Evaluation of miR-222 Expression in HBV Infected Patients in Comparison with HDV and HBV Co-infected Patients

2021 ◽  
Author(s):  
Zahra Sokhanvar ◽  
Ameneh Elikaei ◽  
Zohreh Sharifi
Keyword(s):  
Gene Expression ◽  
Liver Disease ◽  
Quantitative Pcr ◽  
Internal Control ◽  
Liver Diseases ◽  
Cdna Synthesis ◽  
Severe Liver ◽  
Serum Samples ◽  
Complementary Dna ◽  
Expression Of Genes

Background: Liver disease is more severe in HDV+HBV co-infected patients than HBV infected patients which seems to be related to differences in the expression of genes and other factors such as MicroRNAs (miRNAs). The aim of this study was to investigate miR-222 expression in HBV infected patients in comparison with HDV+HBV co-infected patients. Methods: First, total RNA was extracted from the serum samples and then, complementary DNA (cDNA) was produced using cDNA synthesis kit. Finally, miR-222 gene expression was measured using U6 as the internal control by quantitative PCR (qPCR). Results: The level of miR-222 expression in HDV+HBV co-infected samples was significantly up regulated. The fold change of the miR-222 expression between two groups was 3.3 (95% CI; 0.011- 17.63) with p<0.001. Conclusion: The expression of miR-222 was higher in HBV+HDV co-infected patients than HBV infected patients. Further studies should be conducted to confirm whether miR-222 can be a biomarker for prognosis of severe liver diseases.

scholarly journals The Course Of Chronic Liver Disease In Patients With Covid-2019 (Literature Review And Own Data)

2021 ◽  
Vol 03 (09) ◽  
pp. 69-74
Author(s):  
Muxamedova Z.R. ◽  
Keyword(s):  
Liver Disease ◽  
Literature Review ◽  
Liver Diseases ◽  
Chronic Liver ◽  
Chronic Liver Diseases ◽  
Biochemical Activity ◽  
Severe Liver ◽  
Risk Of Mortality ◽  
The World ◽  
Severe Liver Damage

The pandemic of the new coronavirus COVID-19 has switched medicine around the world on the primary fight against this infection. Patients with chronic liver diseases require increased attention of doctors during an epidemic, since against the background of an exacerbation of their disease, not only the risk of contracting the COVID 19 viral infection increases, but also its more severe course. Patients with confirmed COVID-19 with severe liver damage - high biochemical activity. According to some reports, patients with a severe course of COVID-19 have an increase in ALT levels, a decrease in the number of platelets, a decrease in the level of albumin, and a connection (although not all indicators) with a higher risk of mortality is possible.

scholarly journals Patients with chronic liver disease and COVID-19 (literature review and own data)

2021 ◽  
Vol 2 (2/S) ◽  
pp. 498-503
Author(s):  
D.H. Yuldasheva ◽  
Z.X. Muxamedova ◽  
N.S. Shadjanova
Keyword(s):  
Liver Disease ◽  
Literature Review ◽  
Liver Diseases ◽  
Chronic Liver ◽  
Chronic Liver Diseases ◽  
Biochemical Activity ◽  
Severe Liver ◽  
Risk Of Mortality ◽  
The World ◽  
Severe Liver Damage

The pandemic of the new coronavirus COVID-19 has switched medicine around the world on the primary fight against this infection. Patients with chronic liver diseases require increased attention of doctors during an epidemic, since against the background of an exacerbation of their disease, not only the risk of contracting the COVID 19 viral infection increases, but also its more severe course. Patients with confirmed COVID-19 with severe liver damage - high biochemical activity. According to some reports, patients with a severe course of COVID-19 have an increase in ALT levels, a decrease in the number of platelets, a decrease in the level of albumin, and a connection (although not all indicators) with a higher risk of mortality is possible.

