Risk Factors For Liver Fibrosis Research Articles

Association between Serum Ferritin Levels and Metabolic-associated Fatty Liver Disease in Adults: a Cross-sectional Study Based on the NHANES.

Ferritin, initially acting as an iron-storage protein, was found to be associated with metabolic diseases. Our study was designed to investigate the association between serum ferritin and metabolic-associated fatty liver disease (MAFLD) using data from the National Health and Nutrition Examination Survey (NHANES) of the United State of America. A cross-sectional study was conducted, enrolling a total of 2145 participants from the NHANES in the 2017-2018 cycles. Hepatic steatosis and liver fibrosis were assessed by ultrasound images and several non-invasive indexes. Multiple regression analysis was conducted to determine the associations between serum ferritin concentration and MAFLD and liver fibrosis. The analysis revealed that participants with higher serum ferritin levels (Q3 and Q4 groups) had a higher prevalence of MAFLD than those with the lowest serum ferritin levels [Q3 vs. Q1: OR=2.17 (1.33, 3.53), P<0.05 in fatty liver index (FLI); Q4 vs. Q1: OR=3.13 (1.91, 5.13), P<0.05 in FLI]. Additionally, participants with the highest serum ferritin levels (Q4 group) displayed a higher prevalence of liver fibrosis [Q4 vs. Q1: OR=2.59 (1.19, 5.62), P<0.05 in liver stiffness measurement; OR=5.06 (1.12, 22.94), P<0.05 in fibrosis-4 index], with significantly increased risk observed in participants with concomitant diabetes [OR=7.45 (1.55, 35.72), P=0.012]. Our study revealed that elevated serum ferritin levels are associated with a higher prevalence of MAFLD and advanced liver fibrosis in patients. Elevated serum ferritin levels combined with diabetes are important risk factors for liver fibrosis.

Isolation of mucosa-associated microbiota dysbiosis in the ascending colon in hepatitis C virus post-sustained virologic response cirrhotic patients.

Achieving sustained virologic response (SVR) in patients infected with hepatitis C virus (HCV) reduces all-cause mortality. However, the mechanisms and risk factors for liver fibrosis and portal hypertension post-SVR remain incompletely understood. In the gut-liver axis, mucosa-associated microbiota (MAM) substantially influence immune and metabolic functions, displaying spatial heterogeneity at the anatomical intestinal site. We analyzed MAM composition and function to isolate the locoregional MAM involved in chronic liver disease progression in HCV post-SVR patients. We collected MAM samples from three intestinal sites (terminal ileum, ascending colon, and sigmoid colon) via brushing during colonoscopy in 23 HCV post-SVR patients and 25 individuals without liver disease (controls). The 16S rRNA of bacterial DNA in specimens collected with a brush and in feces was sequenced. The molecular expression of intestinal tissues and hepatic tissues were evaluated by quantitative real-time PCR. In the post-SVR group, the microbial β-diversity of MAM, especially in the ascending colon, differed from the control group and was associated with liver fibrosis progression. In PICRUSt analysis, MAM in the ascending colon in the liver cirrhosis (LC) group showed compromised functions associated with the intestinal barrier and bile acid production, and FGF19 expression was markedly decreased in the terminal ileum biopsy tissue in the LC group. At the genus level, six short-chain fatty acid (SCFA)-producing bacterial genera, Blautia, Alistipes, Roseburia, Agathobaculum, Dorea, and Pseudoflavonifractor were reduced in the ascending colon of post-SVR LC patients. In patients of HCV post-SVR, we identified the association between the degree of liver fibrosis and dysbiosis of mucosa-associated SCFA-producing bacterial genera that may be related to intestinal barrier and bile acid production in the ascending colon.

Development and validation of a noninvasive prediction model for significant hepatic liver fibrosis in Chinese patients with autoimmune hepatitis

Introduction and ObjectivesAutoimmune hepatitis (AIH) is a prevalent noninfectious liver disease. However, there is currently a lack of noninvasive tests appropriate for evaluating liver fibrosis in AIH patients. The objective of this study was to develop and validate a predictive model for noninvasive assessment of significant liver fibrosis (S ≥ 2) in patients to provide a reliable method for evaluating liver fibrosis in individuals with AIH. Materials and MethodsThe clinical data of 374 AIH patients were analyzed. A prediction model was established through logistic regression in the training set, and bootstrap method was used to validate the models internally. In addition, the clinical data of 109 AIH patients were collected for external verification of the model.The model was expressed as a nomogram, and area under the curve (AUC) of the receiver operating characteristic (ROC), calibration curve, and decision curve analysis were used to evaluate the accuracy of the prediction model. ResultsLogistic regression analysis revealed that age, platelet count (PLT), and the A/G ratio were identified as independent risk factors for liver fibrosis in AIH patients (P < 0.05). The diagnostic model that was composed of age, PLT and A/G was superior to APRI and FIB-4 in both the internal validation (0.872, 95%CI: 0.819–0.924) and external validation (0.829, 95%CI: 0.753–0.904). ConclusionsOur predictive model can predict significant liver fibrosis in AIH patients more accurately, simply, and noninvasively.

