Liver Damage In Patients Research Articles

MiR-103–3p attenuates liver injury with severe acute pancreatitis by inhibiting pyroptosis through miR-103–3p/NLRP1 axis

BackgroundSevere acute pancreatitis (SAP) is a common digestive system disorder in clinical practice, and it is often associated with liver damage in patients with severe acute pancreatitis. Several studies have indicated that pyroptosis plays a role in liver damage following severe acute pancreatitis (SAP). However, the precise mechanisms remain unclear. This study aims to elucidate the association and specific mechanisms between liver injury following SAP and pyroptosis, providing theoretical support for research on SAP-induced liver injury. MethodsA rat model of SAP with concomitant liver injury was successfully established. The expression levels of miR-103–3p across different liver tissue groups were quantified using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). Bioinformatic analyses and dual-luciferase reporter assays confirmed that NLRP1 is a direct target of miR-103–3p. In vivo assessments of miR-103–3p levels were performed, and the extent of cell pyroptosis during liver injury post-SAP was evaluated through western blotting, qRT-PCR, scanning electron microscopy, histopathology, immunofluorescence, and immunohistochemistry. The role of miR-103–3p in regulating NLRP1-mediated pyroptosis and its impact on SAP-induced liver injury were validated. ResultsThis study reports that following SAP-induced liver injury, the expression of miR-103–3p in liver tissue was significantly decreased, and cell pyroptosis was involved in the process of liver injury. Experimental validation indicated that NLRP1 was a downstream target of miR-103–3p. Overexpression of miR-103–3p in vitro significantly alleviated the severity of liver injury following SAP, while simultaneously inhibiting cell pyroptosis. ConclusionThese findings indicate that pyroptosis may be linked to SAP-induced liver injury and that miR-103–3p mitigates hepatocyte pyroptosis by reducing liver injury through the suppression of NLRP1 expression.

Liver damage in patients hospitalized with acute decompensated heart failure, depending on the degree of glucose metabolism disorder

Aim. To study the frequency of cardiohepatic syndrome and steatosis by the value of controlled attenuation parameter (CAP), fibrosis, and their combination, depending on the degree of glucose metabolism disorder in patients with acute decompensated heart failure (ADHF).Materials and methods. The study included 280 patients (53% men, average age 70.1 ± 10.8 years) with ADHF: 72.5% of patients had a history of arterial hypertension, 60% of patients had coronary heart disease. The HbA1c test was performed in all patients to assess the status of glucose metabolism. The patients were divided into groups depending on the results obtained: at HbA1c values < 5.7%, patients were included in the group without glucose metabolism disorders, at HbA1c 5.7–6.4% – in the prediabetes group, at HbA1c ≥ 6.5% – in the type 2 diabetes group. All patients underwent a standard physical examination at admission and at discharge. Clinical and comprehensive assessments of congestion were performed – NT-proBNP, lung ultrasound, liver fibroscan with CAP, and bioelectrical impedance analysis of body composition.Results. The frequency of glucose metabolism disorders in patients hospitalized with ADHF was 57.5% (n = 161), while prediabetes was detected in 17.1% (n = 48) and type 2 diabetes – in 40.4% (n = 113) of patients. We revealed significantly higher incidence of steatosis by CAP value (69 vs. 42%, p < 0.001), fibrosis (80 vs. 64%, p < 0.001), and their combination (59 vs. 30%, p < 0.001), as well as cardiohepatic syndrome (87 vs. 61%, p < 0.001) in patients with ADHF and glucose metabolism disorders compared to individuals with ADHF without glucose metabolism disorders, respectively. The group of ADHF patients with glucose metabolism disorders and a combination of steatosis / fibrosis was characterized by more pronounced manifestations of metabolic syndrome, impaired kidney and liver function, and more pronounced manifestations (both clinical and laboratory) of congestion.Conclusion. In patients with ADHF with glucose metabolism disorders, liver function test and liver fibroscan with CAP allow for identifying the most severe group of patients with a combination of steatosis/fibrosis and pronounced congestion.

Liver Fibrosis Is Enhanced by a Higher Egg Burden in Younger Mice Infected with S. mansoni.

