.14, 95 % CI 1.07-1.22). MR revealed a negative association between telomere length and liver fibrosis (IVW method: OR = 0.63288, 95 % CI 0.42498-0.94249). The gene APOLD1 was identified as a potential target through the intersection of the GEO dataset and eQTL genes.

Conclusions: This study emphasized the link between biological aging and fibrosis in young to middle-aged obese MASLD patients. We introduced phenotypic age as a clinical indicator and identified APOLD1 as a potential therapeutic target.

Introduction and objectives: Public health policies in metabolic dysfunction-associated steatotic liver disease (MASLD) are still lacking. This study aims to estimate the prevalence and severity of MASLD in primary health care (PHC) through non-invasive markers.

Patients and methods: Two-phase study, including a retrospective (RETR) and a prospective (PROS) one, was carried out in PHC in Brazil. In RETR, metabolic and hepatic profiles of 12,054 patients, including FIB-4, were evaluated. In PROS, 350 patients were randomly selected and submitted to a clinical and nutritional assessment.

Results: RETR (65.4 % women, mean age 55.3 years old): dyslipidemia, hypertension, and type 2 diabetes mellitus (T2DM) present in 40.8 %, 34.3 %, and 12.2 % of the electronic health records, respectively. Fasting glucose >100 mg/dL in 34.5 %, and glycated hemoglobin higher than 5.7 % in 51.5 %, total cholesterol >200 mg/dL and triglycerides >150 mg/dL in 40.8 % and 32.1 %, respectively. Median FIB-4 was of 1.33, 5 % >2.67. No one had MASLD as a diagnostic hypothesis; PROS (71.8 % women, mean age 58 years old): body mass index (BMI) ≥30 kg/m² in 31.8 %. MASLD prevalence (FLI≥ 30 + cardiometabolic features) of 62.1 %; 39.4 % of patients had FLI ≥60, with higher BMI, waist circumference, fasting glucose, triglycerides, AST, ALT and GGT, as well as lower HDL-cholesterol (p < 0.001). FIB-4>1.3 in 40 % and NAFLD Fibrosis Score (NFS)>-1.45 in 59.2 % of steatotic patients.

Conclusions: There is a high prevalence of MASLD in PHC, with a significant risk of liver fibrosis. These findings reinforce we need to develop public policies to defeat MASLD epidemics.