scholarly journals A Comparison of the Liver Fat Score and CT Liver-to-Spleen Ratio as Predictors of Fatty Liver Disease by HIV Serostatus

Author(s):  
Lauren E Mellor Crummey ◽  
Jordan E Lake ◽  
Holly Wilhalme ◽  
Chi Hong Tseng ◽  
Philip M Grant ◽  
...  
2021 ◽  
Author(s):  
Cerda-Reyes Eira ◽  
Ojeda-Yuren Alicia Sarahi ◽  
Torres-Vazquez Julián ◽  
Herrero Maceda María del Rosario ◽  
Vázquez-Medina Martín Uriel ◽  
...  

The prevalence of non-alcoholic fatty liver disease (NAFLD) has increased in the last years up to 25% in the adult population. This disease includes a large spectrum of disorders, from simple fatty liver disease to cirrhosis and Hepatocellular Carcinoma (HCC), and they are related to chronic metabolic conditions. NAFLD is characterized by the presence of at least 5% of hepatic steatosis without evidence of hepatocellular injury. The diagnosis of this disease should be of exclusion and focused on its progression, treatment, and identification of the prognosis. The European Association for the Study of the Liver (EASL), the National Institute for Health and Care Excellence (NICE), the Italian Association for the Study of the Liver (AISF), and the American Association for the Study of the Liver (AASLD), published their Clinical Guidelines that have identified the criteria for the diagnosis of NAFLD, several, using imaging or histological diagnostic methods, although they imply a different approach and screening. The Fatty Liver Index and the NAFLD Liver Fat Score are used by 3 out of 5 Guidelines and they are easily calculated using blood tests and clinical information. Other non-invasive scales for NAFLD are the NAFLD fibrosis score (NFS), Fib-4, AST/ALT ratio index; also the ELF panel, Fibrometer, Fibrotest, Hepascore; and some imaging techniques that include transient elastography, magnetic resonance elastography (MRE), and shear wave elastography. Finally, proteomic’s and glycomic’s technologic biomarkers are currently under investigation and recent use, such as Cytokeratin 18 and Sirtuin 1. Still, liver biopsy remains the gold standard to distinguish between steatohepatitis and simple steatosis, using the histological classification and staging scoring systems of NAFLD Activity Score (NAS) and the Steatosis Activity Fibrosis (SAF), to evaluate the disease’s activity.


2017 ◽  
Author(s):  
Jelica Bjekic-Macut ◽  
Ivana Bozic-Antic ◽  
Konstantinos Tziomalos ◽  
Dusan Ilic ◽  
Danijela Vojnovic-Milutinovic ◽  
...  

World Science ◽  
2019 ◽  
Vol 1 (10(50)) ◽  
pp. 30-36
Author(s):  
Oleg Babak ◽  
Anna Bashkirova

The aim of the study was to conduct a cluster analysis of pathogenetic relationships between metabolic parameters, endothelial lipase levels, the severity of steatosis, and clinical parameters in patients with non-alcoholic fatty liver disease with hypertension. To analyze pathogenetic relationships, a cluster analysis was performed with the distribution of parameters into 4 clusters using the Ward's method. The most dense metabolic link by cluster analysis endothelial lipase forms with NAFLD liver fat score (2.639 cu), HbA1C (2.084 cu), total cholesterol (2.272 cu), and alcohol units (2.797 cu).


Metabolites ◽  
2020 ◽  
Vol 11 (1) ◽  
pp. 22
Author(s):  
Alessandro Mantovani ◽  
Graziana Petracca ◽  
Alessandro Csermely ◽  
Giorgia Beatrice ◽  
Giovanni Targher

Recent randomized controlled trials (RCTs) tested the efficacy of sodium-glucose cotransporter-2 (SGLT-2) inhibitors to specifically treat nonalcoholic fatty liver disease (NAFLD). We systematically searched three electronic databases (up to 31 October 2020) for identifying placebo-controlled or head-to-head RCTs that used SGLT-2 inhibitors for treatment of NAFLD. No published RCTs with paired liver biopsy data were available for the meta-analysis. Primary outcome measures were changes in serum liver enzyme levels and liver fat content on imaging techniques. Overall, we included a total of twelve RCTs testing the efficacy of dapagliflozin (n = six RCTs), empagliflozin (n = three RCTs), ipragliflozin (n = two RCTs) or canagliflozin (n = one RCT) to specifically treat NAFLD for a median period of 24 weeks with aggregate data on 850 middle-aged overweight or obese individuals with NAFLD (90% with type 2 diabetes). Compared to placebo/reference therapy, treatment with SGLT-2 inhibitors significantly decreased serum alanine aminotransferase (weighted mean differences (WMD): −10.0 IU/L, 95%CI −12.2 to −7.79 IU/L; I2 = 10.5%) and gamma-glutamyltransferase levels (WMD: −14.49 IU/L, 95%CI −19.35 to −9.63 IU/L, I2 = 38.7%), as well as the absolute percentage of liver fat content on magnetic resonance-based techniques (WMD: −2.05%, 95%CI −2.61 to −1.48%; I2 = 0%). In conclusion, SGLT-2 inhibitors seem to be a promising treatment option for NAFLD.


