Explore the vast range of titles available.

We aimed to compare the association of metabolic dysfunction‐associated fatty liver disease (MAFLD), metabolic dysfunction‐associated steatotic liver disease (MASLD), alcohol‐related liver disease (ALD), metabolic dysfunction and ALD (MetALD), and MASLD with viral hepatitis (MASLD‐Viral) with risks of cirrhosis, liver cancer, and mortality. The data of 464,556 adults from the UK Biobank (UKB), 13,526 adults from the National Health and Nutrition Examination Survey (NHANES), and 2554 adults from BeijngFH Health Cohort Study (FHCS) were included. Adjusted hazard ratios (aHR) and odds ratios were calculated using Cox and Logistic regression models, respectively. Compared with non‐SLD, the risk of liver cancer increased from MetALD (aHR 1.70 [95% CI 1.37, 2.09]), MASLD (1.91 [1.66, 2.21]), MAFLD (2.01 [1.76, 2.29]), ALD (3.16 [2.54, 3.93]), to MASLD‐Viral (22.0 [10.8, 44.4]) in a stepwise manner in the UKB; the risk of all‐cause mortality increased from MetALD, MASLD, MAFLD, ALD, to MASLD‐Viral in the NHANES. The odds ratio of liver fibrosis increased from MASLD, MAFLD, to MASLD‐Viral in the FHCS. In patients with diabetes, metformin plus other drugs were associated with higher risks of cirrhosis, liver cancer, and all‐cause mortality in MASLD or MAFLD. Prevention rather than antiglycemic treatment is important for patients with diabetic MASLD or MAFLD. This study analyzed the UK Biobank, NHANES III, and FHCS data to assess the prognostic and associative effects of new steatotic liver disease nomenclatures. It found that MAFLD, MASLD, and MetALD were associated with higher risks of liver‐related conditions and mortality, with diabetes and certain antiglycemic medications further heightening these risks .

Metabolic dysfunction‐associated steatotic liver disease (MASLD) has become the most prevalent chronic liver disease globally. Previous studies have shown that MASLD is an independent risk factor for chronic kidney disease (CKD), but the variations in estimated glomerular filtration rate (eGFR) levels across countries with different ethnic backgrounds have not been extensively reported. We enrolled 3308 participants with biopsy‐proven MASLD from 34 centers in this multinational study and analyzed the associations between eGFR and histological severity of liver fibrosis in different countries. European participants had lower eGFR levels (92.2 ± 20.7 vs. 104.7 ± 17.3 mL/min/1.73 m2) and significant liver fibrosis (61.4 vs. 32.4%) than Asian individuals. In Asia, Chinese participants had the highest mean eGFR level at 105.8 mL/min/1.73 m2, while Malaysian participants had the lowest at 87.3 mL/min/1.73 m2 (p < 0.001). In Europe, French participants had the highest mean eGFR level at 95.3 mL/min/1.73 m2, while Romanian individuals had the lowest at 81.1 mL/min/1.73 m2 (p < 0.001). eGFR levels were inversely associated with liver fibrosis in Asian individuals (OR: 0.793, 95%CI: 0.685–0.917, p = 0.002), even after adjusting for traditional renal risk factors, but not in Europeans. Our findings provide the basis for further investigation of the burden of MASLD on CKD risk in different countries. A total of 3308 participants with biopsy‐proven MASLD from 34 centers were enrolled in the study. We collected liver biopsy pathological scores and clinical parameters and conducted correlation analysis. We finally found that eGFR levels are inversely associated with liver fibrosis in Asians, even after adjusting for traditional renal risk factors.

