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Farzana, Taposhi, Pijush Karmakar, Jakia Haque, Md Farhan Joha, and Eshrat Jahan Eami. "Study Of Serum Triglyceride And Ldl-cholesterol Among Patients Suffereing From Liver Cirrhosis And Its Relation With Severity of The Disease." Central Medical College Journal 5, no. 1 (June 12, 2022): 25–29. http://dx.doi.org/10.3329/cemecj.v5i1.60201.
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Background: Cirrhosis is characterized by abnormal structure and function of the liver. Liver synthesizes the various lipoproteins involved in transporting cholesterol and lipids throughout the body. This makes liver an important site for lipid metabolism as well as its transport. Thus liver cirrhosis is associated with lipid abnormalities and the amount of decrement is expected to be significantly correlated with increasing severity of liver damage.
Aims and objectives: To determine serum TG and LDL-C in patients with cirrhosis and study their relationship to the severity of cirrhosis.
Materials & Method: This cross-sectional study was carried out in the Department of Biochemistry, Sylhet MAG Osmani Medical College, Sylhet during the period from January to December 2016. Fifty cirrhosis of liver patients fulfilling the inclusion criteria were enrolled as group-A and 50 age-sex matched healthy adults were selected as the control group (group-B).
Result: Fasting serum TG and LDL-C were estimated. Severity of liver Cirrhosis was categorized according to Child-Pugh scoring system and increasing severity was categorized as Child Pugh class A, B and C. TG and LDL-C were decreased in patients with liver cirrhosis. The level of severity of liver damage significantly affects the serum LDL-C level in cirrhosis; and may be considered as marker of severity of liver damage in cirrhosis.
Conclusion: It may be concluded that hypolipidemia exists in patients with liver cirrhosis and screening for severity of cirrhosis by LDL-C is important for intervention with appropriate therapy to reduce the severity of the disease.
Central Medical College Journal Vol 5 No 1 Jan 2021 PP 25-29
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Spogis, Jakob, Florian Hagen, Wolfgang M. Thaiss, Tatjana Hoffmann, Nisar Malek, Konstantin Nikolaou, Christoph P. Berg, et al. "Sonographic findings in coronavirus disease-19 associated liver damage." PLOS ONE 16, no. 2 (February 19, 2021): e0244781. http://dx.doi.org/10.1371/journal.pone.0244781.
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Purpose This study was conducted to evaluate the role of liver sonography in patients with coronavirus disease 2019 (COVID-19) and elevated liver enzymes. Materials and methods In this retrospective study, patients tested positive for SARS-CoV-2 in our emergency ward between January 01 and April 24, 2020 and elevated liver enzymes were included (Cohort 1). Additionally, the local radiology information system was screened for sonographies in COVID-19 patients at the intensive care unit in the same period (Cohort 2). Liver sonographies and histologic specimen were reviewed and suspicious findings recorded. Medical records were reviewed for clinical data. Ultrasound findings and clinical data were correlated with severity of liver enzyme elevation. Results Cohort 1: 126 patients were evaluated, of which 47 (37.3%) had elevated liver enzymes. Severity of liver enzyme elevation was associated with death (p<0.001). 8 patients (6.3%) had suspicious ultrasound findings, including signs of acute hepatitis (n = 5, e.g. thickening of gall bladder wall, hepatomegaly, decreased echogenicity of liver parenchyma) and vascular complications (n = 4). Cohort 2: 39 patients were evaluated, of which 14 are also included in Cohort 1. 19 patients (48.7%) had suspicious ultrasound findings, of which 13 patients had signs of acute hepatitis and 6 had vascular complications. Pathology was performed in 6 patients. Predominant findings were severe cholestasis and macrophage activation. Conclusion For most hospitalized COVID-19 patients, elevated liver enzymes cause little concern as they are only mild to moderate. However, in severely ill patients bedside sonography is a powerful tool to reveal different patterns of vascular, cholestatic or inflammatory complications in the liver, which are associated with high mortality. In addition, macrophage activation as histopathologic correlate for a hyperinflammatory syndrome seems to be a frequent complication in COVID-19.
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Effenberger, Maria, Christoph Grander, Gernot Fritsche, Rosa Bellmann-Weiler, Frank Hartig, Sophie Wildner, Stefanie Seiwald, et al. "Liver stiffness by transient elastography accompanies illness severity in COVID-19." BMJ Open Gastroenterology 7, no. 1 (July 2020): e000445. http://dx.doi.org/10.1136/bmjgast-2020-000445.
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ObjectiveSevere liver damage is associated with worse outcome in COVID-19. Our aim was to explore the degree of liver damage, liver stiffness (LS) and severity of illness in patients with COVID-19.DesignWe investigated 32 patients with COVID-19 admitted to the University Hospital of Innsbruck in a prospective cross-sectional study. We performed laboratory testing, liver and spleen sonography and elastography to measure organ stiffness.Results12 patients (38%) showed elevated aminotransferases and gamma-glutamyltransferase levels. LS was positively correlated with elevated aminotransferase levels in patients with COVID-19 compared with those without elevated enzymes. Even mild liver damage raised LS significantly in COVID-19 as it was in patients with gastrointestinal symptoms. Furthermore, higher LS measurements were significantly associated with illness severity like pneumonia, need for mechanical ventilation, and even death.ConclusionTransient elastography is a useful and non-invasive tool to assess onset and severity of acute liver injury in patients with COVID-19 patients. Increased LS seems to be predictive for a more severe and complicated course of disease.
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Casey, Carol A., Benita L. McVicker, Terrence M. Donohue, Melinda A. McFarland, Robert L. Wiegert, and Amin A. Nanji. "Liver asialoglycoprotein receptor levels correlate with severity of alcoholic liver damage in rats." Journal of Applied Physiology 96, no. 1 (January 2004): 76–80. http://dx.doi.org/10.1152/japplphysiol.00375.2003.
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It has been demonstrated that the oral administration of ethanol (Lieber-DeCarli liquid diet) to rats results in a decreased expression and content of the asialoglycoprotein receptor (ASGP-R) in the resultant fatty liver. In the present study, we wanted to determine whether the extent of impaired receptor content was correlated with the severity of liver pathology by using the intragastric feeding model. When ASGP-R protein and mRNA levels were measured in animals infused with ethanol or dextrose in the presence of fish oil (FO) or medium-chain triglyceride as the source of fat, more significant impairments to the ASGP-R were observed in the FO-ethanol group compared with the medium-chain triglyceride-ethanol group. Furthermore, only the FO-ethanol group showed pathological liver changes. These results demonstrate that a correlation exists between the progression of alcohol-associated liver injury, as defined by the severity of liver pathology, and an ethanol-induced decline in ASGP-R content.
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Sayfullin, M. A., N. N. Zvereva, E. A. Nurmuhametova, N. P. Blohina, E. Yu Pylaeva, K. S. Konyaev, and O. V. Shamsheva. "Liver damage with measles." Journal Infectology 12, no. 4 (October 17, 2020): 78–86. http://dx.doi.org/10.22625/2072-6732-2020-12-4-78-86.
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Objective: to determine the incidence of liver damage with measles, the specificity of these changes, to identify risk groups, to assess the dynamics of the development of hyperfermentemia in various stages of the disease.Materials and methods: a retrospective cohort study of medical records of patients hospitalized with measles (n = 101), divided into 4 groups: children (n = 23), men (n = 32), women (n = 24) and pregnant women (n = 22). Patients with laboratory-confirmed influenza (n = 61) were taken as a comparison group. The analysis of the frequency of detecting changes in biochemical parameters, average values, standard error and confidence intervals.Results: An increase in ALT in measles patients was observed in 56 (55.4%), above 5 norms – in 15 patients (14.8%), an increase in AST was detected in 80 (79.2%) patients, above 5 norms – in 10 (9.9%). These changes are specific for measles, which was established by comparing the indicators of patients with measles and influenza. The greatest frequency and severity of the observed changes was observed in men. Determination of bilirubin concentration was carried out in 95 patients. An increase in total bilirubin above 20 μmol / L was observed in 10 (10.5%), direct above 5 μmol / L – in 13 (13.6%) patients.Conclusion: given the frequency of occurrence of the identified changes, it is advisable to conduct a biochemical blood test for measles patients. Therapeutic tactics should be determined taking into account the possible development of hepatitis with measles.
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Dhefer, Iqbal Hanash. "Liver damage during infections with coronavirus." Journal of Techniques 3, no. 2 (June 30, 2021): 79–85. http://dx.doi.org/10.51173/jt.v3i2.302.
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The pathogen of the new 2019 coronavirus disease (COVID-19), the sever acute respiratory syndrome coronavirus 2 (SARS-Cov-2), presented a significant risk to health care. The WHO has described the SARS-CoV-2 infection outbreak as an international public health emergency. The main damage caused by the infection with SARS-CoV-2 was known to be lung infections. Previous research revealed that liver damage is prevalent in patients infected with the additional widely zoonotic coronaviruses, Severe Acute Respiratory Syndrome (SARS) and Middle East Respiratory Syndrome (MERS), and has been reviewed in relation to the severity of MERS, SARS, and COVID-19 diseases. Likewise, the mechanism and features of liver damage and liver injury has also been observed, as outlined in this review, which results in extreme cases during the phases of the disease.
