Severe Fatty Liver Research Articles

Ultrasound image analysis for detection of fatty liver and grading its severity in buffaloes at Mosul, Iraq

The study aimed to (ⅰ) examines whether quantitative and qualitative digital analysis of hepatic ultrasound images can be used to detect fatty liver and grading its severity, (ⅱ) to estimate the concentration of serum β-hydroxybutyrate content in normal and diseased animals. A total of 50 buffaloes (15 clinically normal and 35 suffered from decreased milk production, loss of appetite, and loss of body weight) 2-4 weeks after parturition were studied. Buffaloes were examined by real-time ultrasound using a 3.5 MHz convex probe. Ultrasound images were saved for qualitative and quantitative analysis, using computer aid Fatty-Liver software (programmed in Matlab language). Based on the digital analysis of ultrasound images, the diseased buffaloes were classified as mild (n=20), moderate (n=7) and severe (n=8) fatty liver affection. Results indicated that the concentration of β-hydroxybutyrate estimated via ELISA were 0.409, 0.735, 0.923, 1.708 mmol/dL in normal, mild, moderate, and severe diseased buffaloes respectively. However, a significant difference has been encountered among normal and diseased animals. It has been concluded that buffaloes at Mosul suffered from fatty liver and digital analysis of ultrasound images was a suitable method for clinical diagnosis, furthermore, estimation of β-hydroxybutyrate was a suitable method for laboratory diagnosis.

Clinical exome sequencing for diagnosing severe cryptogenic liver disease in adults: A case series.

Liver diseases remain unexplained in up to 30% of adult patients; genetic analysis could help establish the correct diagnosis. In six adult patients with cryptogenic liver disease, we performed whole-exome sequencing (WES) and evaluated the individual predisposition to progressive fatty liver disease by polygenic risk scores (PRS). In one patient, WES was allowed to diagnose the Hermansky-Pudlak syndrome. In the other two patients, genetic variants in LDLRAP1/MSH6 and ALDOB genes were identified, contributing to explaining the clinical presentation and disease pathogenesis (50% diagnostic uptake). In the other three patients, rare variants with a high likelihood of disrupting protein function in APOB, ATP7B, ABCB4 and ATP8B1 were identified. One patient who developed hepatocellular carcinoma during the follow-up had a high PRS value. The study supports the role of WES, combined with risk stratification by PRS and accurate clinical assessment in improving the diagnosis and informed management in patients with cryptogenic liver disease, a positive family history or severe fatty liver not fully accounted for by environmental triggers.

Sesame Oil Ameliorates Alanine Aminotransferase, Aspartate Aminotransferase, and Fatty Liver Grade in Women with Nonalcoholic Fatty Liver Disease Undergoing Low-Calorie Diet: A Randomized Double-Blind Controlled Trial.

Background The type and amount of dietary fats play an important role in fat accumulation in the liver. Sesame oil (SO) is a good source of monounsaturated acids (MUFAs) and polyunsaturated fatty acids (PUFAs). Objective This trial aimed at examining the effect of SO consumption on the levels of liver enzymes and the severity of fatty liver in women with nonalcoholic fatty liver disease (NAFLD) undergoing a weight loss diet. Methods This randomized, double-blind, controlled trial was carried out on 60 women with NAFLD. Subjects were randomly assigned to the SO group (n = 30) and sunflower oil (SFO) group (n = 30), each person consuming 30 grams of oil per day for 12 weeks. All the participants received a hypocaloric diet (−500 kcal/day) during the study. Fatty liver grade and liver enzymes were assessed at pre- and postintervention phases. Results 53 patients completed the study. Significant reductions in body weight, body mass index (BMI), waist circumference (WC), and fatty liver grade were observed in both groups (P < 0.05). Following SO, significant decreases in serum aspartate and alanine aminotransferases (AST and ALT) were observed. After adjusting for confounders, ALT, AST, and fatty liver grade of the SO group were significantly reduced compared to the SFO group (P < 0.05). However, the changes in serum alkaline phosphatase (ALP) were not significant (P > 0.05). Conclusions The desired effects of weight loss were reinforced by the consumption of SO through improving fatty liver severity and serum ALT and AST levels in NAFLD patients. Moreover, low-calorie diets may lead to favorable outcomes for NAFLD patients through mitigation of obesity and fatty liver grade.