The liver plays a central role in the pharmacokinetics of the majority of drugs. Liver dysfunction may not only reduce the blood/plasma clearance of drugs eliminated by hepatic metabolism or biliary excretion, it can also affect plasma protein binding, which in turn could influence the processes of distribution and elimination. Portal-systemic shunting, which is common in advanced liver cirrhosis, may substantially decrease the presystemic elimination (i.e., first-pass effect) of high extraction drugs following their oral administration, thus leading to a significant increase in the extent of absorption. Chronic liver diseases are associated with variable and non-uniform reductions in drug-metabolizing activities. For example, the activity of the various CYP450 enzymes seems to be differentially affected in patients with cirrhosis. Glucuronidation is often considered to be affected to a lesser extent than CYP450-mediated reactions in mild to moderate cirrhosis but can also be substantially impaired in patients with advanced cirrhosis. Patients with advanced cirrhosis often have impaired renal function and dose adjustment may, therefore, also be necessary for drugs eliminated by renal exctretion. In addition, patients with liver cirrhosis are more sensitive to the central adverse effects of opioid analgesics and the renal adverse effects of NSAIDs. In contrast, a decreased therapeutic effect has been noted in cirrhotic patients with β-adrenoceptor antagonists and certain diuretics. Unfortunately, there is no simple endogenous marker to predict hepatic function with respect to the elimination capacity of specific drugs. Several quantitative liver tests that measure the elimination of marker substrates such as galactose, sorbitol, antipyrine, caffeine, erythromycin, and midazolam, have been developed and evaluated, but no single test has gained widespread clinical use to adjust dosage regimens for drugs in patients with hepatic dysfunction. The semi-quantitative Child-Pugh score is frequently used to assess the severity of liver function impairment, but only offers the clinician rough guidance for dosage adjustment because it lacks the sensitivity to quantitate the specific ability of the liver to metabolize individual drugs. The recommendations of the Food and Drug Administration (FDA) and the European Medicines Evaluation Agency (EMEA) to study the effect of liver disease on the pharmacokinetics of drugs under development is clearly aimed at generating, if possible, specific dosage recommendations for patients with hepatic dysfunction. However, the limitations of the Child-Pugh score are acknowledged, and further research is needed to develop more sensitive liver function tests to guide drug dosage adjustment in patients with hepatic dysfunction.

Introduction Metabolic dysfunction‐associated steatotic liver disease (MASLD) has become the most common hepatic condition globally. The prevalence of MASLD continues to increase, paralleling the consistent rising rates of risk factors such as obesity and type 2 diabetes. Literature suggests that human immunodeficiency virus‐infected (HIV‐infected) individuals may have an increased risk of developing MASLD due to a complex interplay of factors including antiretroviral therapy. Since the development and widespread use of effective antiretroviral therapy (ART), HIV‐induced liver disease has continued to be the predominant cause of liver‐related morbidity and mortality. This protocol serves to narrate the methods that will be employed in conducting the published literature search for the systematic review and meta‐analysis which will report on the global prevalence of MASLD on people living with HIV and on ARV treatment. Methods The search of literature will be done using search engines or electronic databases including PubMed, Google Scholar, African Journal Online, and ResearchGate. Specific keywords will be used to search literature that has reported on the prevalence of MASLD among HIV patients receiving antiretroviral treatment, this will ensure the reproducibility of the study. Cross‐sectional and longitudinal observational studies, retrospective cohort studies, clinical trial studies, meta‐analyses, and systematic reviews that were published in the English language from 1990 to 2024 will be included. Animal studies will be excluded. Three independent reviewers will conduct the selection process and select studies that meet the eligibility criteria. A quality assessment tool, Downs and Blacks will be used to assess the risk of bias of the selected studies. A review manager will be used for meta‐analysis of collected data and the Grading of Recommendations Assessment, Development, and Evaluation tool will assess the strength of evidence. Ethics, dissemination, and registration The review will not require ethical clearance as it will only include data that is publicly available in published reports. The results of this review will be disseminated through publications. This study is registered with PROSPERO (CRD42024516814).

The revised fourth edition of Evidence-Based Gastroenterology and Hepatology continues to provide the most current, evidence-based information for determining the appropriate medical and surgical options for screening for, diagnosing, and treating gastrointestinal conditions.