Obesity and harmful alcohol consumption are predictors for advanced liver disease in the disease management program for type 2 diabetes.

Type 2 diabetes mellitus (T2DM) is a major risk factor for advanced liver disease. The aim of this prospective cohort study was to assess the prevalence and associated risk factors of liver fibrosis and cirrhosis in primary care centers participating in the diabetes disease management program (DMP) in Germany. A total of 175 participants with the diagnosis of T2DM were enrolled in two primary care centers. Steatotic liver disease (SLD; hepatic steatosis, ≥275dB/m), fibrosis (≥8kPa), and cirrhosis (≥15kPa) were assessed non-invasively using vibration-controlled transient elastography. Multivariable logistic regression analysis was performed to identify clinical predictors of fibrosis and cirrhosis. The AUDIT questionnaire was used to screen for alcohol consumption, and a score ≥8 was considered harmful alcohol consumption. The majority of participants were male (62%), and the median age was 66years (interquartile range 59; 71). The median body mass index was 31.1kg/m2 , with 58.9% of the participants being obese. Harmful alcohol consumption was prevalent in 8.0% and 20.0% of the entire cohort and in those with cirrhosis, respectively. The prevalence of SLD, fibrosis, and cirrhosis was 77.1%, 42.3%, and 12.0%, respectively. In multivariable logistic regression analysis, obesity, and harmful alcohol consumption were associated with the highest odds of fibrosis (odds ratio [OR] 5.198, 95% confidence interval [CI] 2.269-11.908) and cirrhosis (OR 5.615, 95% CI 1.274-24.756), respectively. The prevalence of fibrosis and cirrhosis in patients seen in the diabetes DMP in Germany is high. Obesity and harmful alcohol consumption increase the risk of fibrosis and cirrhosis in people with T2DM. Screening for advanced liver disease and associated risk factors within the DMP program may reduce the liver disease burden in this high-risk population.

Associated factors with liver fibrosis in rheumatoid arthritis patients treated with methotrexate.

There are conflicting findings on the link between liver fibrosis and cumulative methotrexate dosages. We aimed to determine the frequency of liver fibrosis in rheumatoid arthritis patients treated with methotrexate and to identify its associated factors. We conducted a cross-sectional study over 9 months (April-December 2021), including rheumatoid arthritis patients treated with methotrexate. Demographic and clinical data were collected. Liver stiffness was assessed by FibroScan. Fibrosis and significant liver fibrosis were defined as liver stiffness higher than 6 and 7.2 kPa, respectively. Liver tests, albuminemia, lipid profile, and blood glycemia were measured. Metabolic syndrome was also evaluated. Statistical analyses were performed using SPSS. We included 21 men and 47 women. The mean age was 51.60 ± 1.82 years. The mean disease duration was 8.29 ± 6.48 years. The mean weekly intake of methotrexate was 13.76 ± 3.91 mg. The mean methotrexate duration was 4.67 ± 4.24 years. The mean cumulative dose was 3508.87 ± 3390.48 mg. Hypoalbuminemia and metabolic syndrome were found in 34% and 25% of cases. We noted increased alkaline phosphatase levels in four cases. The mean liver stiffness was 4.50 ± 1.53kPa. Nine patients had liver fibrosis, and four had significant fibrosis. Associated factors with liver fibrosis were as follows: age ≥ 60 years (OR:22.703; 95%CI [1.238-416.487]; p = 0.035), cumulated dose of methotrexate ≥ 3 g (OR: 76.501; 95%CI [2.383-2456.070]; p = 0.014), metabolic syndrome (OR: 42.743; 95%CI [1.728-1057.273]; p = 0.022), elevated alkaline phosphatase levels (OR: 28.252; 95%CI [1.306-611.007]; p = 0.033), and hypoalbuminemia (OR: 59.302; 95%CI [2.361-1489.718]; p = 0.013). Cumulating more than 3 g of methotrexate was associated with liver fibrosis in rheumatoid arthritis patients. Having a metabolic syndrome, higher age, hypoalbuminemia, and elevated alkaline phosphatase levels were also likely to be independently associated with liver fibrosis. Key points • Rheumatoid arthritis patients require monitoring hepatic fibrosis when the cumulated dose of methotrexate is above 3 g. • Metabolic syndrome is a risk factor for liver fibrosis, suggesting that its management is necessary to prevent this complication. • Hypoalbuminemia and elevated alkaline phosphatase levels (twice the upper limit) in rheumatoid arthritis patients treated with methotrexate were associated with liver fibrosis.