Associations of muscle mass and grip strength with severe NAFLD: A prospective study of 333,295 UK Biobank participants

Cross-sectional studies have reported that lower muscle mass and strength are risk factors for non-alcoholic fatty liver disease (NAFLD). However, the evidence from prospective studies is limited. This study examined both the strength and pattern of the associations between these 2 physical capability markers and severe NAFLD using data from the UK Biobank study. A total of 333,295 participants were included in this prospective study. Grip strength was measured using a Jamar J00105 hydraulic hand dynamometer, and the Janssen equation was used to estimate skeletal muscle mass by bioelectrical impedance. Muscle mass was adjusted for body weight and all exposures were sex-standardised. Associations of muscle mass and strength with severe NAFLD (defined as hospital admission or death) were first investigated by tertile of each exposure using Cox proportional hazard models. Non-linear associations were investigated using penalised cubic splines fitted in the Cox proportional hazard models. After a median follow-up of 10 years (IQR 9.3 to 10.7 years), 3,311 individuals had severe NAFLD (3,277 hospitalisations and 34 deaths). Compared with the lowest tertile of muscle mass, the risk of severe NAFLD was lower in the middle (hazard ratio 0.76; 95% CI 0.70-0.83) and the highest tertile (hazard ratio 0.46; 95% CI 0.40-0.52). Tertiles of grip strength showed a similar pattern. Non-linearity was only identified for muscle mass (p <0.001). Being on the lower tertile of grip strength and muscle mass accounted for 17.7% and 33.1% of severe NAFLD cases, respectively. Lower muscle mass and grip strength were associated with higher risk of developing severe NAFLD. Interventions to improve physical capability may be protective, but this needs to be investigated in appropriately designed trials. Lower muscle mass - both quantity and quality - were associated with a higher risk of severe non-alcoholic fatty liver disease. Therefore, improving muscle mass might be a protective factor against this increasing public health problem.

Severe Acute Fatty Liver of Pregnancy (AFLP) Associated with Unknown Factor VII Deficiency

We present a case of acute fatty liver of pregnancy (AFLP) associated with unknown factor VII deficiency. The final diagnosis for our patient, a 28 year old female, G2P1, has been a challenge and required multiple treatments included a postpartum emergent laparotomy with haemostatic hysterectomy. Multidisciplinary approach with other specialists was crucial for the outcome of this patient who required a massive amount of resources both diagnostically and therapeutically

Clinical Application of Quantitative CT Technique in Assessing Liver Fat Content in Patients with Schizophrenia.

This paper investigates the clinical application value of quantitative CT (QCT) technique in evaluating liver fat content in patients with schizophrenia. 457 patients with schizophrenia underwent abdominal CT and QCT scans. QCT postprocessing software (QCT Pro version 6.1) measures the percentage of liver fat content in all patients and calculates the average value. Then, the CT workstation displays the corresponding liver/spleen CT value ratio. SPSS 25.0 software is used for statistical analysis of data, and the correlation coefficient between the mean liver fat content. The ratio of liver/spleen CT values is calculated and the consistency between the results is compared. The ROC curve is used to define the cutoff value of the target and evaluate its diagnostic efficiency. There is a high negative correlation between the mean liver fat content and the ratio of liver/spleen CT value in all schizophrenia patients (r = −0.935, P < 0.05). The identification rate of patients with mild fatty liver by QCT technology is 4 times higher than that of the liver and spleen CT value ratio (50.98% Vs 12.47%). Taking the ratio of the liver to the spleen as the standard, the ROC curve of the liver fat content in QCT is drawn, the cutoff values of the mean liver fat content of the normal liver and mild fatty liver and mild and moderate fatty liver were 9.35% and 19.4%, respectively. Comparing this result with the results obtained by the existing QCT for the fatty liver diagnosis and grading standard value (American standard) shows that there is a difference of about 5% between the two. Compared with the semiquantitative liver/spleen ratio, QCT technology can quantify the liver fat content. Given the particularity of patients with schizophrenia, QCT can be used as an important test for identifying early fatty liver and assessing the severity of fatty liver.