Use of ulipristal acetate and risk of liver disease: a nationwide cohort study

2021 ◽  
Author(s):  
Eileen L Yoon ◽  
Jin-Sung Yuk
Keyword(s):  
Liver Disease ◽  
Gnrh Agonist ◽  
Liver Diseases ◽  
Uterine Fibroids ◽  
Gnrh Agonists ◽  
Severe Liver ◽  
Health Insurance Data ◽  
Ulipristal Acetate ◽  
Severe Liver Disease ◽  
Insurance Data

Abstract Context Large-scale clinical trials on the hepatotoxicity of ulipristal acetate (UPA) are lacking. Objective To determine the incidence of liver disease with UPA versus gonadotropin-releasing hormone (GnRH) agonists. Design Retrospective cohort study. Setting National health insurance data in South Korea. Patients or Other Participants Women with uterine fibroids from the Korean Health Insurance Data 2010-2018. Intervention(s) Women with uterine fibroids were divided into two treatment groups: the UPA (5 mg/day) and GnRH agonist groups. Main Outcome Measure(s) Presence or absence of severe liver disease, mild liver disease, and liver transplantation. Results Among the patients with uterine fibroids,17,207 patients were treated with GnRH agonists and 20,926 patients with UPA. After 1:1 propensity score matching for each group, there were 11,445 individuals. Neither group had a liver transplantation case. In the conditional logistic regression analysis, the incidences of total liver diseases (relative risk [RR] 1.111, 95% confidence interval [CI] 1.015-1.216) and mild liver diseases (RR 1.094, 95% CI 1-1.196) were higher in the UPA group than in the GnRH agonist group, but those of severe liver diseases (RR 0.07, 95% CI 0.001-4.412) and toxic liver disease (RR 1.256, 95% CI 0.845-1.867) did not differ between the groups. Conclusions The incidences of severe liver disease, hepatic failure, and toxic liver disease were not different between the UPA and GnRH agonist groups. However, the incidence of mild liver disease was higher in the UPA group than in the GnRH agonist group. The incidence of hepatic damage with UPA was very low.

scholarly journals Abundance of Immunologically Active Alanine Aminotransferase in Sera of Liver Cirrhosis and Hepatocellular Carcinoma Patients

2009 ◽  
Vol 55 (5) ◽  
pp. 1022-1025 ◽  
Author(s):  
Hyun Jeong Kim ◽  
Sang Wook Oh ◽  
Dong Joon Kim ◽  
Eui Yul Choi
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Cirrhosis ◽  
Liver Disease ◽  
Enzymatic Activity ◽  
Enzyme Immunoassay ◽  
Roc Curve ◽  
Alanine Aminotransferase ◽  
Liver Diseases ◽  
Serum Samples ◽  
Sandwich Enzyme Immunoassay

Abstract Background: Although alanine aminotransferase (ALT) is a widely used indicator of liver function, ALT enzymatic activity may not always reflect the degree of liver damage. Improved methods or approaches would be useful. Methods: Monoclonal antibodies (mAbs) to ALT were generated to develop a sandwich enzyme immunoassay system. We used an immunoassay to measure ALT mass concentration and a common biochemical analyzer to assay ALT enzymatic activity in serum samples from patients with liver diseases and healthy individuals. The results from the 2 methods were compared and analyzed by ROC curve analysis. Results: The ALT sandwich enzyme immunoassay system demonstrated reliable performance in linearity, recovery, and imprecision studies. The ALT activity assay exhibited a higher diagnostic accuracy in acute hepatitis (AH) patients, but the ALT immunoassay exhibited higher sensitivity and specificity in patients with chronic liver diseases. The areas under the ROC curve for ALT mass and enzymatic activity were 0.82 and 0.98, respectively, in AH, 0.99 and 0.52 in hepatocellular carcinoma (HCC), and 0.94 and 0.45 in liver cirrhosis (LC). Serum samples from HCC and LC patients had higher amounts of ALT–immunoglobulin complexes [median A450, 1.7 (interquartile range, 1.4–1.9)] than the other groups [1.3 (interquartile range, 0.9–1.6)]. Conclusions: Our analysis of sera from the HCC and LC patient groups revealed considerable amounts of immunologically active but catalytically inactive ALT. The amount of the ALT–immunoglobulin complex increased with the severity of the liver disease. The 2-site immunoassay method may be useful in the differential diagnosis of some causes of liver disease.