Personalized Risk Assessment of Hepatic Fibrosis after Cholecystectomy in Metabolic-Associated Steatotic Liver Disease: A Machine Learning Approach.

Metabolic Associated Fatty Liver Disease (MASLD) is a condition that is often present in patients with a history of cholecystectomy. This is because both situations share interconnected metabolic pathways. This study aimed to establish a predictive model that allows for the identification of patients at risk of developing hepatic fibrosis following this surgery, with potential implications for surgical decision-making. A retrospective cross-sectional analysis was conducted in four hospitals using a database of 211 patients with MASLD who underwent cholecystectomy. MASLD diagnosis was established through liver biopsy or FibroScan, and non-invasive test scores were included for analysis. Various Machine Learning (ML) methods were employed, with the Adaptive Boosting (Adaboost) system selected to build the predictive model. Platelet level emerged as the most crucial variable in the predictive model, followed by dyslipidemia and type-2 diabetes mellitus. FIB-4 score proved to be the most reliable non-invasive test. The Adaboost algorithm improved the results compared to the other methods, excelling in both accuracy and area under the curve (AUC). Moreover, this system holds promise for implementation in hospitals as a valuable diagnostic support tool. In conclusion, platelet level (<150,000/dL), dyslipidemia, and type-2 diabetes mellitus were identified as primary risk factors for liver fibrosis in MASLD patients following cholecystectomy. FIB-4 score is recommended for decision-making, particularly when the indication for surgery is uncertain. This predictive model offers valuable insights into risk stratification and personalized patient management in post-cholecystectomy MASLD cases.

Crohn´s disease is an independent risk factor for liver fibrosis in patients with inflammatory bowel disease and non-alcoholic fatty liver disease

Background and aimsControversial data have been reported regarding the prevalence of Non-Alcoholic Fatty Liver Disease (NAFLD) in Inflammatory Bowel Disease (IBD) population and IBD-related risk factors. The aim of the study was to assess the prevalence and risk factors associated with NAFLD and liver fibrosis in IBD participants compared with non-IBD controls. MethodsCross-sectional, case-control study including 741 IBD cases and 170 non-IBD controls, matched by sex and age. All participants underwent liver ultrasound, transient elastography and laboratory tests. A logistic regression multivariable analysis was performed adjusting for classic metabolic risk factors and history of systemic steroid use. ResultsThe prevalence of NAFLD and significant liver fibrosis was 45 % and 10 % in IBD group, and 40 % and 2.9 % in non-IBD group (p = 0.255 and 0.062, respectively). Longer IBD duration (aOR 1.02 95% CI (1.001–1.04)) and older age at IBD diagnosis (aOR 1.02 95 % CI (1.001–1.04)) were independent risk factors for NAFLD in IBD group. Crohn´s Disease was an independent risk factor for significant liver fibrosis in participants with IBD and NAFLD (aOR 3.97 95 % CI (1.78–8.96)). NAFLD occurred at lower BMI levels in IBD group with NAFLD compared to non-IBD group with NAFLD (aOR 0.92 95 % CI (0.87–0.98)). ConclusionsAlthough we found no differences in the prevalence of NAFLD and liver fibrosis between IBD group and non-IBD group, our findings suggest that liver fibrosis progression should be closely monitored in patients with concomitant CD and NAFLD, more in particular in those with long standing active disease.

NAFLD is associated with less severe liver fibrosis in chronic hepatitis B: A multi-center, retrospective study

Introduction and ObjectivesChronic hepatitis B (CHB) may progress to more serious liver diseases and it is often accompanied by non-alcoholic fatty liver disease (NAFLD). NAFLD and CHB share risk factors for liver fibrosis and cirrhosis, but the influence of NAFLD on fibrosis progression is controversial. This retrospective study evaluated the prevalence of NAFLD in patients with CHB and investigated associations between NAFLD and liver fibrosis in a large multi-center cohort of hepatitis B patients submitted to liver biopsy. Patients and MethodsTreatment-naïve patients with CHB who underwent liver biopsy were analyzed. Propensity score matching (PSM) was performed to adjust the confounders between patients with and without NAFLD. ResultsA total of 1496 CHB patients were included. Two hundred and ninety (19.4%) patients were diagnosed with NAFLD by liver biopsy. The proportions of significant liver fibrosis (52.8% vs. 63.9%, P<0.001), advanced liver fibrosis (27.2% vs. 36.5%, P=0.003), and cirrhosis (13.4% vs. 19.7%, P=0.013) was considerably lower in CHB patients with NAFLD compared to those without NAFLD. 273 patients were included in each group after PSM adjusted for age, sex, hepatitis B envelope antigen status, and hepatitis B virus DNA. Liver fibrosis remained less severe in CHB patients with NAFLD than those without NAFLD (P<0.05) after PSM. The presence of NAFLD was considered an independent negative factor of significant liver fibrosis (odds ratio (OR) 0.692, P=0.013) and advanced liver fibrosis (OR 0.533, P = 0.002) in CHB patients. ConclusionsNAFLD is not uncommon in CHB patients with the prevalence of 19.4%. The presence of NAFLD is associated with less severe liver fibrosis in CHB patients. Registration No. of the study/trialNCT03097952.