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T.Farzana, T.F.Chowdhury, S.K Mandal, R.A. Saeed, and B.R. Rehan. "Study of Serum Total Cholesterol in Cirrhosis of Liver And Its Relation With Severity of The Disease." Journal of Sylhet Women’s Medical College 11, Number 1 (January 1, 2021): 33–38. http://dx.doi.org/10.47648/jswmc2021v11-04.
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Background: Lipid metabolism is impaired in different directions in liver cirrhosis. Dyslipidaemia seen in cirrhosis of the liver differs from that found in most of the additional reasons of secondary dyslipidaemias because lipoproteins in circulation are not only present in unusual amount but they also often have unusual composition, electrophoretic movement and forms (Nangliya et al., 2015). Materials & Method: This cross-sectional study was carried out in the Department of Biochemistry, Sylhet MAG Osmani Medical College, Sylhet during the period from 1st January 2016 to 31st December 2016.Fiftypatients with cirrhosis of liver fulfilling the inclusion criteria were enrolled as group-A and 50 age-sex matched healthy adults were selected as the control group (group-B). Result: Fasting serum total cholesterol was estimated. Severity of liver Cirrhosis was categorized according to Child-Pugh scoring system and increasing severity was categorized as Child Pugh class A, B and C.Serum total cholesterol is decreased in patients with liver cirrhosis. The level of severity of liver damage significantly affects the serum total cholesterol level in cirrhosis; and may be considered as markers of severity of liver damage in cirrhosis. Conclusion: It may be concluded that hypocholesterelemia exists in patients with liver cirrhosis and screening for severity of cirrhosis by serum total cholesterol is important for intervention with appropriate therapy to reduce the severity of the disease. Key words: Liver cirrhosis,Serum total cholesterol , Child-Pugh score.
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Prokofieva, Natalia A., Igor G. Bakulin, Elena G. Nemtsova, Olga Yu Chizhova, Tatiana S. Fil, Anastasiya G. Sushilova, Elena Yu Pavlova, and Maria S. Orlenko. "New coronavirus infection and liver lesions." Russian Family Doctor 27, no. 2 (July 20, 2023): 65–72. http://dx.doi.org/10.17816/rfd404456.
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BACKGROUND: According to published research outcomes, liver dysfunction is one of the predictors of adverse outcome COVID-19.
AIM: To study the frequency and severity of liver damage in COVID-19 and suggest therapeutic and prevention approaches to liver damage.
MATERIALS AND METHODS: The study included 171 patients with SARS-CoV-2 pneumonia at the age of 2194 (mean age 59.85 14.96). Clinical and biochemical blood tests, coagulogram, blood ammonia test, number linkage test, multislice computed tomography of the chest, and 13C-metacetin breath test. Patients were divided into two groups depending on the volume of lung injury. Statistical processing of the results was performed with the software SPSS 26.
RESULTS: The most frequent symptoms were manifestations of intoxication syndrome, respiratory failure, the severity of which correlated with the volume of lung tissue damage according to multislice computed tomography of the chest. In both groups, the activity of alanine aminotransferase, aspartate aminotransferase, gamma-glutamyltranspeptidase, and alkaline phosphate increased. However, significant distinctions in the groups were revealed only for gamma-glutamyltranspeptidase and alkaline phosphate levels. The level of C-reactive protein in both groups directly correlated with the level of cytolysis and cholestasis, indicating a significant role of the liver in pathological processes in COVID-19. Conclusion: Hyperammonemia and decreased liver functional reserve of various severity were observed in all patients.
CONCLUSIONS: The findings indicate the diagnostic value of the studied parameters for the evaluation of liver damage, as well as the applications of prevention and treatment measures for liver lesions in patients with COVID-19.
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Reshetnyak, V. I., I. V. Maev, T. M. Reshetnyak, S. V. Zhuravel, and V. M. Pisarev. "Liver Diseases and the Hemostasis (Rewiew) Part 1. Non-Cholestatic Diseases of the Liver and Hemostasis." General Reanimatology 15, no. 5 (November 9, 2019): 74–87. http://dx.doi.org/10.15360/1813-9779-2019-5-74-87.
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In liver diseases, most commonly in the terminal stage of liver failure, a variety of hemostatic defects affecting almost all parts of the blood coagulation system are developing. This leads to diminishing the capabilities of patients with liver diseases to correctly maintain the hemostatic balance.The severity of hemostatic disorders depends on the nosological form and degree of a liver damage. Depending on the imbalance of the hemostasis system and accumulated clinical/laboratory data, patients with liver diseases can be subdivided into three groups as exhibiting: 1. non-cholestatic liver damage; 2. cholestatic liver damage and 3. liver damage of vascular origin.The first part of the review discusses multiple alterations in the hemostasis system in patients with noncholestatic liver diseases, which are commonly accompanied by hypocoagulation.
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Neuman, Manuela G., and Lawrence B. Cohen. "Inflammation and Liver Cell Death in Patients with Hepatitis C Viral Infection." Current Issues in Molecular Biology 43, no. 3 (November 16, 2021): 2022–35. http://dx.doi.org/10.3390/cimb43030139.
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Hepatitis C virus (HCV)-induced liver disease contributes to chronic hepatitis. The immune factors identified in HCV include changes in the innate and adaptive immune system. The inflammatory mediators, known as “inflammasome”, are a consequence of the metabolic products of cells and commensal or pathogenic bacteria and viruses. The only effective strategy to prevent disease progression is eradication of the viral infection. Immune cells play a pivotal role during liver inflammation, triggering fibrogenesis. The present paper discusses the potential role of markers in cell death and the inflammatory cascade leading to the severity of liver damage. We aim to present the clinical parameters and laboratory data in a cohort of 88 HCV-infected non-cirrhotic and 25 HCV cirrhotic patients, to determine the characteristic light microscopic (LM) and transmission electron microscopic (TEM) changes in their liver biopsies and to present the link between the severity of liver damage and the serum levels of cytokines and caspases. A matched HCV non-infected cohort was used for the comparison of serum inflammatory markers. We compared the inflammation in HCV individuals with a control group of 280 healthy individuals. We correlated the changes in inflammatory markers in different stages of the disease and the histology. We concluded that the serum levels of cytokine, chemokine, and cleaved caspase markers reveal the inflammatory status in HCV. Based upon the information provided by the changes in biomarkers the clinician can monitor the severity of HCV-induced liver damage. New oral well-tolerated treatment regimens for chronic hepatitis C patients can achieve cure rates of over 90%. Therefore, using the noninvasive biomarkers to monitor the evolution of the liver damage is an effective personalized medicine procedure to establish the severity of liver injury and its repair.
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Travenko, E. N., and V. A. Porodenko. "Diagnostics of Fibrosis in Alcoholic Liver Damage." Kuban Scientific Medical Bulletin 26, no. 4 (September 15, 2019): 76–83. http://dx.doi.org/10.25207/1608-6228-2019-26-4-76-83.
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Aim. In this article, the authors determine the severity (index) of histological activity (HAI) and fi brosis in various forms of alcoholic liver disease drawing on the autopsy material, as well as suggest a marker for detecting fi brosis.Materials and methods. The authors studied 110 autopsies and histopathological studies of people who died from ethanol poisoning in the setting of various forms of alcoholic liver damage (95) and traumatic brain injury – control (15). Alcohol dehydrogenase (ADH) activity was studied through histochemical methods; values were estimated through the quantitative morphometry of the histochemical reaction product using the MORFOLOG program developed at the Department for Forensic Medicine (V.A. Porodenko, 1996). Statistical analysis was performed using the STATISTICA 10 software package and a created Exсel database. In order to determine the signifi cance between two compared values, the Student’s t-test was employed. Correlations were estimated using the Spearman’s rank correlation coeffi cient (r).Results. The study revealed various degrees of histological activity and fi brosis in the setting of alcoholic steatosis, hepatitis and cirrhosis. The initial liver damage is characterised by minimal / weak activity and F0–F2 stage of fi brosis. With the progression of the pathological process in the liver, HAI is estimated as moderate and severe (F2–F4 stage of fi brosis). There is a correlation between the development of perisinusoidal and pericellular fi broses (r = –0.655), septae (r = –0.435), connective tissue in the portal tracts and around a vein (r = –0.517) and the number of medium caliber vessels in the liver, as well as between the portal vein diameter and the development of perisinusoidal and pericellular fi broses (r = 0.377). The authors noted high and moderate positive correlation between the ADH activity in zone 3 of the liver acini and the development of necroses and fi brosis, minor cholestases, expansion of the perisinusoidal spaces. The calculated index of fi brosis and ischemic liver damage correlates with its impaired morphofunctional state.Conclusion. The obtained data indicate that fi brosis develops in the early stages of alcoholic liver damage, whose severity can be assessed using the proposed method for determining the index of fi brosis and ischemic liver damage, given that it refl ects both the structural and functional state of the organ.