Schistosomiasis affects over 250 million people worldwide, with the highest prevalence at the age of 10-14 years. The influence of the host's age on the severity of liver damage is unclear. We infected male 8, 14, and 20-week-old mice with S. mansoni. Hepatic damage, inflammation, fibrosis, and metabolism were analyzed by RT-qPCR, Western blotting, ELISA, immunohistochemistry, and mechanistic transwell chamber experiments using S. mansoni eggs and human hepatic stellate cells (HSCs) or primary mouse hepatocytes. Major results were validated in human biopsies. We found that hepatosplenomegaly, granuloma size, egg load, inflammation, fibrosis, and glycogen stores all improved with the increasing age of the host. However, serum alanine transaminase (ALT) levels were lowest in young mice infected with S. mansoni. Hepatic carbohydrate exploitation was characterized by a shift towards Warburg-like glycolysis in S. mansoni-infected animals. Notably, S. mansoni eggs stimulated hepatic stellate cells to an alternatively activated phenotype (GFAP+/desmin+/αSMA-) that secretes IL-6 and MCP-1. The reduction of fibrosis in older age likely depends on the fine-tuning of regulatory and inflammatory cytokines, alternative HSC activation, and the age-dependent preservation of hepatic energy stores. The current results emphasize the significance of investigations on the clinical relevance of host age-dependent liver damage in patients with schistosomiasis.

The structure of liver damage in patients with acute decompensated heart failure, the prognostic role of steatosis and liver density

Abstract Funding Acknowledgements None. Aim To study the spectrum of liver damage in patients with acute decompensated heart failure (ADHF). Materials and methods Included were 566 patients hospitalized with ADHF, NYHA class II–IV, 66% men, mean age 72,4±11,4 years. All patients underwent laboratory and instrumental examination, the degree of steatosis and liver density were determined by transient elastometry methods, with an assessment of the controlled ultrasound attenuation parameter (CAP - Controlled Attenuation Parameter, S, dB/m) using a device according to standard methods. CAP values <294 dB/m with steatosis degree 0 - S0, 295-309 dB/m - S1, 310-330 dB/m - S2, ≥331 dB/m - S3. Liver density was used: ≤5,8 kPa – normal liver density, ≥5,9 – stage F1, ≥7,2 kPa – F2, ≥9,5 kPa – F3, ≥12,5 kPa – F4. Laboratory manifestations of liver damage were considered to be increased aspartate aminotransferase, alanine aminotransferase, gamma-glutamyl transpeptidase and alkaline phosphatase. Results The incidence of hepatic steatosis (≥S1) among patients with ADHF was 29%. Among patients with liver steatosis, minimal steatosis (S1) was detected in 19% of cases, moderate steatosis (S2) - 28,6%, severe steatosis S3 - 52,4%. In patients with steatosis, the frequency of laboratory indicators of liver damage was 53%, and in patients without steatosis - 49,2%. Liver density ≥ F1 was observed in 79,5% of patients. Stage F1 was diagnosed in 10,4% of cases, F2 - in 11%, F3 - 12,7%, F4 - 44,5%. However, no relationship was found between the severity of steatosis and liver density (p>0,05). Multivariate Cox regression analysis showed that extremely low CAP values (<234 dB/m) were associated with a worse prognosis and higher risk of HF mortality during the 3-year follow-up period (adjusted hazard ratio (aHR) 1,57 95% confidence interval (CI) 1,08–2,31, p=0,019) after adjustment for established risk factors and potential confounders. The presence of increased liver density >15,9 kPa was also associated with a worse prognosis of the risk of death from HF during the 3-year follow-up period by Cox multivariate analysis (aHR 1,24, 95% CI 1,01–1,52, p= 0,040). Conclusion Thus, extremely low CAP values (<234 dB/m) and the presence of a marked increase in liver density (>15,9 kPa) were associated with a worse prognosis in patients with ADHF during the 3-year follow-up period.

Gut symbionts alleviate MASH through a secondary bile acid biosynthetic pathway

The gut microbiota has been found to play an important role in the progression of metabolic dysfunction-associated steatohepatitis (MASH), but the mechanisms have not been established. Here, by developing a click-chemistry-based enrichment strategy, we identified several microbial-derived bile acids, including the previously uncharacterized 3-succinylated cholic acid (3-sucCA), which is negatively correlated with liver damage in patients with liver-tissue-biopsy-proven metabolic dysfunction-associated fatty liver disease (MAFLD). By screening human bacterial isolates, we identified Bacteroides uniformis strains as effective producers of 3-sucCA both invitro and invivo. By activity-based protein purification and identification, we identified an enzyme annotated as β-lactamase in B.uniformis responsible for 3-sucCA biosynthesis. Furthermore, we found that 3-sucCA is a lumen-restricted metabolite and alleviates MASH by promoting the growth of Akkermansia muciniphila. Together, our data offer new insights into the gut microbiota-liver axis that may be leveraged to augment the management of MASH.