Biology ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 122
Author(s):  
Jun-Hyuk Lee ◽  
Hye-Sun Lee ◽  
Byoung-Kwon Lee ◽  
Yu-Jin Kwon ◽  
Ji-Won Lee

Although sarcopenia is known to be a risk factor for non-alcoholic fatty liver disease (NAFLD), whether NAFLD is a risk factor for the development of sarcopenia is not clear. We investigated relationships between NAFLD and low skeletal muscle mass index (LSMI) using three different datasets. Participants were classified into LSMI and normal groups. LSMI was defined as a body mass index (BMI)-adjusted appendicular skeletal muscle mass <0.789 in men and <0.512 in women or as the sex-specific lowest quintile of BMI-adjusted total skeletal muscle mass. NAFLD was determined according to NAFLD liver fat score or abdominal ultrasonography. The NAFLD groups showed a higher hazard ratios (HRs) with 95% confidence intervals (CIs) for LSMI than the normal groups (HRs = 1.21, 95% CIs = 1.05–1.40). The LSMI groups also showed a higher HRs with 95% CIs for NAFLD than normal groups (HRs = 1.56, 95% CIs = 1.38–1.78). Participants with NAFLD had consistently less skeletal muscle mass over 12 years of follow-up. In conclusion, LSMI and NAFLD showed a relationship. Maintaining muscle mass should be emphasized in the management of NAFLD.


Circulation ◽  
2013 ◽  
Vol 127 (suppl_12) ◽  
Author(s):  
Lisa B VanWagner ◽  
Christina M Shay ◽  
Hongyan Ning ◽  
John Wilkins ◽  
Cora E Lewis ◽  
...  

Background: Nonalcoholic Fatty Liver Disease (NAFLD) and excess visceral adipose tissue (VAT) are associated with cardiovascular disease (CVD). Recent studies suggest that NAFLD and coronary artery calcification (CAC) are related independent of VAT. In a population-based cross-sectional sample of black and white adults free from prevalent liver or heart disease, we tested the hypothesis that NAFLD is associated with the presence of CAC and abdominal aortoiliac calcification (AAC) independent of VAT and other CVD risk factors. Methods: Participants from the Coronary Artery Risk Development in Young Adults study (Y25 exam) with concurrent computed tomography quantification of liver fat, CAC and AAC were included (n=2,163). NAFLD was defined as liver attenuation ≤ 40 Hounsfield Units after exclusion of other causes of liver fat (medication/alcohol use). Using the Agatston method, CAC/AAC presence was defined as a score > 0. Logistic regression models were used to calculate odds ratios and 95% confidence intervals. Results: Participant age was 49.9 (3.7) years and the sample was equally distributed by sex (55.6% female) and race (50.1% black). Mean BMI was 30.6 (7.1). The CAC and AAC prevalence was 26.5% and 49.6%. NAFLD prevalence was 9.6%. NAFLD participants were 50.1 (3.7) years old and more likely to be male (59.8% vs. 51.7%, p<0.0001), white (56.5% vs. 49.3%, p<0.05) and have the metabolic syndrome (70.1% vs. 22.6%, p<0.0001) than those with no NAFLD. They were also more likely to have CAC (37.2%) and AAC (60.9%) than those with no NAFLD (25.4% and 49.4%, respectively). In multivariable analyses adjusted for demographics and health behaviors, NAFLD was associated with the presence of CAC and AAC (Table 1). This association was attenuated after adjustment for CVD risk factors and VAT. Effect modification by race and sex was not statistically significant. Conclusion: In contrast to prior studies, our results suggest that the relationship between NAFLD and subclinical CVD is mediated by the presence of other CVD risk factors.


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