Outcomes of Nonalcoholic Fatty Liver Disease In Covid Positive Diabetic Patients: Cross Sectional Study

Background: SARS-CoV-2 principally invades the respiratory system. ACE receptor are also abundant throughout the hepatobiliary system and their increased expression on hepatocyte make patients with NAFLD more vulnerable. Aim: To see outcomes of COVID positive diabetic patients suffering from Nonalcoholic fatty liver disease (NAFLD). Study design: Cross Sectional Study. Methodology: 150 diabetic and COVID PCR positive were recruited from COVID ward of Services Hospital in Lahore. Clinical parameters like BMI, SpO2, Hepatomegaly and lab parameters like HbA1C, AST ALT were noted in spreadsheet. Statistical analysis was done using SPSS v.25. Statistical significance for difference in proportions is calculated using Pearson’s Chi-Squared test. P less than 0.05 was considered statistically significant. Results: Around 84(56%) were males and 66(44%) females, smoked were 27(18%), mean age (years) was 59.7333 ±11.35023, mean BMI (kg/m²) was 30.1425±7.30673, 87(58%) patients had NAFLD, who experienced sever disease (53.2%; x^2=0.010) and more mortalities (60.2%;x^2=0.453) as compared to those who do not had condition. Conclusion: We concluded that NAFLD makes COVID-19 infected patients more fragile. Such patients experienced sever disease and more mortalities however need of mechanical ventilation remains almost equal between those who has NAFLD and those who didn’t had. Keywords: Nonalcoholic fatty liver disease, COVID-19, Diabetes, Mortality and Severity.

Quantification of Liver Fat Content after Radiofrequency Ablation for Liver Cancer: Correlation with Hepatic Perfusion Disorders.

Purpose: To quantitatively investigate the correlation between liver fat content and hepatic perfusion disorders (HPD) after radiofrequency ablation (RFA) for liver cancer using magnetic resonance imaging (MRI)-determined proton density fat fraction (PDFF). Materials and methods: A total of 150 liver cancer patients underwent liver MRI examination within one month after RFA and at four months after RFA. According to the liver fat content, they were divided into non-, mild, moderate, and severe fatty liver groups. The liver fat content and hepatic perfusion disorders were determined using PDFF images and dynamic contrast-enhanced MRI images. The relationship between the liver fat content and HPD was investigated. Results: At the first postoperative MRI examination, the proportion of patients in the nonfatty liver group with hyperperfused foci (11.11%) was significantly lower than that in the mild (30.00%), moderate (42.86%), and severe fatty liver (56.67%) groups (p < 0.05), whereas the proportions of patients with hypoperfused foci (6.67%, 7.5%, 5.71%, and 6.67%, respectively) were not significantly different among the four groups (p > 0.05). In the nonfatty liver group, the liver fat content was not correlated with hyperperfusion abnormalities or hypoperfusion abnormalities. By contrast, in the three fatty liver groups, the liver fat content was correlated with hyperperfusion abnormalities but was not correlated with hypoperfusion abnormalities. At the second postoperative MRI examination, six patients in the nonfatty liver group were diagnosed with fatty liver, including two patients with newly developed hyperperfusion abnormalities and one patient whose hypoperfusion abnormality remained the same as it was in the first postoperative MRI examination. Conclusion: There was a high correlation between the liver fat content and hyperperfusion abnormalities after RFA for liver cancer. The higher the liver fat content was, the higher the was risk of hyperperfusion abnormalities. However, there was little correlation between liver fat content and hypoperfusion abnormalities, and the increase in postoperative liver fat content did not induce or alter the presence of hypoperfused foci.

Dietary-Induced Elevations of Triglyceride-Rich Lipoproteins Promote Atherosclerosis in the Low-Density Lipoprotein Receptor Knockout Syrian Golden Hamster.