scholarly journals Pre-clinical and clinical investigations of metabolic zonation in liver diseases: The potential of microphysiology systems

2017 ◽  
Vol 242 (16) ◽  
pp. 1605-1616 ◽  
Author(s):  
Alejandro Soto-Gutierrez ◽  
Albert Gough ◽  
Lawrence A Vernetti ◽  
DL Taylor ◽  
Satdarshan P Monga
Keyword(s):  
Gene Expression ◽  
Liver Disease ◽  
Disease Progression ◽  
Liver Diseases ◽  
Human Liver ◽  
Liver Zonation ◽  
Metabolic Zonation ◽  
Liver Disease Progression ◽  
And Function

The establishment of metabolic zonation within a hepatic lobule ascribes specific functions to hepatocytes based on unique, location-dependent gene expression patterns. Recently, there have been significant developments in the field of metabolic liver zonation. A little over a decade ago, the role of β-catenin signaling was identified as a key regulator of gene expression and function in pericentral hepatocytes. Since then, additional molecules have been identified that regulate the pattern of Wnt/β-catenin signaling within a lobule and determine gene expression and function in other hepatic zones. Currently, the molecular basis of metabolic zonation in the liver appears to be a ‘push and pull’ between signaling pathways. Such compartmentalization not only provides an efficient assembly line for hepatocyte functions but also can account for restricting the initial hepatic damage and pathology from some hepatotoxic drugs to specific zones, possibly enabling effective regeneration and restitution responses from unaffected cells. Careful analysis and experimentation have also revealed that many pathological conditions in the liver lobule are spatially heterogeneous. We will review current research efforts that have focused on examination of the role and regulation of such mechanisms of hepatocyte adaptation and repair. We will discuss how the pathological organ-specific microenvironment affects cell signaling and metabolic liver zonation, especially in steatosis, viral hepatitis, and hepatocellular carcinoma. We will discuss how the use of new human microphysiological platforms will lead to a better understanding of liver disease progression, diagnosis, and therapies. In conclusion, we aim to provide insights into the role and regulation of metabolic zonation and function using traditional and innovative approaches. Impact statement Liver zonation of oxygen tension along the liver sinusoids has been identified as a critical liver microenvironment that impacts specific liver functions such as intermediary metabolism of amino acids, lipids, and carbohydrates, detoxification of xenobiotics and as sites for initiation of liver diseases. To date, most information on the role of zonation in liver disease including, non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma (HCC) have been obtained from animal models. It is now possible to complement animal studies with human liver, microphysiology systems (MPS) containing induced pluripotent stem cells engineered to create disease models where it is also possible to control the in vitro liver oxygen microenvironment to define the role of zonation on the mechanism(s) of disease progression. The field now has the tools to investigate human liver disease progression, diagnosis, and therapeutic development.

scholarly journals Investigating fibrosis and inflammation in an ex vivo NASH murine model

2020 ◽  
Vol 318 (2) ◽  
pp. G336-G351
Author(s):  
Emilia Gore ◽  
Emilia Bigaeva ◽  
Anouk Oldenburger ◽  
Yvette J. M. Jansen ◽  
Detlef Schuppan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lipid Metabolism ◽  
Liver Disease ◽  
Nonalcoholic Steatohepatitis ◽  
Ex Vivo ◽  
Ex Vivo Model ◽  
Nonalcoholic Fatty Liver ◽  
Liver Slices ◽  
Expression Of Genes

Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease, characterized by excess fat accumulation (steatosis). Nonalcoholic steatohepatitis (NASH) develops in 15–20% of NAFLD patients and frequently progresses to liver fibrosis and cirrhosis. We aimed to develop an ex vivo model of inflammation and fibrosis in steatotic murine precision-cut liver slices (PCLS). NASH was induced in C57Bl/6 mice on an amylin and choline-deficient l-amino acid-defined (CDAA) diet. PCLS were prepared from steatohepatitic (sPCLS) and control (cPCLS) livers and cultured for 48 h with LPS, TGFβ1, or elafibranor. Additionally, C57Bl/6 mice were placed on CDAA diet for 12 wk to receive elafibranor or vehicle from weeks 7 to 12. Effects were assessed by transcriptome analysis and procollagen Iα1 protein production. The diets induced features of human NASH. Upon culture, all PCLS showed an increased gene expression of fibrosis- and inflammation-related markers but decreased lipid metabolism markers. LPS and TGFβ1 affected sPCLS more pronouncedly than cPCLS. TGFβ1 increased procollagen Iα1 solely in cPCLS. Elafibranor ameliorated fibrosis and inflammation in vivo but not ex vivo, where it only increased the expression of genes modulated by PPARα. sPCLS culture induced inflammation-, fibrosis-, and lipid metabolism-related transcripts, explained by spontaneous activation. sPCLS remained responsive to proinflammatory and profibrotic stimuli on gene expression. We consider that PCLS represent a useful tool to reproducibly study NASH progression. sPCLS can be used to evaluate potential treatments for NASH, as demonstrated in our elafibranor study, and serves as a model to bridge results from rodent studies to the human system. NEW & NOTEWORTHY This study showed that nonalcoholic steatohepatitis can be studied ex vivo in precision-cut liver slices obtained from murine diet-induced fatty livers. Liver slices develop a spontaneous inflammatory and fibrogenic response during culture that can be augmented with specific modulators. Additionally, the model can be used to test the efficacy of pharmaceutical compounds (as shown in this investigation with elafibranor) and could be a tool for preclinical assessment of potential therapies.

scholarly journals Identification of Serum Biomarkers in End Stage Liver Disease

2010 ◽  
Vol 3 (1) ◽  
pp. 1-6
Author(s):  
D. Koutsogiannis ◽  
K. Summers ◽  
B. George ◽  
P. Adams ◽  
P. Marotta ◽  
...  
Keyword(s):  
Cell Death ◽  
Liver Disease ◽  
Liver Diseases ◽  
Serum Markers ◽  
Control Group ◽  
Serum Samples ◽  
Alcoholic Fatty Liver ◽  
End Stage Liver Disease ◽  
Luminex Technology ◽  
End Stage

Background: Progressive fibrosis and cirrhosis, clinically presenting as end-stage liver disease are common outcomes in alcoholic hepatitis as well as non-alcoholic fatty liver disease(NAFLD). In these processes, a series of changes occurs in liver tissues leading to cell death, remodeling, fibrosis and regeneration. The aim of this study is to identify potential novel biomarkers for non-invasive diagnosis of cirrhosis due to alcoholic etiology or NAFLD. Methods: Serum from patients with biopsy proven end-stage liver disease of various etiologies, namely NAFLD(n=9), alcohol( n=5), and other end-stage liver diseases(n=6), who underwent liver transplant during the first six months of 2007 were utilized for retrospective analysis. Serum samples were also collected from a group of healthy volunteers (n=7). The samples were analysed using Luminex technology or ELISA for 27 biomarkers that are known to be involved in pathologic processes such as cell death, regeneration and fibrosis. Results: Of the 27 serum markers examined, 16 were elevated in the serum in all groups with end-stage liver diseases compared with the control group. They include adipokines, apoptosis and inflammatory mediators and growth factors. Interestingly, the serum of NAFLD patients showed significantly elevated HGF levels and trend towards increase in sFAS, TGF􀀁1, TNFR-1, TNFR-2 and leptin. The level of serum markers showed excellent correlation with each other indicating a complex interdependent pathogenetic mechanism. Conclusions: The data from this study indicate that a large number of serum markers are altered in end-stage liver diseases. A panel of such markers may potentially be useful in assessing advanced fibrosis and cirrhosis in patients with chronic end stage liver diseases.