Poor correlation of 2D shear wave elastography and transient elastography in Fontan-associated liver disease: A head-to-head comparison.

Fontan-associated liver disease (FALD) is a long-term complication of the Fontan procedure. Guidelines recommend elastography, but the utility of transient elastography (TE) and two-dimensional shear wave elastography (2D SWE) is unknown. We aimed to evaluate the relationship between TE and 2D SWE in FALD. This prospective cohort study included 25 patients managed in a specialist clinic between January 2018 and August 2021. Trained clinicians performed 2D SWE (GE Logiq-E9) and TE (FibroScan 503 Touch) on the same day under the same conditions. Laboratory, echocardiography, and imaging data were collected. The atrioventricular systolic-to-diastolic duration (AVV S/D ratio) was calculated as a measure of cardiac diastolic function. We analyzed 40 paired measurements. Median age was 22 years. Median liver stiffness measurement (LSM) was 15.4 kPa (12.1-19.6) by TE and 8.0 kPa (7.0-10.3) (P = 0.001) by 2D SWE. There was weak correlation between the modalities (r = 0.41, P = 0.004). There was no correlation between time since Fontan and LSM by TE (r = 0.15, P = 0.19) or 2D SWE (r = 0.19, P = 0.13). There was no difference in LSM irrespective of whether sonographic cirrhosis was present or absent by TE (17.4 kPa [15.9-23.6] vs. 14.9 kPa [12.0-19.4], respectively, P = 0.6) or 2D SWE (9.0 kPa [2.8-10.5] vs. 8.0 kPa [6.7-10.1], P = 0.46). There was no correlation between AVV S/D ratio and LSM by TE (r = 0.16, P = 0.18) or 2D SWE (r = 0.02, P = 0.45). In FALD, TE and 2D SWE are poorly correlated. LSM by either modality was not associated with known risk factors for liver fibrosis or Fontan function. Based on these data, the role of elastography in FALD is uncertain.

Galectin-12 modulates Kupffer cell polarization to alter the progression of nonalcoholic fatty liver disease.

Nonalcoholic fatty liver disease is caused by an imbalance in lipid metabolism and immune response to pose a risk factor for liver fibrosis. Recent evidence indicates that M2 macrophages secrete transforming growth factor-β1, which contributes to liver fibrosis. Galectin-12 has been demonstrated to regulate lipid metabolism and macrophage polarization. The purpose of this study is to investigate the role of galectin-12 in the development of nonalcoholic fatty liver disease and fibrosis. Liver tissue from wild-type C57BL/6 mice fed with a high-fat diet containing cholesterol and cholic acid for 4-12weeks was used to examine galectin-12 expression and its correlation with nonalcoholic fatty liver disease. Furthermore, the effects of galectin-12 on M2 macrophages during the progression of nonalcoholic fatty liver disease were investigated by studying Kupffer cells from galectin-12 knockout mice and doxycycline-inducible Gal12-/-THP-1 cells. Ablation of galectin-12 promoted M2 polarization of Kupffer cells, as indicated by higher levels of M2 markers, such as arginase I and chitinase 3-like protein 3. Furthermore, the activation of signal transducer and activator of transcription 6 was significantly higher in Gal12-/- macrophages activated by interleukin-4, which was correlated with higher levels of transforming growth factor-β1. Moreover, Gal12-/- macrophage-conditioned medium promoted hepatic stellate cells myofibroblast differentiation, which was indicated by higher α-smooth muscle actin expression levels compared with those treated with LacZ control medium. Finally, we demonstrated that galectin-12 knockdown negatively regulated the suppressor of cytokine signaling 3 levels. These findings suggested that galectin-12 balances M1/M2 polarization of Kupffer cells to prevent nonalcoholic fatty liver disease progression.