Elevated triglycerides are associated with an increased risk of cardiovascular disease (CVD). Therefore, it is very important to understand the metabolism of triglyceride-rich lipoproteins (TRLs) and their atherogenic role in animal models. Using low-density lipoprotein receptor knockout (LDLR−/−) Syrian golden hamsters, this study showed that unlike LDLR−/− mice, when LDLR−/− hamsters were fed a high cholesterol high-fat diet (HFD), they had very high plasma levels of triglycerides and cholesterol. We found that LDLR−/− hamsters exhibited increased serum TRLs and the ApoB100 and 48 in these particles after being fed with HFD. Treatment with ezetimibe for 2 weeks decreased these large particles but not the LDL. In addition, ezetimibe simultaneously reduced ApoB48 and ApoE in plasma and TRLs. The expression of LRP1 did not change in the liver. These findings suggested that the significantly reduced large particles were mainly chylomicron remnants, and further, the remnants were mainly cleared by the LDL receptor in hamsters. After 40 days on an HFD, LDLR−/− hamsters had accelerated aortic atherosclerosis, accompanied by severe fatty liver, and ezetimibe treatment reduced the consequences of hyperlipidemia. Compared with the serum from LDLR−/− hamsters, that from ezetimibe-treated LDLR−/− hamsters decreased the expression of vascular adhesion factors in vascular endothelial cells and lipid uptake by macrophages. Our results suggested that in the LDLR−/− hamster model, intestinally-derived lipoprotein remnants are highly atherogenic and the inflammatory response of the endothelium and foam cells from macrophages triggered atherosclerosis. The LDL receptor might be very important for chylomicrons remnant clearance in the Syrian golden hamster, and this may not be compensated by another pathway. We suggest that the LDLR−/− hamster is a good model for the study of TRLs-related diseases as it mimics more complex hyperlipidemia.

Fatty liver on computed tomography scan on admission is a risk factor for severe coronavirus disease

ObjectivesTo alleviate the overflow of coronavirus disease 2019 (COVID-19) patients in hospitals, less invasive and simple criteria are required to triage the patients. We evaluated the relationship between COVID-19 severity and fatty liver on plain computed tomography (CT) scan performed on admission. MethodsIn this retrospective cohort study, we considered all COVID-19 patients at a large tertiary care hospital between January 31 and August 31, 2020. COVID-19 severity was categorized into severe (moderate and severe) and non-severe (asymptomatic and mild) groups, based on the Japanese National COVID-19 guidelines. Fatty liver was detected on plain CT scan. Multivariate logistic regression analysis was performed to evaluate factors associated with severe COVID-19. ResultsOf 222 patients (median age: 52 years), 3.2%, 58.1%, 20.7%, and 18.0% presented with asymptomatic, mild, moderate, and severe COVID-19, respectively. Although 59.9% had no fatty liver on plain CT, mild, moderate, and severe fatty liver occurred in 13.1%, 18.9%, and 8.1%, respectively. Age and presence of fatty liver were significantly associated with severe COVID-19. ConclusionOur study showed that fatty liver on plain CT scan on admission can become a risk factor for severe COVID-19. This finding may help clinicians to easily triage COVID-19 patients.

What the New Definition of Metabolic Dysfunction-Associated Fatty Liver Disease (MAFLD) Left Behind: Genetically Acquired Fatty Liver Disease (GAFLD).

What the New Definition of Metabolic Dysfunction-Associated Fatty Liver Disease (MAFLD) Left Behind: Genetically Acquired Fatty Liver Disease (GAFLD).

Influencing factors for hepatic fat accumulation in patients with type 2 diabetes mellitus.