Alteration of Gut Microbiota Composition in the Progression of Liver Damage in Patients with Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD).

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a complex disorder whose prevalence is rapidly growing in South America. The disturbances in the microbiota-gut-liver axis impact the liver damaging processes toward fibrosis. Gut microbiota status is shaped by dietary and lifestyle factors, depending on geographic location. We aimed to identify microbial signatures in a group of Chilean MASLD patients. Forty subjects were recruited, including healthy controls (HCs), overweight/obese subjects (Ow/Ob), patients with MASLD without fibrosis (MASLD/F-), and MASLD with fibrosis (MASLD/F+). Both MASLD and fibrosis were detected through elastography and/or biopsy, and fecal microbiota were analyzed through deep sequencing. Despite no differences in α- and β-diversity among all groups, a higher abundance of Bilophila and a lower presence of Defluviitaleaceae, Lachnospiraceae ND3007, and Coprobacter was found in MASLD/F- and MASLD/F+, compared to HC. Ruminococcaceae UCG-013 and Sellimonas were more abundant in MASLD/F+ than in Ow/Ob; both significantly differed between MASLD/F- and MASLD/F+, compared to HC. Significant positive correlations were observed between liver stiffness and Bifidobacterium, Prevotella, Sarcina, and Acidaminococcus abundance. Our results show that MASLD is associated with changes in bacterial taxa that are known to be involved in bile acid metabolism and SCFA production, with some of them being more specifically linked to fibrosis.

Dietary inflammatory index in relation to the progression of hepatic steatosis and liver fibrosis: evaluation by elastography/Fibroscan

One of the proposed mechanisms by which nutrition influences the progression of hepatic steatosis to fibrosis is inflammation. The study investigated how the inflammatory potential of the diet affects the risk of liver damage in patients with nonalcoholic fatty liver disease (NAFLD), a condition where fat accumulates in the liver. This cross-sectional study included 170 outpatients with newly diagnosed NAFLD. This study used a device called Fibroscan® to measure the degree of liver fibrosis, which is the scarring of the liver tissue due to chronic inflammation. The study also used a tool called the Dietary Inflammatory Index (DII) to measure the inflammatory potential of the diet based on the intake of different foods and nutrients. In the findings of the study, patients with more severe fat accumulation in the liver (hepatic steatosis) had higher DII scores, meaning they had more inflammatory diets. The study also found that higher DII scores were associated with higher weight and body mass index (BMI). One standard deviation (SD) increase in DII scores was associated with a 0.29 kilopascal (95% CI: 0.10–0.44; P-value 0.001) increase in the mean liver stiffness, an indicator of liver fibrosis. The study concluded that patients with higher DII scores had a higher risk of developing liver fibrosis than those with lower DII scores, even after adjusting for confounding factors (odds ratio: 5.89; P-value: 0.001). The study suggested that eating less inflammatory foods may help prevent or slow down the progression of hepatic steatosis and liver in patients with NAFLD.

Non-invasive Assessment of Liver Damage Degree in Patients with Viral Hepatitis: Is It Feasible and Acceptable?

Background: Hepatitis C and B virus infections significantly contribute to global chronic liver disease mortality. Objectives: This study explores the role of serum markers (AST/ALT ratio, APRI Score, FIB-4 Score, and Forns index) in non-invasively assessing liver damage in patients with chronic hepatitis C and B. Methods: In this single-center, retrospective, observational study, we analyzed data from 327 patients to establish correlations between serological markers and fibrosis grade using Spearman's correlation. Receiver operator characteristic (ROC) analysis evaluated the ability of these markers to predict advanced fibrosis. Results: In hepatitis B and C cohorts, all markers show significant positive correlations with liver fibrosis (P < 0.001). FIB-4 and the Forns index exhibit moderate correlation (Spearman’s rho 0.48), while AST/ALT and APRI score show mild correlation (Spearman’s rho 0.21 and 0.31). In hepatitis C, the Forns index (0.814) and FIB-4 (0.80) outperform other markers. In hepatitis B, Forns (AUC = 0.73), APRI (AUC = 0.68), and FIB-4 (AUC = 0.68) demonstrate significant predictive ability. Conclusions: FIB-4 and the Forns index hold clinical significance as fibrosis biomarkers in the management of chronic viral hepatitis. FIB-4 is a universal marker, while the interpretation of the Forns index requires consideration of the etiology of chronic viral hepatitis.