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Abd El-Emam, Mahran Mohamed, Mahmoud Mostafa, Amina A. Farag, Heba S. Youssef, Azza S. El-Demerdash, Heba Bayoumi, Mohammed A. Gebba, et al. "The Potential Effects of Quercetin-Loaded Nanoliposomes on Amoxicillin/Clavulanate-Induced Hepatic Damage: Targeting the SIRT1/Nrf2/NF-κB Signaling Pathway and Microbiota Modulation." Antioxidants 12, no. 8 (July 25, 2023): 1487. http://dx.doi.org/10.3390/antiox12081487.
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Amoxicillin/clavulanate (Co-Amox), a commonly used antibiotic for the treatment of bacterial infections, has been associated with drug-induced liver damage. Quercetin (QR), a naturally occurring flavonoid with pleiotropic biological activities, has poor water solubility and low bioavailability. The objective of this work was to produce a more bioavailable formulation of QR (liposomes) and to determine the effect of its intraperitoneal pretreatment on the amelioration of Co-Amox-induced liver damage in male rats. Four groups of rats were defined: control, QR liposomes (QR-lipo), Co-Amox, and Co-Amox and QR-lipo. Liver injury severity in rats was evaluated for all groups through measurement of serum liver enzymes, liver antioxidant status, proinflammatory mediators, and microbiota modulation. The results revealed that QR-lipo reduced the severity of Co-Amox-induced hepatic damage in rats, as indicated by a reduction in serum liver enzymes and total liver antioxidant capacity. In addition, QR-lipo upregulated antioxidant transcription factors SIRT1 and Nrf2 and downregulated liver proinflammatory signatures, including IL-6, IL-1β, TNF-α, NF-κB, and iNOS, with upregulation in the anti-inflammatory one, IL10. QR-lipo also prevented Co-Amox-induced gut dysbiosis by favoring the colonization of Lactobacillus, Bifidobacterium, and Bacteroides over Clostridium and Enterobacteriaceae. These results suggested that QR-lipo ameliorates Co-Amox-induced liver damage by targeting SIRT1/Nrf2/NF-κB and modulating the microbiota.
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Parisse, Simona, Alessandra Gianoncelli, Gloria Isani, Francesco Luigi Gambaro, Giulia Andreani, Emil Malucelli, Giuliana Aquilanti, et al. "Severity of Hepatocyte Damage and Prognosis in Cirrhotic Patients Correlate with Hepatocyte Magnesium Depletion." Nutrients 15, no. 11 (June 3, 2023): 2626. http://dx.doi.org/10.3390/nu15112626.
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We aimed to evaluate the magnesium content in human cirrhotic liver and its correlation with serum AST levels, expression of hepatocellular injury, and MELDNa prognostic score. In liver biopsies obtained at liver transplantation, we measured the magnesium content in liver tissue in 27 cirrhotic patients (CIRs) and 16 deceased donors with healthy liver (CTRLs) by atomic absorption spectrometry and within hepatocytes of 15 CIRs using synchrotron-based X-ray fluorescence microscopy. In 31 CIRs and 10 CTRLs, we evaluated the immunohistochemical expression in hepatocytes of the transient receptor potential melastatin 7 (TRPM7), a magnesium influx chanzyme also involved in inflammation. CIRs showed a lower hepatic magnesium content (117.2 (IQR 110.5–132.9) vs. 162.8 (IQR 155.9–169.8) μg/g; p < 0.001) and a higher percentage of TRPM7 positive hepatocytes (53.0 (IQR 36.8–62.0) vs. 20.7 (10.7–32.8)%; p < 0.001) than CTRLs. In CIRs, MELDNa and serum AST at transplant correlated: (a) inversely with the magnesium content both in liver tissue and hepatocytes; and (b) directly with the percentage of hepatocytes stained intensely for TRPM7. The latter also directly correlated with the worsening of MELDNa at transplant compared to waitlisting. Magnesium depletion and overexpression of its influx chanzyme TRPM7 in hepatocytes are associated with severity of hepatocyte injury and prognosis in cirrhosis. These data represent the pathophysiological basis for a possible beneficial effect of magnesium supplementation in cirrhotic patients.
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Chuang, Wan-Long, Hong-Wen Liu, Wen-Yu Chang, Shinn-Cherng Chen, Ming-Yuh Hsieh, and Liang-Yen Wang. "Natural killer cell activity in patients with liver cirrhosis relative to severity of liver damage." Digestive Diseases and Sciences 36, no. 3 (March 1991): 299–302. http://dx.doi.org/10.1007/bf01318200.
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Zahedi, Kamyar, Sharon L. Barone, Jie Xu, Nora Steinbergs, Rebecca Schuster, Alex B. Lentsch, Hassane Amlal, Jiang Wang, Robert A. Casero, and Manoocher Soleimani. "Hepatocyte-specific ablation of spermine/spermidine-N1-acetyltransferase gene reduces the severity of CCl4-induced acute liver injury." American Journal of Physiology-Gastrointestinal and Liver Physiology 303, no. 5 (September 1, 2012): G546—G560. http://dx.doi.org/10.1152/ajpgi.00431.2011.
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Activation of spermine/spermidine- N1-acetyltransferase (SSAT) leads to DNA damage and growth arrest in mammalian cells, and its ablation reduces the severity of ischemic and endotoxic injuries. Here we have examined the role of SSAT in the pathogenesis of toxic liver injury caused by carbon tetrachloride (CCl4). The expression and activity of SSAT increase in the liver subsequent to CCl4 administration. Furthermore, the early liver injury after CCl4 treatment was significantly attenuated in hepatocyte-specific SSAT knockout mice (Hep-SSAT-Cko) compared with wild-type (WT) mice as determined by the reduced serum alanine aminotransferase levels, decreased hepatic lipid peroxidation, and less severe liver damage. Cytochrome P450 2e1 levels remained comparable in both genotypes, suggesting that SSAT deficiency does not affect the metabolism of CCl4. Hepatocyte-specific deficiency of SSAT also modulated the induction of cytokines involved in inflammation and repair as well as leukocyte infiltration. In addition, Noxa and activated caspase 3 levels were elevated in the livers of WT compared with Hep-SSAT-Cko mice. Interestingly, the onset of cell proliferation was significantly more robust in the WT compared with Hep-SSAT Cko mice. The inhibition of polyamine oxidases protected the animals against CCl4-induced liver injury. Our studies suggest that while the abrogation of polyamine back conversion or inhibition of polyamine oxidation attenuate the early injury, they may delay the onset of hepatic regeneration.
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Alizadeh, Ahmad, Fariborz Mansour-Ghanaei, Ava Roozdar, Farahnaz Joukar, Masood Sepehrimanesh, Seyedeh Amineh Hojati, and Alireza Mansour-Ghanaei. "Laboratory Tests, Liver Vessels Color Doppler Sonography, and FibroScan Findings in Patients with Nonalcoholic Fatty Liver Disease: An Observation Study." Journal of Clinical Imaging Science 8 (April 3, 2018): 12. http://dx.doi.org/10.4103/jcis.jcis_93_17.
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Objective: Determination of the amount of parenchymal damage in nonalcoholic fatty liver disease (NAFLD) is crucial to choose the best treatment and management. Aim: Here, the associations between laboratory data and severity of steatosis and fibrosis plus hepatic vessel Doppler indices in NAFLD patients were investigated. Patients and Methods: Fifty patients (20 males and 30 females) with NAFLD criteria were enrolled. Fatty liver was graded by sonography (SGFL) and FibroScan (FGFL). In addition, liver fibrosis was graded through FGLF. Damages to the portal, hepatic, and splenic veins were evaluated by color Doppler/dopplex. Serum liver enzymes and C-reactive protein (CRP) were also measured. Results: Significant association existed between SGFL and FGFL (P = 0.006). Portal vein pulsatility index (PI) and phasicity plus the triphasic and monophasic pattern of hepatic veins significantly associated with fatty liver grade evaluated by sonography. Splenic vein Peak systolic velocity and PI showed significant association with FGFL. Eventually, elevated liver enzymes and CRP significantly correlated with FGLF. Conclusion: We found that the severity of fatty liver is correlated with hepatic and portal veins damages; however, the degree of parenchymal fibrosis was independent to these indices and can be directly evaluated by FGFL. In addition, elevated liver enzymes and CRP correlated with the degree of fibrosis.
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Qiao, Lichun, Ziwei Guo, Haobiao Liu, Jiaxin Liu, Xue Lin, Huan Deng, Xuan Liu, et al. "Protective Effect of Mitophagy Regulated by mTOR Signaling Pathway in Liver Fibrosis Associated with Selenium." Nutrients 14, no. 12 (June 10, 2022): 2410. http://dx.doi.org/10.3390/nu14122410.
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Background: As a central organ of energy metabolism, the liver is closely related to selenium for its normal function and disease development. However, the underlying roles of mitochondrial energy metabolism and mitophagy in liver fibrosis associated with selenium remain unclear. Methods: 28 rats were randomly divided into normal, low-selenium, nano-selenium supplement-1, and supplement-2 groups for a 12-week intervention. We observed pathological and ultrastructural changes in the liver and analyzed the effects of selenium deficiency and nano-selenium supplementation on liver metabolic activities and crucial proteins expression of mammalian target of the rapamycin (mTOR) signaling pathway. Results: Selenium deficiency caused liver pathological damage and fibrosis with the occurrence of mitophagy by disrupting normal metabolic activities; meanwhile, the mTOR signaling pathway was up-regulated to enhance mitophagy to clear damaged mitochondria. Furthermore, nano-selenium supplements could reduce the severity of pathological damage and fibrosis in livers and maintain normal energy metabolic activity. With the increased concentrations of nano-selenium supplement, swelling mitochondria and mitophagy gradually decreased, accompanied by the higher expression of mTOR and phosphorylation-modified mTOR proteins and lower expression of unc-51 like autophagy activating kinase 1 (ULK1) and phosphorylation-modified ULK1 proteins. Conclusions: Mitophagy regulated by the mTOR signaling pathway plays a dual protective role on low-selenium inducing liver fibrosis and nano-selenium supplements preventing liver fibrosis. Mitochondrial energy metabolism plays an important role in these processes as well.