BACKGROUNDNon-alcoholic fatty liver disease has become the most common chronic liver disease worldwide, which originates from the accumulation of triglyceride (TG) in the liver. Patients with type 2 diabetes mellitus (T2DM) are considered to have a predisposition to hepatic steatosis. However, the influencing factors for hepatic fat accumulation in T2DM patients remain unclear.AIMTo investigate the influencing factors for hepatic fat accumulation in T2DM patients. METHODSWe enrolled 329 T2DM patients admitted to the Endocrinology Department of the First Affiliated Hospital of Soochow University, who underwent MR mDIXON-Quant examination to quantify the hepatic fat fraction (HFF). According to body mass index (BMI), the patients were divided into normal weight, overweight, and obese groups. The differences in general statistics, biochemical parameters, islet function, and HFF were compared among the three groups. The associations between HFF and other parameters and the influences of various parameters on the severity of hepatic fat accumulation were analyzed. RESULTSThe HFF of T2DM patients gradually increased in the normal weight, overweight, and obese groups (P < 0.05). Spearman correlation analysis showed that in T2DM patients, HFF was negatively correlated with age and high-density lipoprotein cholesterol (P < 0.05), whereas it was positively correlated with BMI, waist-hip ratio, fasting plasma glucose, alanine aminotransferase (ALT), aspartate aminotransferase, bilirubin, glutamyl transpeptidase, lactate dehydrogenase, albumin (ALB), uric acid (UA), total cholesterol, TG, low-density lipoprotein cholesterol (LDL-C), C-reactive protein, free triiodothyronine, fasting insulin, fasting C-peptide, and homeostasis model assessment of insulin resistance (P < 0.05). Multiple linear regression analysis showed significant positive influences of BMI, ALT, LDL-C, UA, and ALB on HFF in T2DM patients (P < 0.05). Binary logistic regression analysis showed that BMI, ALT, ALB, and LDL-C were independent risk factors for moderate to severe fatty liver in T2DM patients, and obesity increased the risk of being complicated with moderate to severe fatty liver by 4.03 times (P < 0.05).CONCLUSIONThe HFF of T2DM patients increases with BMI. Higher BMI, ALT, ALB, and LDL-C are independent risk factors for moderate to severe fatty liver in T2DM patients.

CREBH Systemically Regulates Lipid Metabolism by Modulating and Integrating Cellular Functions.

Cyclic AMP-responsive element-binding protein H (CREBH, encoded by CREB3L3) is a membrane-bound transcriptional factor expressed in the liver and small intestine. The activity of CREBH is regulated not only at the transcriptional level but also at the posttranslational level. CREBH governs triglyceride metabolism in the liver by controlling gene expression, with effects including the oxidation of fatty acids, lipophagy, and the expression of apolipoproteins related to the lipoprotein lipase activation and suppression of lipogenesis. The activation and functions of CREBH are controlled in response to the circadian rhythm. On the other hand, intestinal CREBH downregulates the absorption of lipids from the diet. CREBH deficiency in mice leads to severe hypertriglyceridemia and fatty liver in the fasted state and while feeding a high-fat diet. Therefore, when crossing CREBH knockout (KO) mice with an atherosclerosis model, low-density lipoprotein receptor KO mice, these mice exhibit severe atherosclerosis. This phenotype is seen in both liver- and small intestine-specific CREBH KO mice, suggesting that CREBH controls lipid homeostasis in an enterohepatic interaction. This review highlights that CREBH has a crucial role in systemic lipid homeostasis to integrate cellular functions related to lipid metabolism.

Identification of key genes and pathways in mild and severe nonalcoholic fatty liver disease by integrative analysis

BackgroundThe global prevalence of nonalcoholic fatty liver disease (NAFLD) is increasing. The pathogenesis of NAFLD is multifaceted, and the underlying mechanisms are elusive. We conducted data mining analysis to gain a better insight into the disease and to identify the hub genes associated with the progression of NAFLD. MethodsThe dataset GSE49541, containing the profile of 40 samples representing mild stages of NAFLD and 32 samples representing advanced stages of NAFLD, was acquired from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) were identified using the R programming language. The Database for Annotation, Visualization and Integrated Discovery (DAVID) online tool and Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) database were used to perform the enrichment analysis and construct protein–protein interaction (PPI) networks, respectively. Subsequently, transcription factor networks and key modules were identified. The hub genes were validated in a mice model of high fat diet (HFD)-induced NAFLD and in cultured HepG2 cells by real-time quantitative PCR. ResultsBased on the GSE49541 dataset, 57 DEGs were selected and enriched in chemokine activity and cellular component, including the extracellular region. Twelve transcription factors associated with DEGs were indicated from PPI analysis. Upregulated expression of five hub genes (SOX9, CCL20, CXCL1, CD24, and CHST4), which were identified from the dataset, was also observed in the livers of HFD-induced NAFLD mice and in HepG2 cells exposed to palmitic acid or advanced glycation end products. ConclusionThe hub genes SOX9, CCL20, CXCL1, CD24, and CHST4 are involved in the aggravation of NAFLD. Our results offer new insights into the underlying mechanism of NAFLD progression.