Effect of an Airbag-selective Portal Vein Blood Arrester on the Liver after Hepatectomy: A New Technique for Selective Clamping of the Portal Vein.

A novel technique was explored using an airbag-selective portal vein blood arrester that circumvents the need for an intraoperative assessment of anatomical variations in patients with complex intrahepatic space-occupying lesions. Rabbits undergoing hepatectomy were randomly assigned to 4 groups: intermittent portal triad clamping (PTC), intermittent portal vein clamping (PVC), intermittent portal vein blocker with an airbag-selective portal vein blood arrester (APC), and without portal blood occlusion (control). Hepatic ischemia and reperfusion injury were assessed by measuring the 7-day survival rate, blood loss, liver function, hepatic pathology, hepatic inflammatory cytokine infiltration, hepatic malondialdehyde levels, and proliferating cell nuclear antigen levels. Liver damage was substantially reduced in the APC and PVC groups. The APC animals exhibited transaminase levels similar to or less oxidative stress damage and inflammatory hepatocellular injury compared to those exhibited by the PVC animals. Bleeding was significantly higher in the control group than in the other groups. The APC group had less bleeding than the PVC group because of the avoidance of portal vein skeletonization during hepatectomy. Thus, more operative time was saved in the APC group than in the PVC group. Moreover, the total 7-day survival rate in the APC group was higher than that in the PTC group. Airbag-selective portal vein blood arresters may help protect against hepatic ischemia and reperfusion injury in rabbits undergoing partial hepatectomy. This technique may also help prevent liver damage in patients requiring hepatectomy.

Liver pathology in COVID-19 after end of pandemic: Modern view of problem

The COVID‑19 pandemic, first reported in late 2019, despite ending in May 2023, continues to have a devastating impact on global health with significant associated morbidity and mortality rates. Liver injury is a common feature in patients with COVID‑19 and ranges from mild and temporary elevation of liver enzymes to severe liver damage and even acute liver failure. The purpose of this review is to present data on the prevalence, pathophysiological mechanisms, clinical manifestations, diagnosis, course features, complications, and treatment options for liver damage in patients with SARS-CoV‑2. Several pathophysiological mechanisms are responsible for liver damage in COVID‑19, including the direct cytotoxic effect of the virus, cytokine storm, hypoxia and ischemia of the organ, and drug hepatotoxicity. Patients with underlying chronic liver disease (CLD) (liver cirrhosis, non-alcoholic fatty liver disease, alcohol-related liver disease, hepatocellular carcinoma, etc.) may have greater risk to develop both severe COVID‑19 and further liver deterioration. Some COVID‑19 patients experience post-covid syndrome, also known as post-acute COVID‑19, long-term COVID‑19 or long COVID‑19. The most common manifestations of post-covid syndrome in patients with liver pathology, both developed directly in connection with SARS-Cov‑2 infection, and in people with pre-existing CLD, include the phenomena of astheno-vegetative syndrome, as well as clinical and biochemical signs of moderate cytolysis and cholestasis syndrome.

Поражение печени при хронической сердечной недостаточности

Non-alcoholic fatty liver disease (NAFLD) and chronic heart failure (CHF) are characterized by a high and constantly increasing prevalence. Hepatocardial relationships in patients with CHF are based on impaired blood supply and hypoxia. The purpose — to investigate liver damage in patients with CHF using the HSI index. Material and methods. 348 patients with stable CHF in the compensation stage, aged 66.4 (10.4) years, were examined. Liver damage was assessed by the HSI index. Results and conclusions. NAFLD was detected in 54.3% of patients with CHF. The proportion of people with NAFLD decreased with increasing age: 62.8% in the group of < 60 years, 53.6% — 60–75 years, 45.1% — > 75 years. Patients with CHF and NAFLD were more often female (p = 0.002), younger (p = 0.001), with burdened heredity for cardiovascular diseases (p = 0.010), with type 2 diabetes mellitus (p < 0.001). The proportion of patients with CHF IV FC was higher in the presence of NAFLD (p = 0.03). Patients with NAFLD had higher body mass index (BMI) (p<0.001) and metabolic index (p < 0.001). Obesity of 1–3 degrees was more often in patients with NAFLD than without liver damage (p < 0.001). The mass of the left ventricular myocardium (MMLF) in male and female patients with CHF was higher in the presence of NAFLD, compared with patients without NAFLD (p = 0.004 and p = 0.001). A comparison of blood parameters in patients with CHF and NAFLD demonstrated a higher level of glucose (p < 0.001), alanine aminotransferases (ALT) (p < 0.001), uric acid (p = 0.013), total protein (p = 0.013), highly sensitive C-reactive protein (hs-CRP) (p = 0.012) and triglycerides (TG) (p < 0.001). Correlations of HSI with age, BMI, metabolic index, glucose levels, ALT, uric acid, total protein, hs-CRP, total cholesterol, triglycerides, and MMLF were revealed.