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Alavian, Seyed Ehsan, Mohammad Mofidi, and Fahimeh Shahabipour. "Effect of COVID-19 on Serum Activity of Liver Enzymes: Is This Associated with Severity and Mortality Rate?" Ibnosina Journal of Medicine and Biomedical Sciences 14, no. 03 (September 2022): 086–93. http://dx.doi.org/10.1055/s-0042-1759739.
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Abstract Introduction Coronavirus disease 2019 (COVID-19) is a viral infection caused by a novel coronavirus known as the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The disease raises an enormous public health challenge for the international community. Liver enzymes have been reported to be frequently elevated in hospitalized patients with severe COVID-19 disease. Materials and Methods This article is a narrative review of abnormal liver tests and liver injury as a manifestation of progression to severe pneumonia. We collected data from the PubMed database (National Library of Medicine, Bethesda, Maryland, United States). We used the search term “abnormal liver test” and relevant records were measured. The review article was organized thematically. Results This narrative review aims to summarize the available clinical data on abnormal liver enzymes in coronavirus infection and its association with the risk of mortality, severer pneumonia, and systemic inflammation. Some clinical studies refer to abnormal liver tests and liver injury as a manifestation of progression to severe pneumonia. Recent research verified the relationship between hepatic liver enzyme activities and liver damage in patients with COVID-19, which suggested that it might reflect the infection severity and the mortality risk. Thus, this review investigated the correlation between liver serum enzymes level and the severity of COVID-19 patients, by reviewing investigating the relationship between the illness severity in COVID-19 patients with abnormal liver tests, liver pathology, and markers of inflammation. Conclusion In the current pandemic of SARS-CoV-2, abnormalities of liver enzyme tests were commonly observed in patients with COVID-19. However, because of multiorgan damages that observed in COVID-19 patients, various issues should be considered such as the pathology and pathophysiology of the liver tissue, especially on the activation process of the immune response and cytokine storm to prevent the severity of the disease.
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Soegijanto, Soegeng, Desiana W. Sari, Atsushi Yamanaka, Tomohiro Kotaki, Masanori Kameoka, and Eiji Konishi. "AWARENESS OF USING RINGER LACTAT SOLUTION IN DENGUE VIRUS INFECTION CASES COULD INDUCE SEVERITY." Indonesian Journal of Tropical and Infectious Disease 4, no. 4 (October 1, 2013): 35. http://dx.doi.org/10.20473/ijtid.v4i4.231.
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Background: In 2012, serotype of Dengue Virus had changed from Den-2 and Den-3 to Den-1. In 5–10 years ago, serotype of Den-1 case showed a mild clinical manifestation; but now as a primary case it can also show severe clinical manifestation. One of indicator is an increasing liver enzyme, AST and ALT, with level more than 100–200 U/L. Aim: To getting a better solutions for this problem. Method: Obsevasional Study had been done in medical faculty of Airlangga University (Dr. Soetomo and Soerya hospital) Surabaya on Mei–August 2012. There were 10 cases of dengue virus infection were studied, 5 cases got Ringer Acetate solution (Group A) and 5 cases got Ringer Lactate solution (Group B). The diagnosis was based on criteria WHO 2009. Result: Five cases of Dengue Virus Infection had showed a liver damage soon after using Ringer Lactate solution; AST and ALT were increasing more than 100–200 U/L; but the other 5 cases showed better condition. It might be due to use Ringer Acetate that did not have effect for inducing liver damage. By managing carefully, all of the cases had shown full recovery and healthy condition when being discharged. Conclusion: Using Ringer Acetate as fluid therapy in Dengue Virus Infection is better to prevent liver damage than using Ringer Lactate.
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Islam, Md Asiful, Hamid Hasan, Gulnar Yasmin, Minhaj Rashidur Rahman, and Md Titu Miah. "Association of lipid profile with severity of hepatitis B virus related chronic liver disease in adult." Bangladesh Medical Journal Khulna 54, no. 1-2 (July 18, 2022): 8–12. http://dx.doi.org/10.3329/bmjk.v54i1-2.60777.
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Background: Chronic liver disease (CLD) is a major health problem and contributes to a common cause of hepatocellular carcinoma, disability and death worldwide. Hepatitis B virus (HBV) is the leading cause of CLD in our country. Abnormal lipid profile is expected in those with severe liver dysfunction.
Objective: The objective of the study was to determine the alteration of lipid profile (total cholesterol, triglyceride, LDL-C and HDL-C) in HBV positive adult CLD patients and to correlate with severity of liver damage.
Methods: This case control study was conducted for one year between January 2018 to December 2018. One hundred and three patients, >18 years old, admitted with HBV positive CLD in Dhaka Medical College Hospital were recorded as case and 103 age and sex matched, healthy population, were recorded as control. A standard case record form including demographics, histories, clinical examinations and different investigations were completed for each group. Then lipid profile values of cases were compared to controls and different Child-Pugh and MELD scores, were used to see severity of liver damage in CLD patients.
Results: In patients with HBV positive adult CLD, there were a significant decrease in serum total cholesterol. LDL-C and HDL-C levels compared to the control group (mean 131.4 vs 179.3, 72.5 vs 109.6, and 31.0 vs 40.4 mg/dl, respectively; p<0.001). Comparison of lipid profile with pathologic progression of CLD revealed that these values were diminished gradually with progression of liver damage. Overall triglyceride level was decreased marginally in cases when compared to controls (mean 139.2 vs 146.6 and p=0.047) and this reduction was observed in only advanced stage.
Conclusion: Serum total cholesterol, LDL-C and HDL-C level in HBV positive CLD patients were low and diminished gradually with severity of liver damage. Triglyceride level was marginally significant and diminished in advanced CLD.
Bang Med J Khulna 2021; 54 : 08-12
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Chowdhury, Atanu Roy, Ramkrishna Brahmachari, and Soumyojit Saha. "Clinicobiochemical and pathological correlation in alcoholic liver disease among Indian patients." International Journal of Research in Medical Sciences 9, no. 3 (February 25, 2021): 854. http://dx.doi.org/10.18203/2320-6012.ijrms20210890.
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Background: Alcohol is one of the leading causes of “preventable” morbidity and mortality worldwide. It is associated with liver damage. A gray area is temporal relation between clinico-biochemical severity and histological changes in liver, neither this issue has been widely studied.Methods: A hospital based cross sectional clinico-pathological pilot study was undertaken in a tertiary care hospital in West Bengal in patients with a history of alcohol intake who had been admitted in the inpatient department of medicine. Assessment of patients with history of alcohol intake with respect to clinical, biochemical and histopathological examination was performed. The correlation between clinico-biochemical severity and histopathological stages in cases of alcoholic liver disease was evaluated.Results: There was a significant correlation between clinico-biochemical severity and liver biopsy changes. The severity of histopathological changes of alcoholic liver disease was found to correlate significantly with the severity of abdominal parameters with Pearson correlation cofactor of 0.819.Conclusions: Both the clinic-biochemical severity and histological changes had no correlation with the duration of alcohol intake in contrast to earlier studies which had demonstrated a definite correlation of alcoholic liver disease (ALD) with both the amount and duration of alcohol intake. Larger studies will be required to substantiate the findings of this study.
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Iannacone, Matteo, Giovanni Sitia, Masanori Isogawa, Patrizia Marchese, Maria G. Castro, Pedro L. Lowenstein, Francis V. Chisari, Zaverio M. Ruggeri, and Luca G. Guidotti. "Platelets Mediate Cytotoxic T Lymphocyte-Induced Liver Damage." Blood 106, no. 11 (November 16, 2005): 651. http://dx.doi.org/10.1182/blood.v106.11.651.651.