Liver Fibrosis in Non-Alcoholic Fatty Liver Disease and Progression to Hepatocellular Carcinoma in Patients with Inflammatory Bowel Disease: A Systematic Review

The aim of the systematic review is to assess the prevalence and risk factors of liver fibrosis in patients with Inflammatory Bowel Disease (IBD) and Non-Alcoholic Fatty Liver Disease (NAFLD) and to discuss the role of liver fibrosis in the progression to hepatocellular carcinoma (HCC). We performed a structured search in PubMed, Web of Science, Embase, and Scopus up to 3 March 2023 to identify observational studies reporting liver fibrosis in patients with NAFLD and IBD. Quality of studies was assessed using the Newcastle-Ottawa Scale (NOS) score. A total of 23 studies met our inclusion criteria, including 629,781 patients. A total of 10 cross-sectional, 3 case-control, and 10 cohort studies were included. Fourteen studies had a NOS score ≥ 7 points. NAFLD was diagnosed in 2162/6332 (34.1%) IBD participants. However, NAFLD diagnosis was established in 924/2962 (31.2%) healthy individuals without IBD. Advanced liver fibrosis was found in 116 (11.6%) of 992 IBD patients with NAFLD. Most studies found an association between NAFLD and classic cardiovascular risk factors such as older age, male sex, higher BMI, diabetes, hypertension and dyslipidemia. In addition, metabolic syndrome features were also associated with an increased risk of significant and advanced liver fibrosis. Although no strong association between NAFLD and IBD therapy was reported, some studies associated NAFLD with IBD diagnosis, Crohn’s Disease, a complicated course of IBD, disease activity, and IBD duration. Advanced liver fibrosis was also associated with Crohn’s disease in several studies. In conclusion, NAFLD and advanced liver fibrosis are prevalent and clinically relevant extraintestinal manifestations, so its diagnosis and potential progression to HCC should be carefully considered in daily clinical practice.

P68 Liver fibrosis is independent of methotrexate use in patients with moderate-to-severe psoriasis

Abstract Methotrexate has been implicated for liver disease in patients with psoriasis for many years. Liver fibrosis (LF) has various established risk factors, but data on the impact of methotrexate on LF in patients with psoriasis are lacking. This cross-sectional cohort study aimed to determine the prevalence of LF using noninvasive LF markers in patients with psoriasis, and to evaluate the relationship between LF and the cumulative dose of methotrexate and other liver disease risk factors. Adults with moderate-to-severe chronic plaque psoriasis diagnosed by a dermatologist, who were selected for a LF assessment, were recruited from dermatology clinics in a tertiary centre between June 2020 and March 2021. Data were recorded as part of standard clinical care and at the time of recruitment. Patients underwent transient elastography to evaluate LF. Three values for liver stiffness measurement (LSM) were used, indicating ≥ mild LF (≥ 7 kPa), ≥ moderate LF (≥ 7.9 kPa) and ≥ advanced LF (≥ 9.5 kPa). Both continuous and categorical LSM values were used for evaluation. A total of 225 patients were included [median age 48, interquartile range (IQR) 37–57, 51% female]. Fifty-six per cent had a body mass index (BMI) ≥ 30 kg m−2, and the median alcohol use disorders identification test (AUDIT) score was 4 (IQR 1–7, 23% score ≥ 8). Ninety-one per cent had received methotrexate for a median duration of 36 months (IQR 14–78). Prevalence rates of LF were 31%, 21% and 13% using LSM ≥ 7 kPa, ≥ 7.9 kPa and ≥ 9.5 kPa, respectively. There was no association between methotrexate and continuous LSM values [unadjusted coefficient 0.16, 95% confidence interval (CI) 0.49–0.82; P = 0.63] or using the categorical LSM cutoff values: 7 kPa (unadjusted coefficient 1.06, 95% CI 0.98–1.15; P = 0.19), 7.9 kPa (unadjusted coefficient 1.03, 95% CI 0.94–1.12; P = 0.58) and 9.5 kPa (unadjusted coefficient 1.01, 95% CI 0.91–1.12; P = 0.84). Similarly, no significant relationship was found when adjusting for other risk factors for LF. The following risk factors were associated with higher LSM values: BMI (P &amp;lt; 0.001), waist circumference (P &amp;lt; 0.001), metabolic syndrome (P &amp;lt; 0.001), AUDIT score (P = 0.020) and Fib-4 score (P = 0.03). This study confirms a high prevalence of significant LF in patients with moderate-to-severe psoriasis. More importantly, it shows that cumulative methotrexate was not associated with LF, and other risk factors including BMI, waist circumference, metabolic syndrome, alcohol intake and Fib-4 score are important predictors for LF. The findings suggest that these risk factors should be assessed in this group of patients to identify patients requiring regular liver health monitoring. Further research is needed to determine whether methotrexate contributes to the progression of LF in the context of pre-existing LF.