Місце транзієнтної еластографії в діагностиці неалкогольної жирової хвороби печінки

Неалкогольна жирова хвороба печінки включає стеатоз печінки, стеатогепатит та фіброз, що можуть прогресувати до стеатогенного цирозу печінки. З огляду на поширеність цієї патології, погіршення якості життя хворих, зростання смертності від ускладнень зростає інтерес до розробки методів для точної та своєчасної оцінки ступеня жирової дистрофії печінки та прогресування фіброзу. Мета: вивчити діагностичні можливості транзієнтної еластографії у пацієнтів з ідіопатичним підвищенням рівня трансаміназ. Методи. У 52 хворих (20 чоловіків і 32 жінки) з ідіопатичним збільшенням трансаміназ без ознак стеатозу печінки згідно з сонографічним дослідженням визначали контрольований параметр ультразвукового затухання (CAP) і жорсткість печінки (LSM) з використанням апарата FibroScan з М-зондом. Критеріями виключення з дослідження були наявність хронічних вірусних, автоімунних гепатитів та зловживання алкоголем. Результати. 78,8 % пацієнтів мали жирову дистрофію печінки згідно з CAP. При аналізі контрольованого параметра ультразвукового затухання було встановлено, що 63,4 % мали фіброз F0–F1, 29,3 % — F1–F2, а 7,3 % — F3. За показником САР існували вірогідні відмінності між групою з вираженим фіброзом (F3) та групою з мінімальним фіброзом (F0–F1) ((203,0 ± 5,1) проти (243,0 ± 10,1), р &lt; 0,05). При аналізі біохімічних показників були відзначені вірогідні відмінності рівня гамма-глутамілтрансферази у групі з вираженим фіброзом (F3) від показників групи з мінімальним фіброзом (F0–F1) ((40,2 ± 5,7) проти (26,4 ± 3,7), р &lt; 0,05). Отже, у значної частини пацієнтів з ідіопатичним підвищенням рівня трансаміназ чинником запалення є жирова дистрофія печінки, що не виявлялась при рутинному ультразвуковому обстеженні. У групі з більш розвинутим фіброзом спостерігалось зменшення вмісту жиру в печінці та підвищення активності гамма-глутамілтрансферази, що свідчить про посилення холестазу в печінці в даної категорії пацієнтів. Отже, у пацієнтів з ідіопатичним підвищенням трансаміназ навіть за відсутності ознак стеатозу згідно з даними сонографії доцільно проводити визначення CAP апаратом FibroScan, що є більш чутливим у встановленні жирової дистрофії, ніж ультразвукове дослідження.

Effect of a common missense variant in LIPA gene on fatty liver disease and lipid phenotype: New perspectives from a single-center observational study.

Lysosomal acid lipase deficiency (LAL‐D) is an autosomal recessive disease characterized by hypoalphalipoproteinemia, mixed hyperlipemia, and fatty liver (FL) due to mutations in LIPAse A, lysosomal acid type (LIPA) gene. The rs1051338 single‐nucleotide polymorphism (SNP) in LIPA gene, in vitro, could adversely affect the LAL activity (LAL‐A). Nonalcoholic fatty liver disease (NAFLD) is often associated with metabolic syndrome, and the diagnosis requires the exclusion of excess of alcohol intake and other causes of hepatic disease. The aim of the study was to evaluate the impact of rs1051338 rare allele on lipid phenotype, severity of FL, and LAL‐A in patients suffering from dyslipidemia associated with NAFLD. We selected 74 subjects with hypoalphalipoproteinemia or mixed hyperlipemia and evaluated transaminases, liver assessment with controlled attenuation parameter (CAP), LAL‐A, rs1051338 SNP genotype. The presence of rare allele caused higher levels of triglycerides and hepatic transaminase and lower levels of high‐density lipoprotein cholesterol (HDL‐C). Multivariate analysis highlighted independent association between rare allele and FL severity in subjects with NAFLD. The rs1051338 SNP may modulate FL severity and atherogenic dyslipidemia in patients suffering from NAFLD.