Особенности поражения печени у пациентов с тиреотоксикозом: клиническое наблюдение гепатопатии на фоне приема тиреостатиков

Особенности поражения печени у пациентов с тиреотоксикозом: клиническое наблюдение гепатопатии на фоне приема тиреостатиков

Evaluation of systemic inflammatory and fibrosis indices in Saprochaete capitata infections: a retrospective case-control study

Abstract Objectives Evaluation of inflammation and liver fibrosis by using well established indices of serum biomarkers in hepatitis caused by viral agents has been reported in recent studies. But the diagnostic performance and prediction of liver damage in S. capitata infections has not yet been reported. The aim of the current study was to investigate the levels of systemic inflammatory indices based on liver enzymes and platelets, their effectiveness in detecting S. capitata infection and its degree of damage to the liver. Methods We investigated the diagnostic performance of seven serum inflammation and fibrosis markers as fibrosis-4 (FIB-4) score, AST/platelet ratio (APRI), AST/ALT ratio (De Ritis ratio), albumin/ALP ratio (AAR), platelet/albumin ratio (PAR), pan-immune-inflammation value (PIV) and GGT/platelet ratio (GPR) in total 62 S. capitata infected patients using cut-offs through receiver operating characteristics (ROC) analysis. Results Area under the curve of FIB-4 score was statistically significantly higher than ones of De Ritis ratio, AAR, PIV, APR, GPR, APRI index in determining liver damage in patients with S. capitata. The optimal cut off point for FIB-4 score was defined that the levels above 27.57 for FIB-4 score may be used for the diagnosis of S. capitata with 89 % of sensitivity and 91 % of specificity. Conclusions Serum fibrosis and immune-inflammation indices are independent, useful predictors, and FIB4 score is superior to the others in the diagnosis of inflammation and liver damage in S. capitata. These biomarkers may also be useful to specialists to follow up on the medical processes of these patients.

THE REVIEW ARTICLE ON LIVER FUNCTION TEST IN HUMAN BODY

Laboratory Liver function tests (LFT) may be defined as the tests which are useful in the evaluation and treatment of patients with hepatic dysfunction. Theliver is of vital importance in intermediary metabolism, in the detoxification andin the elimination of toxic substances. The biochemical tests are useful in detecting the presence of liver disease. The test are also cheap, non- invasive and widely available and are of value in directing the use of other diagnostic tests such as liver biopsy and imaging. Some of the biochemical markers such asserum Bilirubin, SGPT or Alanine amino transferase (ALT) , SGOT or aspartate amino transferase (AST) , Alkaline phosphatase (ALP), Gamma Glutamyl Transferase (GGT), 5′ nucleotidase, Ceruloplasmin etc. are considered in this article. An isolated or conjugated alteration of biochemical markers of liver damage in patients can challenge the clinicians during the diagnosis of disease related to liver directly or with some other organs.

The effectiveness of hepatotropic complex Lesil in prevention hepatotoxic effects of anti-helicobacter therapy