Full textAbstract:
Abstract We used hepatitis B virus (HBV) transgenic mice as recipients of cytotoxic T cells (CTLs) specific for the immunodominant Env28–39 epitope (Env28) of HbsAg, and C57BL/6J mice acutely infected with a recombinant replication-deficient adenovirus expressing lacZ (RAd35) to show that platelets accumulate in necroinflammatory foci of the liver during the course of a disease similar to acute hepatitis in humans. Liver disease was monitored by quantifying the activity of serum alanine aminotransferase (sALT), a hepatocellular enzyme that is released into the circulation by necrotic hepatocytes, and by evaluating histological changes at the time of autopsy. Livers from mice sacrificed 2 days after CTL transfer were stained with a mixture of rat monoclonal antibodies (α-PLT) against mouse glycoprotein (GP) Ibα, a receptor exclusively expressed on platelets and megakaryocytes. Livers from mice injected with saline (0.9% NaCl) alone served as controls. Platelets were detectable only inside vessels and hepatic sinusoids in saline-injected controls, while they accumulated alongside apoptotic hepatocytes and inflammatory cells within necroinflammatory foci of the liver in CTL-injected or RAd35-infected animals. The injection of α-PLT caused a >97.5% decrease in the number of circulating platelets (less than 2x104 platelets/μl of blood) within 30 min, and similar low counts were maintained for up to 6 days. Mice that received either saline or an irrelevant antibody (α-Irr) exhibited stable platelet counts (8–10 x 105 platelets/μl of blood). Previous platelet depletion in CTL-injected or RAd35-infected animals reduced the intrahepatic accumulation of virus-specific CTLs and the resulting liver damage, as evidenced by an 80% reduction in sALT activity (from 1600 to 300 U/L) and a reduction the size of necroinflammatory foci (from 6724 μm2 to 1245 μm2) as compared to mice that received α-Irr. Infusion of washed mouse platelets expressing human GP Ibα (thus, insensitive to the depleting effect of α-Plt) within hours after CTL transfer or RAd35 infection restored CTL accumulation and liver disease severity, but not when the infused platelets were pretreated with the activation inhibitor, prostaglandin E1. Accordingly, platelet activation was required to promote CTL/platelet interactions under flow conditions in vitro. Fibrin deposition was abundant within hepatic necroinflammatory foci of CTL-injected or RAd35-infected animals, and markedly decreased in animals that were previously made thrombocytopenic. The platelet-dependent intrahepatic deposition of fibrin could be selectively prevented by anticoagulant treatment of the mice, which had no effect on the platelet count, but this did not ameliorate liver injury. Our findings indicate that activated platelets contribute to CTL-induced liver immunopathology by facilitating the accumulation of CTLs at the site of inflammation, independently of procoagulant function.
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Bakulin, I. G., N. V. Bakulina, S. V. Tikhonov, S. A. Vinchuk, V. D. Dekkanova, and N. A. Prokofiev. "Pathogenetic links of liver damage, obesity and COVID‑19." Medical alphabet 1, no. 30 (December 22, 2020): 5–10. http://dx.doi.org/10.33667/2078-5631-2020-30-5-10.
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A retrospective analysis of 73 case histories of COVID‑19 patients were made to study the potential relationship between obesity, liver damage and COVID‑19. The average BMI of the study participants was 30.8 ± 5.8 kg/m2, waist circumference 103.5 ± 13.5 cm, 77 % of patients had abdominal obesity, 71 % of patients had cytolytic syndrome. There was not link between the presence of obesity and the level of transaminases. The degree of transaminases increase depended on the severity of COVID‑19 (level of ferritin, CRP, and oxygen saturation of the blood) and wasn't connected with BMI, waist circumference, and the presence of type 2 diabetes.
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Wang, Leijie, Mingjie Yao, Shuhong Liu, Danli Yang, Xiajie Wen, Jing Ning, Lu Wang, et al. "Serum Golgi Protein 73 as a Potential Biomarker for Hepatic Necroinflammation in Population with Nonalcoholic Steatohepatitis." Disease Markers 2020 (February 4, 2020): 1–7. http://dx.doi.org/10.1155/2020/6036904.
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Aims. Persistent hepatic necroinflammatory damage almost always results in fibrosis/cirrhosis or even hepatocellular carcinoma. Therefore, the presence of active necroinflammation in the liver suggests that nonalcoholic fatty liver disease (NAFLD) patients are in urgent need of treatment. Unfortunately, alanine transaminase (ALT), a routine indicator of liver inflammatory damage, showed a poor performance in nonalcoholic steatohepatitis (NASH) patients. Thus, it will be valuable to find an alternative indicator to identify patients with hepatic necroinflammatory damage. In this study, we evaluated the diagnostic value of serum Golgi protein 73 (GP73) for hepatic necroinflammatory damage in patients with NASH. Methods. The clinical data of 201 patients with NASH diagnosed by liver biopsy according to the Brunt staging system were collected retrospectively. The in situ expression of GP73 protein was measured by immunohistochemistry. The receiver operating characteristic (ROC) curve was used to calculate the area under the ROC curve (AUROC) of serum GP73 for diagnosing hepatic necroinflammatory damage. Results. The serum GP73 levels of NASH patients increased with the aggravation of liver necroinflammation. The median levels significantly increased from 49.98 ng/ml (31.49, 75.05) for G0-1 to 76.61 ng/ml (48.68, 110.03) for G2 and to 116.44 ng/ml (103.41, 162.17) for G3 patients (G0-1 vs. G2, P<0.0001; G2 vs. G3, P=0.0228). In consistent, the gradual increase of GP73 protein expression in situ was also observed in liver tissue, in parallel with the increasing severity of necroinflammatory activity. Therefore, serum GP73 correlated well with the intensity of protein expression in liver tissue. The AUROCs of serum GP73 for G2 and G3 inflammatory activity were 0.742 (0.676 to 0.801) and 0.891 (0.840 to 0.931), respectively. Conclusions. GP73 is a valuable alternative serum marker reflecting the severity of hepatic necroinflammation in NASH patients.
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Shaymaa Hasan Abbas, Rasha Saadi Abbas, and Lubab Tarek Nafea. "Severity and Risk of Death Due to COVID 19." Al Mustansiriyah Journal of Pharmaceutical Sciences 20, no. 4 (April 18, 2022): 1–12. http://dx.doi.org/10.32947/ajps.v20i4.769.
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A novel SARS-CoV2 virus appeared since December 2019 and triggering the Corona virus disease (2019-nCoV or COVID-19). Usually the symptoms begin as mild, with only fever, cough, and occasional dyspnea. The severe symptoms such as
pneumonitis, and acute respiratory distress syndrome (ARDS), may occur 5-8 days into COVID-19 illness in a minority of patients. Method: for this narrative review, more than 25 related scientific articles and reports about COVID- 19 were used from different databases (e.g., PubMed, Google Scholar, and Web of Science) using keywords such as SARS-CoV2, COVID-19, Mortality, and CO-morbidities. Results The results of this review reported that aged people are more vulnerable to severe pattern of COVID-19 disease than people younger than 50 years; probably because of health issues and comorbidities in that population group. Male more than female affected by COVID-19. On the other hand, children might be less probable to infected or might show mild symptoms if infected. The small percentage of current smokers infected with COVID-19 compared with the actual percentage of smokers (50·5%) in China are unlikely to be related with the incidence, severity, or mortality rate of COVID-19. The poorer clinical outcome in COVID-19 infected patients may have related to the presence and number of co morbidities especially hypertension, diabetes and cardiovascular diseases. The direct SARS-COV2 infection of liver cells might be the cause of liver damage but might be related to other reasons such as systemic inflammation and drug toxicity. The data suggested that liver damage is more predominant in severe cases especially with pre-existing liver diseases. patients with cancer might be more prone to COVID 19 due to their immunocompromised status but whether or not they have high risk of poor prognoses and sever event not fully established.
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Sigua, B. V., V. P. Zemlyanoy, Zh E. Badalova, K. D. Yalda, and G. N. Gorbunov. "FEATURES OF SURGICAL TACTICS IN WOUNDS OF THE ANTERIORABDOMINAL WALL AND LUMBAR REGION WITH LIVER DAMAGE." HERALD of North-Western State Medical University named after I.I. Mechnikov 6, no. 4 (December 15, 2014): 16–20. http://dx.doi.org/10.17816/mechnikov20146416-20.
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We analyzed the results of treatment of 339 patients with wounds of abdominal and lumbar regions, that were treated during the period from 1991 to 2010. For the purpose of continuity in providing of the specialized surgical care we used the scales, evaluating the severity of multiple and combined injuries, developed by military surgery department (VPH-P ((R) and (OR))) and the classification of liver damages by E. Moore. Abandonment of liver injury packing in favor of suturing allowed to achieve a significant reduction of post-operative complications in patients with injuries of the abdomen and lumbar region with liver damage from 24.1% (40) to 9.2% (16) (p <0,001), and the level of mortality from 6.1% (10) to 1.2% (p <0.05).
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Gao, Daqing, Chiming Wei, Lei Chen, Jiawen Huang, Shiqi Yang, and Anna Mae Diehl. "Oxidative DNA damage and DNA repair enzyme expression are inversely related in murine models of fatty liver disease." American Journal of Physiology-Gastrointestinal and Liver Physiology 287, no. 5 (November 2004): G1070—G1077. http://dx.doi.org/10.1152/ajpgi.00228.2004.