Relationship Between Nonalcoholic Fatty Liver and Non High Density Lipoprotein to High Density Lipoprotein Ratio

Aim: The aim of this study was to investigate the relationship between non-alcoholic fatty liver and demographic characteristics, laboratory parameters and predictory non-high density lipoprotein to high density lipoprotein ratio. Material and Methods: Between February and September 2020, 329 patients with fatty liver prediagnosis were evaluated prospectively. Laboratory (whole blood counts, transaminases, lipid profiles, 25-oh vitamin d3 levels) and ultrasonography findings, body height, body weight and body mass index of patients were compared between fatty liver and control groups. Results: Fatty liver was diagnosed in 164 patients out of 329 participants. There were significant relationships between existence of fatty liver and age, body weight, body mass index, triglyceride levels, non-high density lipoprotein, non-high density lipoprotein to high density lipoprotein ratios. Also relationships between severity of fatty liver and body weight, alanine aminotransferase and body mass index were found to be significant. There were no relationship between existence of fatty liver and monocyte to high density lipoprotein ratio and vitamin D levels. Linear regression analysis for Non-HDL/ HDL ratio in diagnosis of nonalcoholic fatty liver, revealed a correlation coefficient as r=0.179. Positive and negative predictive values for Non-HDL/HDL ratio in diagnosis of nonalcoholic fatty liver were, 56.3% and 60.9%, respectively . Conclusion: There is a significant relationship between fatty liver and non-high density lipoprotein to high density lipoprotein ratio. This ratio may be a simple and readily available predictor in patients with fatty liver.

Accuracy of FibroTouch in assessing liver steatosis and fibrosis in patients with metabolic-associated fatty liver disease combined with type 2 diabetes mellitus.

Metabolic-associated fatty liver disease (MAFLD) is highly prevalent in type 2 diabetes mellitus (T2DM) patients and can rapidly progress to steatohepatitis, liver fibrosis, and hepatocellular carcinoma (HCC). Accurate evaluation and proper management of MAFLD can help prevent adverse liver outcomes. Here we evaluated the precision of the FibroTouch (FT) in the staging of liver steatosis and fibrosis in patients with MAFLD combined with T2DM using two indicators: controlled attenuation parameter (CAP) and liver stiffness measurement (LSM). Eighty-five adult MAFLD combined with T2DM patients were selected at our center from July 2016 to July 2019 and underwent liver puncture biopsy for histopathology and the FT assay simultaneously. Two blinded pathologists independently reviewed the samples. The severity of fatty liver was classified using two scoring systems: the nonalcoholic fatty liver disease activity score (NAS) and the fibrosis score. Scores were then assessed following the Pathology Working Group of the NASH Clinical Research Network of the National Institutes of Health. Similarly, the severity of nonalcoholic steatohepatitis (NASH) was classified using the European Steatosis Activity Fibrosis (SAF) system. The FT assay was applied to obtain the LSM and the CAP. FT accuracy in diagnosing steatosis and fibrosis was determined by the receiver operating characteristic (ROC) curve and the area under the ROC curve (AUROC). Using biopsy analysis as the gold standard, the AUROCs and cutoff values of CAP in diagnosing liver steatosis were as follows: 0.84 (95% CI: 0.67-1.01) and 278 dB/m for S ≥ S1, 0.88 (95% CI: 0.81-0.95) and 305 dB/m for S ≥ S2, 0.89 (95% CI: 0.82-0.95) and 307 dB/m for S ≥ S3. The AUROCs and cutoff values of LSM in diagnosing liver fibrosis were as follows: 0.76 (95% CI: 0.66-0.86) for F ≥ F2, 0.81 (95% CI: 0.71-0.91) and 13.8 kPa for F ≥ F3, 0.92 (95% CI: 0.85-1.00) and 20.1 kPa for F ≥ F4. In patients of MAFLD with T2DM, CAP and LSM obtained by FT are highly accurate in assess liver steatosis and fibrosis, respectively, with AUROC values ranging from 0.76 to 0.92.