Objective — to evaluate the effectiveness of the hepatotropic complex Lesil® for the prevention of the development of drug‑induced liver damage in patients receiving anti‑Helicobacter therapy (AHT). Materials and methods. Observation involved the main (I) and control (II) groups of 40 people in each. Patients with gastroduodenal diseases were included in the study if Helicobacter pylori (H. pylori) infection was first detected. A 14‑day course of 4‑component AHT was administered: pantoprazole, amoxicillin, clarithromycin, colloidal bismuth subcitrate. The main group additionally received Lesil® (Propharma Plant LLC, Ukraine) in a dose of 2 capsules a day for 6 weeks. Patients’ satisfaction with therapy was assessed using a visual analog scale. Statistical processing of the obtained results was carried out using standard methods. Results. After the course of treatment, eradication of H. pylori was achieved in 76 subjects (95%). After the end of AHT in the I group, no changes in liver tests were registered, whereas in the II group, an increase in the activity of ALT and AST in 2.4 (p<0.05) and 2.9 times (p<0.01) was revealed, as well as an increase in the levels of γ‑glutamyltranspeptidase (p<0.01) and alkaline phosphatase (p<0.01), and increase in the fraction of direct bilirubin. Patients of the II group were less satisfied with the treatment: the indicators of the visual analog scale were 4.97±068, compared to the I group (8.43±1.21, p<0.05). Conclusions. Against the background of AHT (PPI in a standard dose, amoxicillin, clarithromycin, colloidal bismuth subcitrate) for 14 days, signs of drug‑induced liver damage were detected, which persisted for 4 weeks after the end of therapy. Hepatocomplex Lesil® is an effective means to prevent drug damage to the liver. This is confirmed by the absence of signs of cytolytic and cholestatic syndromes in the group of patients who received Lesil® 2 capsules per day for 6 weeks in addition to the AHT. Hepatocomplex Lesil® demonstrated safety and good tolerance by patients who were satisfied with AHT in combination with Lesil®.

Significance of Serum Butyrylcholinesterase in Evaluating the Liver Reserve in Chronic Hepatitis (C) Cirrhotic Patients

Abstract Background Hepatitis C virus can cause both acute and chronic hepatitis. The acute process is self-limited, rarely causes hepatic failure and usually leads to chronic infection. Chronic HCV infection often follows a progressive course over many years and can ultimately result in cirrhosis, HCC and the need for liver transplantation. Liver cirrhosis is one of the major leading causes of morbidity and mortality worldwide including Egypt. Cirrhotic patients evaluated for the presence of complications by using Child-Pugh score. However; the cirrhotic patients particularly those with Child grades B and C with ascites or hemorrhagic tendency are usually treated with albumin or blood transfusion which may affect the numerical value for calculating the Child- Pugh score. Objective To evaluate serum cholinesterase level as a biomarker for detecting liver damage in patients with chronic hepatitis C. Subjects and Methods The aim of this study is to evaluate serum cholinesterase level as a biomarker for detecting liver injury in patients with CHC. For this propose 40 patients with liver cirrhosis due to HCV infection and 10 healthy adults were selected and divided into 3 groups: Group 1: 20 Patients having compensated liver cirrhosis due to HCV infection. Group 2: 20 Patients having decompensated liver cirrhosis due to HCV infection. Group 3: 10 Healthy subjects matched for age and sex as a control. Results Sensitivity of cholinesterase is 100%, its specificity is 100% and its accuracy is 100%, in predicting liver injury in patients with chronic hepatitis C. Cholinesterase is positively correlated with Hb, platelets and albumin. Cholinesterase is negatively correlated with ALT, AST and ALP, total, direct bilirubin, PT, INR, urea, creatinine and AFP. Conclusion Serum cholinesterase is an excellent biomarker of the synthetic function of liver in CLD with hepatitis C. Cholinesterase levels should be routinely checked to assess liver function. It can be effectively used to follow the staging of liver disease in hepatitis C.

Factors affecting the development of liver fibrosis in patients who experienced COVID-19

The aim of the review is to highlight the main factors affecting the development of liver fibrosis and possible mechanisms of liver damage in patients who have experienced COVID-19. A search was carried out using keywords in the Scopus, Web of Science, and PubMed databases in literary sources of the last three years on factors associated with fibrogenesis in novel coronavirus infection.The review presents the main mechanisms of liver damage in COVID-19: direct effects on hepatocytes and cholangiocytes, hypoxia, and immune-mediated and drug-induced damage. We analyzed the significance of factors affecting fibrosis development in patients with COVID-19: chronic diffuse liver diseases, against which COVID-19 occurs, such as non-alcoholic fatty liver disease, alcohol-associated liver disease, chronic hepatitis B, C, and cirrhosis of the liver.Damage to the liver in coronavirus infection develops by several mechanisms. The development of COVID-19 against the background of diffuse liver pathology of various genesis is associated with progression of these diseases (increased fibrogenesis) and a poorer prognosis.