Prevalence of risk factors for liver fibrosis and associations of serum biomarkers with liver fibrosis in a Houston community clinic.

e22518 Background: Liver fibrosis may lead to hepatocellular carcinoma (HCC). Hepatitis B virus (HBV) infection, hepatitis C virus (HCV) infection, metabolic syndrome, and alcohol use disorder (AUD) are risk factors for fibrosis. Early screening for fibrosis using serum biomarkers in community settings is not well established. Methods: Adult patients at the HOPE Clinic, a federally qualified health care center in Houston, were enrolled from January 2021 through January 2023 and surveyed about risk factors for liver fibrosis. We measured vital signs and waist circumference, calculated body mass index (BMI), and performed blood testing. We defined chronic HBV infection as positivity for hepatitis B surface antigen; chronic HCV infection as detectable HCV RNA; metabolic syndrome as the presence of at least 3 of 4 conditions: hyperglycemia, hypertension, dyslipidemia, and obesity; and AUD as an AUDIT-C score of ≥4 for men and ≥3 for women. Transient elastrography was performed to assess for fibrosis, with scores ≥8 kPa indicating ≥F2 fibrosis. Serum biomarkers of fibrosis were defined as Fibrosis-4 (FIB-4) score ≥2.67 (based on ALT, AST, platelets, age); NAFLD Fibrosis Score (NFS) ≥0.675 (based on ALT, AST, platelets, albumin, age, BMI, diabetes); and Fatty Liver Index (FLI) ≥30 (based on triglycerides, gamma-glutamyl transferase, waist circumference, BMI). We described the prevalence of fibrosis risk factors and tested the associations of risk factors and serum biomarkers with ≥F2 fibrosis using Fisher’s exact test. Results: We enrolled 904 patients, 378 men (42%) and 526 women (58%). The median age was 48 years. A total of 456 patients (51%) were White, 245 (27%) were Asian, and 187 (21%) were Black. Among all patients, 365 (41%) were Hispanic. Forty-two percent of patients (n = 377) had BMI ≥30. Five percent of patients (46/869) had chronic HBV infection, &lt; 1% (1/863) had chronic HCV infection, 49% (417/849) had metabolic syndrome, and 13% (115/896) had AUD. Of 826 patients who completed transient elastrography, 79 (10%) had ≥F2 fibrosis. Metabolic syndrome was significantly associated with ≥F2 fibrosis (odds ratio [OR] 2.4, 95% confidence interval [CI] 1.5-4.1) but chronic HBV infection, chronic HCV infection, and AUD were not. Serum biomarkers were predictive of ≥F2 fibrosis: FIB-4 score ≥2.67 (OR 19.1, 95% CI 7.3-50.2); NFS ≥0.675 (OR 12.0, 95% CI 4.2-34.2); and FLI ≥30 (OR 5.9, 95% CI 1.4-25.0). Among patients with metabolic syndrome, FIB-4 score ≥2.67 (OR 22.0, 95% CI 4.3-112.0) and NFS ≥0.675 (OR 11.9, 95% CI 2.8-51.4) were predictive of ≥F2 fibrosis, but FLI ≥30 (OR 4.5, 95% CI 0.7-27.5) was not. Conclusions: In this ongoing community-based study, 1 in 10 patients had fibrosis. Metabolic syndrome was a significant risk factor for ≥F2 fibrosis, along with FIB-4 and NFS among patients with metabolic syndrome. Incorporating biomarkers into clinical algorithms will be useful to prevent HCC. Clinical trial information: NCT04785534 .

High prevalence of metabolic diseases, liver steatosis and fibrosis among Chinese psychiatric patients

BackgroundWe aimed to investigate the differences of metabolic disorders between the general population and psychiatric patients, with an emphasis on the prevalence and influencing factors of liver fibrosis in psychiatric patients.MethodsA total of 734 psychiatric patients and 734 general population matched for age, sex, and BMI were enrolled from Shanghai, China. All participants underwent blood pressure, glucose, lipid profile measurements, and anthropometric parameters including body weight, height and waist circumference. FibroScan examinations were also performed on psychiatric patients. Liver steatosis and fibrosis were diagnosed by controlled attenuation parameter (CAP) and liver stiffness measurement (LSM) by professional staff.ResultsCompared with the general population, psychiatric patients revealed significantly higher burden of metabolic disorders. The overall prevalence of liver steatosis (CAP ≥ 233 dB/m) and fibrosis (LSM ≥ 7.0 kPa) was 48.7% and 15.5% in psychiatric patients. Psychiatric patients with liver steatosis or fibrosis showed worse metabolic profile. Meanwhile, the prevalence of liver fibrosis was also significantly higher in patients with overweight, central obesity, diabetes, hypertension, metabolic syndrome, and liver steatosis. In logistic regression analyses, age, BMI and visceral adiposity index were independent risk factors for liver fibrosis in psychiatric patients. Additionally, antipsychotic medication was suggested to be associated with an increased risk of liver fibrosis in psychiatric patients with liver steatosis.ConclusionsPrevalence of liver steatosis and fibrosis is high in Chinese psychiatric patients. Those with antipsychotic polypharmacy and obesity are at high risk, and may benefit from early liver assessment in preventing fibrosis progression.