Full textAbstract:
Mitochondrial generation of reactive oxygen species (ROS) is increased in mice with fatty livers induced by genetic obesity, chronic consumption of ethanol, or methionine/choline-deficient diets. Both nuclear and mitochondrial (mt) DNA are targets for ROS-induced damage and accumulate hydroxylated bases, such as 8-hydroxy-2′-deoxyguanosine (8-oxoG) and base substitution of adenine with 8-oxoG (A*8-oxoG), that introduce mutations that promote cancer as well as cell death. The mammalian homolog of the bacterial DNA mismatch repair enzyme MutY (MYH) removes A*8-oxoG from nuclear and mtDNA, reduces 8-oxoG accumulation, and restores genomic stability after ROS exposure. Cumulative damage to mtDNA occurs as fatty liver disease progresses. Therefore, differences in hepatic MYH activity may influence the severity of fatty liver disease. To evaluate this hypothesis, we compared mtH2O2 production, MYH expression, oxidative DNA damage, and hepatocyte death in healthy mice and different mouse models of fatty liver disease. The results show that diverse causes of steatohepatitis increase mtROS production, limit repair of mtDNA, and oxidatively damage DNA. However, there are important differences in the DNA repair response to oxidant stress among mouse models of fatty liver disease. Independent of the degree of mtROS generation, models with the least MYH exhibit the greatest accumulation of 8-oxoG and the most hepatocyte death. These findings raise the intriguing possibility that inherited or acquired differences in DNA repair enzyme activity may underlie some of the interindividual differences in fatty liver disease outcomes.
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Cairoli, Victoria, Elena De Matteo, Paola Casciato, Beatriz Ameigeiras, María Victoria Preciado, and Pamela Valva. "The performance of soluble CD163 as a non-invasive biomarker of liver damage in chronically HCV and HCV/HIV infected subjects." PLOS ONE 17, no. 7 (July 7, 2022): e0270911. http://dx.doi.org/10.1371/journal.pone.0270911.
Full textAbstract:
Macrophage activation plays a key role in liver disease progression. Soluble CD163 (sCD163) is a specific macrophage activation biomarker useful for clinical estimating damage severity and predicting outcome in different liver conditions. sCD163 performance as a non-invasive marker of liver damage was evaluated in plasma samples at time of biopsy in 120 patients with different hepatic conditions (56 HCV, 20 HCV/HIV, 10 HBV and 34 MAFLD). sCD163 values were compared with those of healthy donors and analyzed related to histological damage. sCD163 together with other clinical parameters were used to create a logistical regression model to predict significant fibrosis. Only patients with viral hepatitis showed higher sCD163 values compared to the control group (HCV p<0.0001; HCV/HIV p<0.0001; HBV p = 0.0003), but no significant differences regarding fibrosis stages were observed. The proposed model predicts fibrosis severity using the logarithm sCD163 concentration, platelet count and age, it demonstrated to be a good marker for the HCV monoinfected group (AUROC 0.834) and an excellent one for the HCV/HIV co-infected group (AUROC 0.997). Moreover, the model displayed a diagnostic performance similar to FIB-4 in HCV cases and FIB-4 and APRI in HCV/HIV coinfected cases, and it even managed to correctly classify some cases that had been misclassified. The proposed model is able to determine, in a non-invasive way, the liver fibrosis stage of HCV and HCV/HIV patients, so after validation, it could be used in a complementary way in the clinical practice whenever APRI and FIB-4 failed to determine damage severity in HCV and HCV/HIV cases.
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Muhammad Iftikhar Yousaf, Usama Faizan, Humaira Mubeen Afzal, Muhammad Asif, Muhammad Ali Sabir, and Muhammad Haroon Yousaf. "Correlation of fasting serum cholesterol level with severity of chronic liver disease." Professional Medical Journal 30, no. 12 (November 30, 2023): 1551–55. http://dx.doi.org/10.29309/tpmj/2023.30.12.7821.
Full textAbstract:
Objective: To evaluate correlation of fasting serum cholesterol level with severity of chronic liver disease (CLD). Study Design: Cross-sectional Survey. Setting: North Medical Ward, Mayo Hospital Lahore. Period: June 2020 to December 2020. Material & Methods: Patients having chronic liver disease with age 25-85 years and of either gender, were included. After 12 hours of fasting, 5ml of blood was drawn from patients under all aseptic precautions into sterile disposable syringes and blood samples were sent to laboratory for measurement of total cholesterol. Total cholesterol (TC) in mg/dl was noted from their reports. CLD severity patients was defined by using Modified Child Pugh classifications. Data was entered in SPSS version 20 and analyzed by same software. Results: Total 100 cases diagnosed with chronic liver disease (CLD) were studied, with an average age of 53.8±10.76 years. The majority of participants, constituting 72%, were male. Overall average TC was 119.85±31.51mg/dl. Out of all 27% patients belonged to CPT class A, 28% had CPT class B and 45% had CPT class C. Spearman correlation between Child Pugh score and total cholesterol level was calculated. A negative spearman correlation was found as r= -.672. It was significant at the level of 0.01. Conclusion: As per the study conclusion, total serum cholesterol level was observed to be the significantly corelated with degree of liver damage. The significance of this correlation highlights the potential clinical utility of serum total cholesterol as a prognostic tool for evaluating the degree of liver damage.
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Eremin, A. V., E. A. Savina, and O. V. Eremin. "Periodontal pathology in patients with cirrhosis of the liver." Experimental and Clinical Gastroenterology, no. 3 (October 4, 2022): 15–25. http://dx.doi.org/10.31146/1682-8658-ecg-199-3-15-25.
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The frequency and clinical course of chronic generalized periodontitis against the background of liver cirrhosis of various etiologies were studied. 70 patients with chronic generalized periodontitis of varying degrees in combination with liver cirrhosis were examined (23 patients (32.9%) had liver cirrhosis class A, 25 (35.7%) — class B, 22 (31.4%) — class C. Comparison group — 17 patients with periodontitis without somatic pathology. Control group — 20 practically healthy volunteers. A signifi cantly reduced level of oral hygiene was revealed in patients with liver cirrhosis of classes B and C. Periodontal pathogenic microorganisms were signifi cantly more common in the contents of periodontal pockets with cirrhosis. With an increase in the class of CP, the frequency of bacterial expansion increased. The severity of periodontal damage in patients with liver cirrhosis is associated with a loss of bone mineral density by the type of osteopenia (47.2%) or osteoporosis (31.4%), increasing according to the class of liver cirrhosis and the severity of periodontal disease The degree of resorption of the alveolar process is associated with a systemic decrease in bone mineral density. The eff ects of generalized osteopenic syndrome and resorption of the alveolar processes are characteristic of patients with alcoholic liver damage and liver cirrhosis with cholestasis syndrome.
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Del Ben, M., L. Polimeni, F. Baratta, S. Bartimoccia, R. Carnevale, L. Loffredo, P. Pignatelli, F. Violi, and F. Angelico. "Serum Cytokeratin-18 Is Associated with NOX2-Generated Oxidative Stress in Patients with Nonalcoholic Fatty Liver." International Journal of Hepatology 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/784985.
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Background & Aims. Hepatocyte apoptosis may play a role in progression of nonalcoholic fatty liver and oxidative stress seems one of the key mechanisms responsible for liver damage. The aim was to determine the association of oxidative stress with cytokeratin-18 M30 fragment levels, a marker of hepatocyte apoptosis.Methods.Steatosis severity was defined according to Hamaguchi’s echographic criteria in 209 patients with nonalcoholic fatty liver. Serum cytokeratin-18, urinary 8-iso-prostaglandin F2α, soluble NOX2-derived peptide, and adiponectin were measured.Results.Serum cytokeratin-18 progressively increased with steatosis severity (from 169.5 (129.3/183.8) to 176 (140/190) and 180 (169.5/192.5)μIU/mL in mild, moderate, and severe steatosis, respectively;P<0.01). After stratification by cytokeratin-18 tertiles, a significant progression of body mass index, HOMA-IR, triglycerides, urinary 8-iso-PGF2α, soluble NOX2-derived peptide, and of the prevalence of diabetes and severe steatosis was found, while HDL-cholesterol and adiponectin progressively decreased. A positive correlation between cytokeratin-18 and body mass index, HOMA-IR, Hamaguchi’s score, urinary 8-iso-PGF2α, and soluble NOX2-derived peptide and a negative correlation between cytokeratin-18 and HDL-cholesterol and adiponectin were found. Body mass index, adiponectin, and soluble NOX2-derived peptide were independent predictors of serum cytokeratin-18 levels (adjustedR2=0.36).Conclusion.We support an association between oxidative stress and severity of liver damage in patients with nonalcoholic fatty liver.
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Wu, Jing, Ran Xue, Muchen Wu, Xuehong Yin, Bangxiang Xie, and Qinghua Meng. "Nrf2-Mediated Ferroptosis Inhibition Exerts a Protective Effect on Acute-on-Chronic Liver Failure." Oxidative Medicine and Cellular Longevity 2022 (April 16, 2022): 1–23. http://dx.doi.org/10.1155/2022/4505513.