Background Steatotic liver disease (SLD) was a newly proposed disease category derived from metabolic dysfunction-associated fatty liver disease (MAFLD). MAFLD and sarcopenia were independent risk factors for mortality. We aimed to evaluate the impacts of SLD subtypes, MAFLD, and sarcopenia on mortality. Methods A total of 6543 subjects were identified from the National Health and Nutrition Examination Survey 1999–2006 with the latest Linked Mortality file. Hepatic steatosis, advanced fibrosis, and sarcopenia were determined by the laboratory- and anthropometry- based fatty liver index and fibrosis-4 index, and dual-energy X-ray absorptiometry-based appendicular skeletal muscle mass index, respectively. Associations of SLD subtypes, MAFLD, and sarcopenia with mortality were estimated using the weighted Cox proportional hazards model. Results During a mean follow-up time of 15.7 years, 1567 (16.7%) deaths occurred including 494 (4.9%) deaths from cardiovascular diseases and 372 (4.1%) from cancer. The all-cause mortality rates of MAFLD, metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction and alcohol-associated liver disease (MetALD), other aetiology SLD, MASLD without sarcopenia, and MASLD with sarcopenia were 21.0%, 19.8%, 30.2%, 30.9%, 19.2%, and 75.5%, respectively. MAFLD increased the risk of all-cause mortality (hazard ratio [HR] 1.26, 95% confidence interval [CI] 1.00-1.59). MASLD predicted all-cause mortality (HR 1.17, 95% CI 1.03–1.33) but this prediction became insignificant after adjustment for metabolic risks. In contrast, MetALD and other aetiology SLD were significantly associated with all-cause mortality (HR 1.83, 95% CI 1.21–2.76; HR 2.50, 95% CI 1.82–3.44, respectively), predominantly associated with cancer-specific mortality (HR 2.42, 95% CI 1.23–4.74; HR 2.49, 95% CI 1.05–5.90, respectively). MASLD with sarcopenia increased the risk of all-cause mortality by almost twice (HR 2.19, 95% CI 1.37–3.49) and further coexisting advanced fibrosis additively increased mortality (HR 3.41, 95% CI 1.92–6.05). Conclusion SLD definition identified a more homogeneous group with metabolically hepatic steatosis at higher risks of mortality. MASLD or MASLD-related advanced fibrosis and sarcopenia additively increased mortality.

The aim of this study is to determine the effect of laser diode as an alternative treatment on liver dysfunction ( study) that is caused by carbofuran using male mice ( ) strain Balb/C. The samples were divided into three groups, namely, Group C-L- (control group, no treatment), Group C+L- (only treated by carbofuran treatment), and Group C+L+ (treatment group, treated by carbofuran and laser-puncture) with five replications each. After being treated, each liver slice of samples was observed using microscope to get the histology result and then scored. Carbofuran contamination can lead to inflammation of cells and necrosis. The histology results and the scoring test showed that the liver cells repair with the energy dose of laser diode at 0.5 and 1.0 Joule. The optimum energy dose in this study was 1.0 Joule which had the closest score of inflammatory cells and necrosis to normal liver cells.

Extracellular matrix glycoprotein tenascin‑X (TNX) is the largest member of the tenascin family. In the present study, the contribution of TNX to liver dysfunction was investigated by administration of high‑fat and high‑cholesterol diet with high levels of phosphorus and calcium (HFCD) to wild‑type (WT) and TNX‑knockout (KO) mice. After 16 weeks of HFCD administration, the ratio of liver weight to body weight was approximately 22% higher in the HFCD‑fed WT mice compared with the HFCD‑fed TNX‑KO mice, indicating hepatomegaly in HFCD‑fed WT mice. Histological analyses with hematoxylin and eosin staining at 21 weeks revealed that hepatocyte hypertrophy in HFCD‑fed TNX‑KO mice was suppressed to 85% of that in HFCD‑fed WT mice. By contrast, there was a 1.2‑fold increase in lipid deposition in hepatocytes from HFCD‑fed TNX‑KO mice compared with HFCD‑fed WT mice at 18 weeks, as demonstrated by Oil Red O staining. In addition, TNX‑KO mice at 21 weeks and 27 weeks post‑HFCD administration exhibited significant suppression of inflammatory cell infiltrate to 51 and 24% of that in WT mice, respectively. Immunofluorescence analysis for type I collagen and Elastica van Gieson staining demonstrated a clear hepatic fibrosis progression in HFCD‑fed WT mice at 27 weeks, whereas hepatic fibrosis was undetected in HFCD‑fed TNX‑KO mice. The present findings indicated that TNX deficiency suppressed hepatic dysfunction induced by HFCD administration.