Liver fibrosis is closely related to metabolic factors in metabolic associated fatty liver disease with hepatitis B virus infection

This case–control study aimed to identify the clinical characteristics and explore the risk factors for liver fibrosis in metabolic associated fatty liver disease (MAFLD) patients with hepatitis B virus (HBV) infection. The patients were grouped into MAFLD + HBV and MAFLD (without HBV infection). Propensity score matching (PSM) was used to match baseline features between the groups. We included 401 patients with biopsy-proven MAFLD, 179 of whom had HBV infection. A total of 83 pairs were successfully matched via PSM, and steatosis scores and ballooning in the MAFLD + HBV group were lower than those in the MAFLD group, while the inflammation scores and liver fibrosis stages were higher. After adjusted for confounding factors, HBV infection was associated with a higher risk of significant liver fibrosis in patients with MAFLD [odds ratio (OR): 3.140, P = 0.003]. Overall, 43.58% (78/179) of patients in the MAFLD + HBV group had significant liver fibrosis. Further multivariate regression analysis, hypertension (OR: 2.640; P = 0.031), type 2 diabetes (OR: 4.939; P = 0.035), and elevated glutamyl-transferase levels (OR: 3.980; P = 0.001) were risk factors for liver fibrosis in the MAFLD + HBV group. This suggests metabolic rather than viral factors are more closely associated with liver fibrosis in MAFLD patients with HBV infection.

Establishment and validation of a predictive nomogram for liver fibrosis in patients with Wilson disease and abnormal lipid metabolism

To establish and validate predictive nomogram for liver fibrosis in patients with Wilson disease (WD) showing abnormal lipid metabolism. We retrospectively collected the clinical data of 500 patients with WD showing abnormalities in lipid metabolism, who were treated in the Department of Encephalopathy of the First Affiliated Hospital of Anhui University of Chinese Medicine from December, 2018 to December, 2021 and divided into modeling group and validation group. The independent risk factors of liver fibrosis in these patients were screened using LASSO regression and multivariate logistic regression analysis for establishment of the predictive nomogram. The area under the curve (AUC), calibration curve and decision curve of the receiver-operating characteristic curve (ROC) were used for internal and external verification of the nomogram in the modeling and validation group and evaluating the differentiation, calibration and clinical practicability of the model. Triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and apolipoprotein B (Apo-B) were independent risk factors for the development of liver fibrosis in patients with WD and abnormal lipid metabolism (P < 0.05). The predictive nomogram showed good discrimination, calibration and clinical utility in both the modeling and validation groups. The established predictive nomogram in this study has a high accuracy for early identification and risk prediction of liver fibrosis in patients with WD having abnormal lipid metabolism.

Adipose Tissue Insulin Resistance Predicts the Severity of Liver Fibrosis in Patients With Type 2 Diabetes and NAFLD.

Although type 2 diabetes (T2D) is a risk factor for liver fibrosis in nonalcoholic fatty liver disease (NAFLD), the specific contribution of insulin resistance (IR) relative to other factors is unknown. Assess the impact on liver fibrosis in NAFLD of adipose tissue (adipose tissue insulin resistance index [adipo-IR]) and liver (Homeostatic Model Assessment of Insulin Resistance [HOMA-IR]) IR in people with T2D and NAFLD. Participants were screened by elastography in the outpatient clinics for hepatic steatosis and fibrosis, including routine metabolites, cytokeratin-18 (a marker of hepatocyte apoptosis/steatohepatitis), and HOMA-IR/adipo-IR. University ambulatory care practice. A total of 483 participants with T2D. Screening for steatosis and fibrosis with elastography. Liver steatosis (controlled attenuation parameter), fibrosis (liver stiffness measurement), and measurements of IR (adipo-IR, HOMA-IR) and fibrosis (cytokeratin-18). Clinically significant liver fibrosis (stage F ≥ 2 = liver stiffness measurement ≥8.0 kPa) was found in 11%, having more features of the metabolic syndrome, lower adiponectin, and higher aspartate aminotransferase (AST), alanine aminotransferase, liver fat, and cytokeratin-18 (P < 0.05-0.01). In multivariable analysis including just clinical variables (model 1), obesity (body mass index [BMI]) had the strongest association with fibrosis (odds ratio, 2.56; CI, 1.87-3.50; P < 0.01). When metabolic measurements and cytokeratin-18 were included (model 2), only BMI, AST, and liver fat remained significant. When fibrosis stage was adjusted for BMI, AST, and steatosis (model 3), only Adipo-IR remained strongly associated with fibrosis (OR, 1.51; CI, 1.05-2.16; P = 0.03), but not BMI, hepatic IR, or steatosis. These findings pinpoint to the central role of dysfunctional, insulin-resistant adipose tissue to advanced fibrosis in T2D, beyond simply BMI or steatosis. The clinical implication is that targeting adipose tissue should be the priority of treatment in NAFLD.