Fatty Liver Disease, Metabolism and Alcohol Interplay: A Comprehensive Review.

Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease worldwide, and its incidence has been increasing in recent years because of the high prevalence of obesity and metabolic syndrome in the Western population. Alcohol-related liver disease (ArLD) is the most common cause of cirrhosis and constitutes the leading cause of cirrhosis-related deaths worldwide. Both NAFLD and ArLD constitute well-known causes of liver damage, with some similarities in their pathophysiology. For this reason, they can lead to the progression of liver disease, being responsible for a high proportion of liver-related events and liver-related deaths. Whether ArLD impacts the prognosis and progression of liver damage in patients with NAFLD is still a matter of debate. Nowadays, the synergistic deleterious effect of obesity and diabetes is clearly established in patients with ArLD and heavy alcohol consumption. However, it is still unknown whether low to moderate amounts of alcohol are good or bad for liver health. The measurement and identification of the possible synergistic deleterious effect of alcohol consumption in the assessment of patients with NAFLD is crucial for clinicians, since early intervention, advising abstinence and controlling cardiovascular risk factors would improve the prognosis of patients with both comorbidities. This article seeks to perform a comprehensive review of the pathophysiology of both disorders and measure the impact of alcohol consumption in patients with NAFLD.

HBV with precore and basal core promoter mutations exhibits a high replication phenotype and causes ER stress-mediated cell death in humanized liver chimeric mice.

Mutations within the precore (PC) and basal core promoter (BCP) regions of the HBV genome are associated with fulminant hepatitis and HBV reactivation. These mutations may enhance viral replication, but little is known about whether they directly induce damage to the liver. We investigated mechanisms of direct cytopathic effects induced by the infection with PC/BCP mutants in the absence of immune response in vitro and in vivo . Mice with humanized livers and hepatocytes derived from humanized mice were infected with either wild-type or mutant-type PC/BCP HBV, and the HBV replication and human hepatocyte damage were evaluated. HBV proliferated vigorously in mice with PC/BCP-mutant infection, and the severe loss of human hepatocytes with a slight human ALT elevation subsequently occurred only in PC/BCP mutant mice. In PC/BCP mutant infection, the accumulation of HBsAg in humanized livers colocalized with the endoplasmic reticulum, leading to apoptosis through unfolded protein response in HBV-infected hepatocytes. RNA-sequencing revealed the molecular characteristics of the phenotype of PC/BCP mutant infection in a humanized mouse model. Reduced ALT elevation and higher HBV DNA levels in this model are consistent with characteristics of HBV reactivation, indicating that the hepatocyte damage in this model might mimic HBV reactivation followed by hepatocyte damage under immunosuppressive conditions. PC and BCP mutations were associated with enhanced viral replication and cell death induced by ER stress using HBV infection models. These mutations might be associated with liver damage in patients with fulminant hepatitis or HBV reactivation.

Splenic Artery Steal Syndrome in Patients with Liver Cirrhosis: A Retrospective Clinical Study.

BACKGROUND Splenic artery steal syndrome (SASS) can aggravate liver damage in patients with cirrhosis. This study explored whether SASS could be an effective therapeutic target for improving hepatic artery perfusion and liver function in patients with decompensated cirrhosis. MATERIAL AND METHODS Based on inclusion and exclusion criteria, 87 patients with hepatitis B cirrhosis and portal hypertension hypersplenism admitted to our General Surgery Department for splenectomy and pericardial devascularization surgery were selected. A total of 35 cases met the diagnostic criteria of SASS and were assigned to the SASS group; the remaining 52 cases were assigned to the control group. The indicators before, during, and after surgery were compared between the 2 groups. RESULTS There were no significant differences in preoperative and intraoperative indicators between SASS group and control group (P>0.05). The MELD score 7 days after surgery and the hepatic artery diameter and hepatic artery velocity 14 days after surgery in both groups were significantly better than before surgery. The MELD score 7 days after surgery in the SASS group was significantly better than that in the control group, and the hepatic artery diameter and hepatic artery velocity 14 days after surgery in the SASS group were significantly better than those in the control group (P<0.05). CONCLUSIONS Splenectomy and pericardial devascularization surgery was an effective treatment to redirect blood flow to the hepatic artery for cirrhotic patients diagnosed with SASS. The introduction of cirrhotic SASS into clinical practice may benefit more patients with cirrhotic portal hypertension and hypersplenism.