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Although massive hepatocyte cell death and oxidative stress constitute major events of acute-on-chronic liver failure (ACLF), the relationship of ferroptosis with ACLF has yet to be explored. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key regulator of ferroptosis. However, if Nrf2 modulates ACLF through ferroptosis remains unknown. Here, the liver tissues of ACLF patients were collected and murine models of ACLF using carbon tetrachloride, D-galactosamine, and lipopolysaccharide as well as an H2O2-induced hepatocyte injury model were established. Upon ACLF, livers exhibited key features of ferroptosis, including lipid peroxidation (increase in malondialdehyde whereas a decrease in glutathione and nicotinamide adenine dinucleotide phosphate), and increased mRNA expression of prostaglandin-endoperoxide synthase-2 (PTGS2). Ferroptosis inducer RSL-3 treatment aggravated liver damage, while ferroptosis inhibitor Ferrostatin-1 administration alleviated ACLF severity, manifesting with improved liver histopathological lesions and reduced serum ALT and AST. Compared with normal liver tissue, Nrf2 was upregulated in ACLF patients and murine models. Pharmacological activation of Nrf2 (Bardoxolone Methyl) attenuated liver damage, prevented lipid peroxidation, upregulated PTGS2 mRNA expression, and improved ferroptosis-specific mitochondrial morphology in vivo. In contrast, Nrf2 inhibitor ML385 exacerbated lipid peroxidation and liver injury. Collectively, Nrf2 plays a protective role in ACLF progression through repressing ferroptosis, which provides promising therapeutic cues for ACLF.
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Rossi, Chiara, Antonio Salvati, Mariarosaria Distaso, Daniela Campani, Francesco Raggi, Edoardo Biancalana, Domenico Tricò, Maurizia Rossana Brunetto, and Anna Solini. "The P2X7R-NLRP3 and AIM2 Inflammasome Platforms Mark the Complexity/Severity of Viral or Metabolic Liver Damage." International Journal of Molecular Sciences 23, no. 13 (July 4, 2022): 7447. http://dx.doi.org/10.3390/ijms23137447.
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P2X7R-NLRP3 and AIM2 inflammasomes activate caspase-1 and the release of cytokines involved in viral-related liver disease. Little is known about their role in non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steato-hepatitis (NASH). We characterized the role of inflammasomes in NAFLD, NASH, and HCV. Gene expression and subcellular localization of P2X7R/P2X4R-NLRP3 and AIM2 inflammasome components were examined in histopathological preparations of 46 patients with biopsy-proven viral and metabolic liver disease using real-time PCR and immunofluorescence. P2X7R, P2X4R, and Caspase-1 are two- to five-fold more expressed in patients with NAFLD/NASH associated with chronic HCV infection than those with metabolic damage only (p ≤ 0.01 for all comparisons). The AIM2 inflammasome is 4.4 times more expressed in patients with chronic HCV infection, regardless of coexistent metabolic abnormalities (p = 0.0006). IL-2, a cytokine playing a pivotal role during chronic HCV infection, showed a similar expression in HCV and NASH patients (p = 0.77) but was virtually absent in NAFLD. The P2X7R-NLRP3 complex prevailed in infiltrating macrophages, while AIM2 was localized in Kupffer cells. Caspase-1 expression correlated with elastography-based liver fibrosis (r = 0.35, p = 0.02), whereas P2X7R, P2X4R, NRLP3, Caspase-1, and IL-2 expression correlated with circulating markers of disease severity. P2X7R and P2X4R play a major role in liver inflammation accompanying chronic HCV infection, especially when combined with metabolic damage, while AIM2 is specifically expressed in chronic viral hepatitis. We describe for the first time the hepatic expression of IL-2 in NASH, so far considered a peculiarity of HCV-related liver damage.
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Ma, Y. "Anti-SLA antibody is a marker of severity of liver damage in patients with autoimmune liver disease." Journal of Hepatology 34 (April 2001): 212. http://dx.doi.org/10.1016/s0168-8278(01)80785-6.
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Ma, Y., D. P. Bogdanos, R. Willams, G. Mieli-Vergani, and D. Vergani. "Anti-SLA antibody is a marker of severity of liver damage in patients with autoimmune liver disease." Journal of Hepatology 34 (April 2001): 212. http://dx.doi.org/10.1016/s0168-8278(01)81660-3.
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Pereverzev, A. P., and O. D. Ostroumova. "Antineoplastic drugs and drug-induced liver damage with cholestasis." Medical alphabet 1, no. 19 (November 2, 2020): 47–54. http://dx.doi.org/10.33667/2078-5631-2020-19-47-54.
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The number of cases of drug-induced liver injury (DILI) has been increasing since the 1990s. DILIs cause up to 40,000 deaths each year. One of the leaders in the number of DILIs are antineoplastic drugs ms, such as alkylating agents, antimetabolites, targeted drugs, monoclonal antibodies, etc. One of the most effective and safe strategies for the treatment and prevention of DILI is to use hepatoprotective drugs. Currently, on the market of the Russian Federation, is available novel drug Heptrong® (does not have an International Non-proprietary Name), which has anti-inflammatory, antioxidant activity and the ability to stabilize and reduce the permeability of hepatocyte membranes, suppress the activity 5-lipoxygenase, a decrease in the synthesis of leukotriene B4, interleukin-1, interleukin-6, which are pro-inflammatory cytokines. The drug activates the antitoxic function of the liver, improves its protein- and lipid-synthesizing functions. Heptrong® neutralizes the processes of inflammation in the liver, thereby reducing the severity of the clinical manifestations of drug-induced lesions.
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Kamal, Adina M., Florentina Dumitrescu, Adrian Mită, Denisa M. Săbiescu, Dragoș O. Alexandru, Codruța E. Gheorghe, Monalisa M. Filip, et al. "Liver Function Tests and FIB-4 Score as Predictors of Severity in COVID-19 Patients from the South-West of Romania." Life 12, no. 7 (June 22, 2022): 934. http://dx.doi.org/10.3390/life12070934.
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Background: The coronavirus disease 2019 pandemic (COVID-19) is the most important global health crisis to date. In this study, we performed an analysis to find the association between liver damage, FIB-4 score and the severity of COVID-19 disease. Methods: We included a total of 580 patients that tested positive for SARS-CoV-2 infection and were hospitalized. No patient included had any known history of liver disease. Liver function tests were performed, and FIB-4 score was calculated in order to assess their involvement in the disease progression. Results: More than half of the patients had elevated liver function tests. Age, high body mass index, associated heart disease and diabetes were associated with poor outcome. Corticosteroids, antibiotics, and anticoagulants strongly correlated with liver injuries. Liver impairment and injury, as well as a FIB-4 score higher than 3.5, also correlated with higher degrees of disease severity. Conclusion: Liver injury and elevated FIB-4 score were associated with poor clinical outcome and disease severity, as well as being a valuable tool to predict COVID-19-related mortality.
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Zhang, Tao, Jian Gu, Jianrong Guo, Ke Chen, Huili Li, and Jiliang Wang. "Renalase Attenuates Mouse Fatty Liver Ischemia/Reperfusion Injury through Mitigating Oxidative Stress and Mitochondrial Damage via Activating SIRT1." Oxidative Medicine and Cellular Longevity 2019 (December 16, 2019): 1–21. http://dx.doi.org/10.1155/2019/7534285.
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Liver ischemia/reperfusion (IR) injury is a severe complication of liver surgery. Moreover, nonalcoholic fatty liver disease (NAFLD) patients are particularly vulnerable to IR injury, with higher rates of postoperative morbidity and mortality after liver surgeries. Our previous study found that renalase (RNLS) was highly sensitive and responsive to oxidative stress, which may be a promising biomarker for the evaluation of the severity of liver IR injury. However, the role of RNLS in liver IR injury remains unclear. In the present study, we intensively explored the role and mechanism of RNLS in fatty liver IR injury in vivo and in vitro. C57BL/6 mice were divided into 2 groups feeding with high-fat diet (HFD) and control diet (CD), respectively. After 20 weeks’ feeding, they were suffered from portal triad blockage and reflow to induce liver IR injury. Additionally, oleic acid (OA) and tert-butyl hydroperoxide (t-BHP) were used in vitro to induce steatotic hepatocytes and to simulate ROS burst and mimic cellular oxidative stress following portal triad blockage and reflow, respectively. Our data showed that RNLS was downregulated in fatty livers, and RNLS administration effectively attenuated IR injury by reducing ROS production and improving mitochondrial function through activating SIRT1. Additionally, the downregulation of RNLS in the fatty liver was mediated by a decrease of signal transduction and activator of transcription 3 (STAT3) expression under HFD conditions. These findings make RNLS a promising therapeutic strategy for the attenuation of liver IR injury.
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Haider, Rehan. "Alcoholic Hepatitis." Journal of Clinical Research and Reports 15, no. 1 (January 31, 2024): 01–11. http://dx.doi.org/10.31579/2690-1919/351.
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Alcoholic hepatitis is a serious liver condition characterized by inflammation and liver damage caused by excessive alcohol consumption. This condition represents a significant health concern worldwide as it can progress to more severe liver diseases, including cirrhosis and liver failure. This abstract provides an overview of alcoholic hepatitis, including its causes, symptoms, diagnosis, and treatment. Long-term alcohol consumption is the primary cause of alcoholic hepatitis. When alcohol is metabolized in the liver, it generates toxic byproducts that can lead to inflammation and cellular damage. Over time, repeated episodes of damage can result in alcoholic hepatitis. Patients with this condition may present with various symptoms including jaundice, abdominal pain, nausea, vomiting, fever, and an enlarged liver. Diagnosis of alcoholic hepatitis typically involves a combination of medical history assessment, physical examination, blood tests, and imaging studies. Elevated levels of liver enzymes, such as AST and ALT, are common laboratory findings. A liver biopsy may be required to confirm the diagnosis and assess the extent of liver damage. Treatment of alcoholic hepatitis primarily focuses on alcohol cessation, which is essential to prevent further liver damage and improve the chances of recovery. Supportive care, such as nutritional supplementation and the management of complications, is also essential. Hospitalization may be necessary for severe cases. The prognosis varies depending on the severity of the condition and the patient's response to treatment. Complete abstinence from alcohol significantly improves the chances of recovery; however, some individuals may progress to advanced liver disease or even liver failure. Liver transplantation may be considered for those with end-stage liver disease. key words Alcoholic hepatitis Liver inflammation Excessive alcohol consumption Liver damage Cirrhosis Liver failure Symptoms Jaundice Abdominal pain Nausea Vomiting Fever Enlarged liver Diagnosis Liver enzymes AST (Aspartate Aminotransferase) ALT (Alanine Aminotransferase) Liver biopsy Treatment Alcohol cessation.