Noninvasive assessment and risk factors of liver fibrosis in pediatric patients with beta thalassemia major using transient elastography

BackgroundIn beta-thalassemia major (TM) patients, levels of liver iron overload and the presence of chronic hepatitis C are directly correlated with the onset and severity of liver fibrosis. A noninvasive approach that can evaluate cirrhosis and liver fibrosis in these patients is transient elastography (TE). We aimed to find out the role of noninvasive elastography in the assessment of liver fibrosis in young beta-thalassemia major patients receiving frequent blood transfusions. Identifying the patients' risk factors for liver fibrosis is another goal. The study comprised 53 patients, all of whom had a thorough history-taking procedure, clinical examination, and investigations such as CBC, serum ferritin, HCV and HBV serology, and liver function testing. It was carried out transient elastography to find liver fibrosis.ResultsAccording to transient elastography, 52.8% of the patients had severe fibrosis (F2 and higher). 9.4% of people had positive HCV serology results. Significant liver fibrosis was correlated with all serum ferritin levels (708.2 ± 182.1, 3213.5 ± 1272.9, nonsignificant vs. significant fibrosis), HCV infection, age, blood transfusion frequency, and irregular chelation therapy. But no significant correlation regarding sex and BMI was detected.ConclusionTransient elastography is an alternate noninvasive approach that assesses liver fibrosis in beta-thalassemia major patients. The risk of liver fibrosis is related to iron overload, HCV seropositivity, advanced age, frequent blood transfusion, and irregular chelation therapy.

Evaluation of Six Noninvasive Methods for the Detection of Fibrosis in Chinese Patients with Obesity and Nonalcoholic Fatty Liver Disease.

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the world, and liver fibrosis has been proven to be associated with liver diseaserelated events and total mortality. Several noninvasive methods have been developed, but whether those methods are suitable for the detection of fibrosis in Chinese patients with obesity and NAFLD has not been completely elucidated. This study aimed to compare the efficacy of fibrosis-4 (FIB-4), aspartate transaminase to platelet ratio index (APRI), modified aspartate transaminase to platelet ratio index (m-APRI), BARD (BARD (BMI (body mass index) > 28 = 1 point, AAR (aspartate aminotransferase/alanine aminotransferase) > 0.8 = 2 points, DM (diabetes mellitus) = 1 point)), NAFLD fibrosis score (NFS), and shear wave elastography (SWE) in the evaluation of the degree of liver fibrosis in Chinese patients with obesity and NAFLD. A retrospective study consisted of 100 patients. The accuracy of FIB-4, APRI, m-APRI, BARD, NFS, and SWE in the assessment of significant or advanced liver fibrosis in Chinese patients with obesity and NAFLD was compared. Weight and alanine aminotransferase (ALT) were independent risk factors for liver fibrosis. SWE, APRI, and m-APRI had significant efficiency in the diagnosis of significant fibrosis in patients with obesity and NAFLD. APRI and SWE were superior to the other methods in the diagnosis of significant and advanced liver fibrosis in patients with obesity and NAFLD. APRI and SWE showed no statistically significant difference in diagnostic efficiency. Weight and ALT are independent risk factors for liver fibrosis progression in NAFLD patients. SWE and APRI have predictive value for significant and advanced fibrosis of NAFLD in Chinese patients with obesity.

Liver Stiffness is Reduced to Normal After Successful Renal Transplantation: A Prospective Cohort Study

Liver stiffness (LS) may be falsely elevated in patients on maintenance hemodialysis (MHD) due to fluid overload. We measured LS change by transient elastography (TE) in MHD patients before and after successful renal transplantation. Adults on ≥2 years of MHD, without additional risk factors for liver fibrosis or fluid overload, and planned for renal transplantation were prospectively recruited. LS was measured on two occasions, i.e., within two weeks before transplantation (pre-Tx LS) and after ≥ 3 months after successful transplantation (post-Tx LS). The participants with pre-Tx LS≤7.0KPa and >7.0KPa were classified as "Group I" and "Group II," respectively. Categorical and numerical data are expressed as ratio/proportions and mean (SD), respectively. Paired data from 43 participants (males 42 [97.7%]; age 32 [11] years) were analyzed. The pre-Tx and post-Tx LS of the entire cohort, measured at 307 (198) days of interval, were 8.5 (7.3) KPa and 6.7 (3.1) KPa, respectively. Before transplantation, 21 (49%) participants belonged to Group II and 22 (51%) to Group I. Among the Group II participants, 12 (57%) showed LS normalization after 312 (182) days of transplantation. Of the 22 participants in Group I, three (13.6%) showed LS elevation to >7.0KPa after 303 (217) days of transplantation. The mean LS changes among the overall cohort, Group II, and Group I were -1.8KPa, -4.1KPa, and+0.2KPa, respectively. LS in people on MHD may be falsely elevated, which is likely to normalize after successful renal transplantation.