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Background: This diagnostic prospective study compared the feasibility and diagnostic accuracy of Pocket-size Ultrasound Devices (PUDs) against standard ultrasound (US) in detecting liver steatosis using the controlled attenuation parameter (CAP) and liver biopsy as reference standards.
Materials And Methods: Consecutive patients with chronic liver diseases were assessed for the presence of steatosis using PUD and US. A CAP cut-off value >275 dB/m was applied to establish ≥S1. A 26-patient subgroup underwent liver biopsy. PUD reproducibility was evaluated using Cohen's k statistic. Diagnostic accuracy of PUD and US was given as Sensibility (Sn), Specificity (Sp), Positive and Negative Predictive Values (PPV, NPV), positive and negative Likelihood Ratio (LR+, LR-).
Results: 81 consecutive patients (69% males) with multiple etiologies were enroled. PUD inter-observer agreement was good (k 0.77, 95%CI 0.62-0.93). PUD and US identified ≥S1 according to CAP values respectively with Sn 0.87, Sp 0.61, PPV 0.49, NPV 0.91, LR+ 2.04, LR- 0.07, AUROC 0.74 and Sn 0.96, Sp 0.54, PPV 0.47, NPV 0.97, LR+ 2.10, LR- 0.07, AUROC 0.75.
Conclusions: PUD shows good reproducibility and diagnostic accuracy in ruling liver steatosis out, representing a useful point-of-care tool to avail of hepatologists interested in excluding NAFLD, but with basic US skills.
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http://dx.doi.org/10.1016/j.dld.2023.11.014 | DOI Listing |
J Gastroenterol
September 2025
Department of General Surgery (Hepatopancreatobiliary Surgery), Department of Biliary-Pancreatic Center, The Affiliated Hospital of Southwest Medical University, 25 Taiping Street, Jiangyang District, Luzhou City, 646000, Sichuan Province, China.
Background And Aims: Inflammatory cell infiltration in the liver is a hallmark of metabolic dysfunction-associated fatty liver disease (MAFLD). However, the pathological events that trigger the infiltration of inflammatory cells to mediate MAFLD pathogenesis remains poorly understood. This study aims to investigate the function and mechanism of Hic-5 on hepatic inflammation of MAFLD.
View Article and Find Full Text PDFKaohsiung J Med Sci
September 2025
Hepatitis Research Center, College of Medicine; Center for Metabolic Disorders and Obesity; Center for Liquid Biopsy and Cohort Research, Kaohsiung Medical University, Kaohsiung, Taiwan.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is an increasingly prevalent chronic liver condition that can progress to severe complications such as metabolic dysfunction-associated steatohepatitis (MASH). Despite its growing burden, there are no reliable non-invasive biomarkers for tracking disease progression. In this study, we established a murine MASLD/MASH model using a high-fat diet and chemical (CCl) induction.
View Article and Find Full Text PDFGen Physiol Biophys
September 2025
Department of Endocrinology and Metabolism, Central People's Hospital of Zhanjiang, Zhanjiang City, Guangdong Province, China.
This study explores how human antigen R (HuR) stabilizes fibroblast growth factor 19 (FGF19) mRNA, inhibiting Kupffer cell (KC) activation to reduce inflammation and fibrosis in non-alcoholic fatty liver disease (NAFLD). An animal model of NAFLD was established in mice by administering a high-fat diet (HFD). In vitro study utilized a lipopolysaccharide-induced immortalized mouse KC model.
View Article and Find Full Text PDFAnalyst
September 2025
Institute of Basic Theory for Chinese Medicine, China Academy of Chinese Medical Sciences, Beijing, China.
: Postmenopausal conditions can lead to metabolic disorders such as obesity and steatosis. (PT), a prominent traditional Chinese medicine, exerts potential therapeutic effects against hepatic injury. Nevertheless, the extent to which PT ameliorates liver damage resulting from estrogen deficiency, along with the associated mechanisms, remains poorly understood.
View Article and Find Full Text PDFJ Obes
September 2025
School of Natural Sciences, University of Lincoln, Lincoln, UK.
To investigate the genetic determinants of fat distribution across anatomical sites and their implications for health outcomes. We analyzed neck-to-knee MRI data from the UK Biobank ( = 37,589) to measure fat at various locations and used Mendelian randomization to assess effects on 26 obesity-related diseases and 94 biomarkers from FinnGen and other consortia. We identified genetic loci associated with 10 fat depots: abdominal subcutaneous adipose tissue ( = 2 loci), thigh subcutaneous adipose tissue (25), thigh intermuscular adipose tissue (15), visceral adipose tissue (7), liver proton density fat fraction (PDFF) (8), pancreas PDFF (11), paraspinal adipose tissue (9), pelvic bone marrow fat (28), thigh bone marrow fat (27), and vertebrae bone marrow fat (5).
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