Влияние содержания витаминов D и B12 на частоту стеатогепатоза у детей с избыточной массой тела и ожирением

Актуальность. Неалкогольный стеатогепатоз у детей приводит к росту заболеваемости и смертности во взрослом возрасте. В последние годы опубликованы противоречивые данные о взаимосвязи между уровнями витаминов D и B12 и частотой неалкогольного стеатогепатоза. Цель исследования: оценить взаимосвязь между уровнем витаминов D и B12 и инсулинорезистентностью (ИР) и частотой неалкогольного стеатогепатоза у детей с ожирением и избыточной массой тела. Материалы и методы. В проспективное исследование были включены 167 детей с избыточной массой тела и ожирением в возрасте от 5 до 18 лет. Определяли антропометрические показатели, включая массу тела, рост, индекс массы тела (ИМТ) (вес/рост2, кг/м2). У детей и подростков с ИМТ ≥ 95-го перцентиля для возраста и пола диагностировали ожирение, а ИМТ от 85-го до 94-го перцентиля классифицировали как избыточную массу тела. Дети и подростки были разделены на две группы: со стеатогепатозом и без нарушения функционального состояния печени. Дополнительно оценивали состояние печени с помощью ультразвукового исследования. Определяли демографические характеристики участников исследования, проводили общеклинический обзор, лабораторные исследования, включая анализы на выявление уровня витамина В12 и 25(OH)D в сыворотке крови и определение индекса ИР. Результаты. Из 167 обследованных 103 (61,7 %) были мужского пола, 64 (38,3 %) — женского, их средний возраст составил 11,48 ± 2,99 года. Согласно ИМТ в 26,3 % случаев была выявлена избыточная масса тела, а в 73,7 % — ожирение. Стеатогепатоз диагностирован в 70,7 % случаев (n = 118), его частота была достоверно выше у пациентов мужского пола (79,6 %), чем женского (p = 0,001). Средний показатель ИР был статистически выше в группе детей со стеатогепатозом (11,15 ± 13,39), чем в контрольной группе (6,95 ± 6,20) (р = 0,029). Кроме того, установлены статистически значимые различия уровней ИР по степени выраженности стеатогепатоза (р = 0,013). Не наблюдалось достоверной взаимосвязи между дефицитом витаминов D и B12, наличием и тяжестью стеатогепатоза (p &gt; 0,05). Также не было выявлено статистически значимых различий между средним содержанием витаминов D и В12 и индексом ИР среди детей с ожирением и избыточной массой тела. Выводы. Полученные результаты подтверждают опубликованные ранее данные о том, что дефицит витаминов D и B12 не способствует развитию стеатогепатоза у детей с избыточной массой тела и ожирением. Инсулинорезистентность является фактором риска возникновения и прогрессирования стеатогепатоза.

Close association between non-alcoholic fatty liver disease and ossification of the posterior longitudinal ligament of the spine

Ossification of the posterior longitudinal ligament (OPLL) of the spine is a disease of unknown etiology occurring frequently in individuals with metabolic disturbances. Obesity has been suggested as a potential risk factor for the severity of OPLL. We aimed to investigate whether non-alcoholic fatty liver disease (NAFLD) is associated with OPLL severity. We assessed the severity of NAFLD by a liver-to-spleen (L/S) ratio on computed tomography (CT) scans of 85 symptomatic OPLL patients at a single institution in Japan. We also assessed the severity of OPLL by CT reconstruction sagittal and axial images. The prevalence of NAFLD in middle-aged patients (age < 70 years, n = 50) was 80.3%, which was 2.5–8 times higher than that in the general Japanese population (9–30%). The ossification index of the spinal ligaments increased in proportion to the severity of fatty liver. The L/S ratio was revealed as a significant risk factor associated with the total ossification index (standardized β: -0.40, 95% confidence interval − 54.34 to − 4.22). This study suggests the potential contribution of NAFLD to the progression of OPLL. The close association between NAFLD and OPLL demonstrated in this study warrants further study to elucidate the causal nature of this relationship.