Background Fatty liver disease in the absence of excessive alcohol consumption is an increasingly common condition with a global prevalence of ~ 25–30% and is also associated with cardiovascular disease (CVD). Since systemic metabolic dysfunction underlies its pathogenesis, the term metabolic (dysfunction)-associated fatty liver disease (MAFLD) has been proposed for this condition. MAFLD is closely intertwined with obesity, type 2 diabetes mellitus and atherogenic dyslipidemia, which are established cardiovascular risk factors. Unlike CVD, which has received attention in the literature on fatty liver disease, the CVD risk associated with MAFLD is often underestimated, especially among Cardiologists. Methods and results A multidisciplinary panel of fifty-two international experts comprising Hepatologists, Endocrinologists, Diabetologists, Cardiologists and Family Physicians from six continents (Asia, Europe, North America, South America, Africa and Oceania) participated in a formal Delphi survey and developed consensus statements on the association between MAFLD and the risk of CVD. Statements were developed on different aspects of CVD risk, ranging from epidemiology to mechanisms, screening, and management. Conculsions The expert panel identified important clinical associations between MAFLD and the risk of CVD that could serve to increase awareness of the adverse metabolic and cardiovascular outcomes of MAFLD. Finally, the expert panel also suggests potential areas for future research.

Background Understanding the relationship between relative skeletal muscle mass and newly proposed steatotic liver disease (SLD) is crucial, but research gaps still exist. Based on a cohort study, we investigated the impact of relative skeletal muscle mass on incident SLD and its subtypes and explored potential mediators involved in these relationships. Methods We followed 1964 subjects aged 55–70 years (median age: 61.4 [58.4–65.1] years; 45.5% male participants). Appendicular skeletal muscle mass (ASM) was measured using bioelectrical impedance analysis and adjusted for height squared (ASM/height2), weight (ASM/weight) and body mass index (ASM/BMI) to quantify relative skeletal muscle mass. SLD was diagnosed using ultrasonography and classified into metabolic dysfunction–associated steatotic liver disease (MASLD), metabolic dysfunction and alcohol‐associated liver disease (MetALD) and alcohol‐associated liver disease (ALD). Results Over a mean 4.3‐year follow‐up period, 598 participants (30.4%) developed SLD: 539 MASLD (27.4%), 38 MetALD (1.9%) and 21 ALD (1.1%). Higher ASM/weight and ASM/BMI were associated with lower risks of SLD and MASLD (RR per SD [95% CI]: 0.71 [0.61–0.82], 0.59 [0.46–0.76]; 0.66 [0.58–0.76], 0.51 [0.40–0.64]; all p < 0.001). Associations of ASM/height2 with SLD and MASLD shifted from positive to negative after adjustment for BMI (from 1.67 [1.51–1.84] to 0.77 [0.67–0.89]; from 2.30 [1.92–2.76] to 0.61 [0.47–0.79], all p < 0.001). ASM/height2 and ASM/weight were negatively associated with MetALD (0.49 [0.26–0.94], p = 0.031; 0.50 [0.27–0.93], p = 0.029), whereas ASM/BMI was inversely associated with ALD (0.40 [0.18–0.88], p = 0.023). The effects of ASM/height2, ASM/weight and ASM/BMI on incident MASLD were partially mediated by adiponectin (percentage mediated [95% CI]: 6.3% [2.5%–11.1%]; 9.4% [5.0%–14.6%]; 9.5% [5.1%–15.5%]), uric acid (4.7% [1.6%–8.9%]; 5.3% [2.6%–8.5%]; 5.3% [2.4%–8.8%]), triglyceride (7.1% [3.9%–11.1%]; 7.5% [4.4%–10.9%]; 8.7% [5.3%–13.4%]) and homeostasis model assessment of insulin resistance (13.9% [9.5%–20.4%]; 15.0% [10.0%–20.2%]; 14.5% [9.9%–20.7%]). The effects of ASM/weight and ASM/BMI on incident MASLD were mediated by cholinesterase (8.2% [3.6%–13.1%]; 10.5% [6.1%–16.3%]), prealbumin (6.2% [2.9%–9.8%]; 6.0% [3.0%–10.1%]), retinol‐binding protein‐4 (5.4% [3.0%–8.5%]; 4.6% [1.9%–8.5%]) and osteocalcin (2.1% [0.1%–4.5%]; 2.9% [0.6%–5.7%]). Conclusions Relative skeletal muscle mass adjusted for weight or BMI, rather than height alone, better reflects protective effects against SLD. Mediation analysis reveals key metabolic factors linking muscle mass and liver health, offering insights into the pathogenic pathways involved in muscle–liver crosstalk.