scholarly journals Different types of hyperammonemia in clinical practice

2018 ◽  
pp. 34-42 ◽  
Author(s):  
E. Yu. Plotnikova ◽  
A. S. Sukhikh
Keyword(s):  
Clinical Practice ◽  
Liver Disease ◽  
Clinical Features ◽  
Generic Drug ◽  
Metabolic Disorder ◽  
Liver Diseases ◽  
Fatal Outcome ◽  
Severe Liver ◽  
Pharmaceutical Equivalence ◽  
Different Types

Hyperammonemia is a metabolic disorder, which is caused as a result of high levels of ammonia present in the blood. Hyperammonemia is related to severe liver diseases, primarily to cirrhosis in 90% of cases. Non-cirrhotic causes should be considered in the remaining 10%. The article describes various causes and clinical features of hyperammonemia related to the pre-cirrhotic stages of liver disease, especially to non-alcoholic fatty dystrophy. The authors also provide other etiologies that cause hyperammonemia of varying severity, from minimal to very severe, leading to fatal outcome. The paper provides an analysis of the efficacy of L-ornithine-L-aspartate in hyperammonemia, and the results of own original author’s pharmaceutical equivalence study of the original and generic drug L-ornithine-L-aspartate.

scholarly journals Immunologic Effects of Stereotactic Body Radiotherapy in Dogs with Spontaneous Tumors and the Impact of Intratumoral OX40/TLR Agonist Immunotherapy

2022 ◽  
Vol 23 (2) ◽  
pp. 826
Author(s):  
Mary-Keara Boss ◽  
Remy Watts ◽  
Lauren G. Harrison ◽  
Sophie Hopkins ◽  
Lyndah Chow ◽  
...  
Keyword(s):  
Gene Expression ◽  
T Cells ◽  
Stereotactic Body Radiotherapy ◽  
Tumor Model ◽  
Large Animal ◽  
Serum Samples ◽  
Expression Of Genes ◽  
Tlr Agonist ◽  
Immunological Effects ◽  
The Impact

Stereotactic body radiotherapy (SBRT) is known to induce important immunologic changes within the tumor microenvironment (TME). However, little is known regarding the early immune responses within the TME in the first few weeks following SBRT. Therefore, we used the canine spontaneous tumor model to investigate TME responses to SBRT, and how local injection of immune modulatory antibodies to OX40 and TLR 3/9 agonists might modify those responses. Pet dogs with spontaneous cancers (melanoma, carcinoma, sarcoma, n = 6 per group) were randomized to treatment with either SBRT or SBRT combined with local immunotherapy. Serial tumor biopsies and serum samples were analyzed for immunologic responses. SBRT alone resulted at two weeks after treatment in increased tumor densities of CD3+ T cells, FoxP3+ Tregs, and CD204+ macrophages, and increased expression of genes associated with immunosuppression. The addition of OX40/TLR3/9 immunotherapy to SBRT resulted in local depletion of Tregs and tumor macrophages and reduced Treg-associated gene expression (FoxP3), suppressed macrophage-associated gene expression (IL-8), and suppressed exhausted T cell-associated gene expression (CTLA4). Increased concentrations of IL-7, IL-15, and IL-18 were observed in serum of animals treated with SBRT and immunotherapy, compared to animals treated with SBRT. A paradoxical decrease in the density of effector CD3+ T cells was observed in tumor tissues that received combined SBRT and immunotherapy as compared to animals treated with SBRT only. In summary, these results obtained in a spontaneous large animal cancer model indicate that addition of OX40/TLR immunotherapy to SBRT modifies important immunological effects both locally and systemically.

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