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Tarasenko, S. V., D. A. Glotov, O. D. Peskov, S. N. Sokolova, U. V. Zhuchkova, T. S. Rakhmaev, I. V. Bakonina, et al. "COVID-19 liver damage. Features of laboratory and instrumental diagnostics." Experimental and Clinical Gastroenterology, no. 11 (March 26, 2024): 146–52. http://dx.doi.org/10.31146/1682-8658-ecg-219-11-146-152.
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The aim of the study - to analyze the pathogenesis of liver damage in COVID-19, as well as to study the features of diagnosis. Research materials: literature and own data on the peculiarities of the pathogenesis of liver damage were analyzed, as well as an assessment of laboratory and instrumental diagnostics in patients with COVID-19. The results of the research. In patients, liver damage was manifested by an increase in liver enzymes, as well as a diffuse decrease in its density during CT. The severity of the disease is caused by a cytokine storm caused by a dysfunctional immune response to the virus, viral virulence factors, as well as the presence of concomitant diseases, especially those associated with liver pathology, such as cirrhosis or steatosis. Conclusions. The new COVID-19 coronavirus infection caused by SARS-CoV-2 continues to spread worldwide. The main target is the organs of the respiratory system. However, among the patients with COVID-19, there were lesions of the central nervous system, intestines, myocardium and liver. Liver dysfunction in most cases should be considered as a result of secondary damage due to CVD, ARDS, hypoxia, multiple organ failure, exposure to immune factors, and taking hepatotoxic drugs.
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Williams, Jessica A., Hong-Min Ni, Yifeng Ding, and Wen-Xing Ding. "Parkin regulates mitophagy and mitochondrial function to protect against alcohol-induced liver injury and steatosis in mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 309, no. 5 (September 1, 2015): G324—G340. http://dx.doi.org/10.1152/ajpgi.00108.2015.
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Alcoholic liver disease claims two million lives per year. We previously reported that autophagy protected against alcohol-induced liver injury and steatosis by removing damaged mitochondria. However, the mechanisms for removal of these mitochondria are unknown. Parkin is an evolutionarily conserved E3 ligase that is recruited to damaged mitochondria to initiate ubiquitination of mitochondrial outer membrane proteins and subsequent mitochondrial degradation by mitophagy. In addition to its role in mitophagy, Parkin has been shown to have other roles in maintaining mitochondrial function. We investigated whether Parkin protected against alcohol-induced liver injury and steatosis using wild-type (WT) and Parkin knockout (KO) mice treated with alcohol by the acute-binge and Gao-binge (chronic plus acute-binge) models. We found that Parkin protected against liver injury in both alcohol models, likely because of Parkin's role in maintaining a population of healthy mitochondria. Alcohol caused greater mitochondrial damage and oxidative stress in Parkin KO livers compared with WT livers. After alcohol treatment, Parkin KO mice had severely swollen and damaged mitochondria that lacked cristae, which were not seen in WT mice. Furthermore, Parkin KO mice had decreased mitophagy, β-oxidation, mitochondrial respiration, and cytochrome c oxidase activity after acute alcohol treatment compared with WT mice. Interestingly, liver mitochondria seemed able to adapt to alcohol treatment, but Parkin KO mouse liver mitochondria had less capacity to adapt to Gao-binge treatment compared with WT mouse liver mitochondria. Overall, our findings indicate that Parkin is an important mediator of protection against alcohol-induced mitochondrial damage, steatosis, and liver injury.
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Rakhman, Mahendra Aulia, Vitasari Indriani, and Dwi Arini E. "CORRELATION OF ASPARTATE AMINOTRANSFERASE TO PLATELET RATIO INDEX (APRI) WITH THE DEGREE OF SEVERITY LIVER ORGAN IN CIRRHOSIS HEPATIC PATIENTS." Mandala Of Health 14, no. 1 (June 30, 2021): 16. http://dx.doi.org/10.20884/1.mandala.2021.14.1.3074.
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Background: Cirrhosis hepatic is a chronic liver disease characterized by the replacement of liver tissue into scar tissue resulting in decreased liver function. The patient's diagnosis is gold standard for cirrhosis hepatic by invasive assessment cause tissue damage. The development of the way of diagnosis with secondary markers is APRI score was considered quite good in determining cirrhosis hepatic. On the other to, there is a method for assessing the severity of the liver organ in patients with cirrhosis hepatic using the Child-Pugh score. APRI scores and Child-Pugh scores are based on the calculation of secondary markers caused by hepatocyte cell fungtional damage. This is very useful in the early diagnosis of cirrhosis hepatic patients using simple markers and predicting the severity of the liver organ to assess further prognosis and management.
Objective: To knowing the correlation of APRI index with the degree of severity liver organ in cirrhosis hepatic patients in RSUD Prof. dr. Margono Soekarjo. Specifically, it aims to determine the APRI score and Child-Pugh score in patients with cirrhosis hepatic.
Methods: This study used a cross sectional design with a sample of 31 patients with a diagnosis of cirrhosis hepatic which was selected using a consecutive sampling technique. Primary data were obtained from a one-time blood sampling calculation and secondary data were obtained from medical records from patients with a diagnosis of liver cirrhosis from the physician in charge. Hypothesis analysis using Pearson correlation test.
Resuls: Pearson test results showed a significant difference p = 0.024 (p <0.05) with the strength of the relationship r = 0.404 and the direction of a positive relationship on the correlation of APRI scores and Child-Pugh scores.
Conclusions: There is a significant correlation between APRI scores with the degree of severity liver organ in cirrhosis hepatic patients in RSUD Prof. dr. Margono Soekarjo. The average APRI score in patients cirrhosis hepatic is 3, 107. The Child-Pugh score for the degree of severity liver organ is 8 or in the category of Child-Pugh B or moderate category.
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Salleh, F., Y. M. Goh, S. F. Lau, P. A. M. A. Rani, R. Radzi, M. Mazlan, A. R. Alashraf, et al. "Elucidating Hepatic Lipidosis in Stray Cats Through Serum Biochemistry, Liver Histopathology and Liver RNA Expression of PPAR-δ and PPAR-γ." Sains Malaysiana 51, no. 7 (July 31, 2022): 1957–68. http://dx.doi.org/10.17576/jsm-2022-5107-01.
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Early detection of feline hepatic lipidosis (FHL) with appropriate treatment can increase prognosis significantly. This study looks into the serum biochemistry and lipid composition of serum and liver samples in a group of stray cats (N=18) collected from pounds in Klang Valley, Malaysia. Alanine aminotransferase (ALT) in blood serum was used to detect for liver damage possibly due to FHL, confirmed through light microscopy, serum biochemistry (triglyceride, cholesterol, creatinine, and urea), liver triglyceride and cholesterol concentrations, and liver RNA expression of lipid droplet regulators peroxisome proliferator-activated receptors (PPARs). Differing severity of FHL in samples were divided and grouped using an adapted scoring method observing fatty change of liver (FCL) with trends between FCL groups investigated. Elevated serum ALT reflective of increasing FCL severity was observed with elevated concentrations of liver TAG and cholesterol levels. Serum TAG and cholesterol decreased with heightened FCL pointing to fatty acid oxidation and lipid restoration in the liver, supported by PPAR-γ expression which also propose macrophage activation for liver recovery alongside PPAR-δ for lipogenesis and inflammatory reactions. Elevated serum creatinine and urea levels with increasing FCL severity propose overall intact hepatic function in the stray cat samples.
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Egresi, Anna, Gabriella Lengyel, and Krisztina Hagymási. "Non-invasive assessment of fatty liver." Orvosi Hetilap 156, no. 14 (April 2015): 543–51. http://dx.doi.org/10.1556/oh.2015.30123.
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As the result of various harmful effects (infectious agents, metabolic diseases, unhealthy diet, obesity, toxic agents, autoimmune processes) hepatic damage may develop, which can progress towards liver steatosis, and fibrosis as well. The most common etiological factors of liver damages are hepatitis B and C infection, alcohol consumption and non-alcoholic fatty liver disease. Liver biopsy is considered as the gold standard for the diagnosis of chronic liver diseases. Due to the dangers and complications of liver biopsy, studies are focused on non-invasive markers and radiological imaging for liver steatosis, progression of fatty liver, activity of the necroinflammation and the severity of the fibrosis. Authors review the possibilities of non-invasive assessment of liver steatosis. The statistical features of the probes (positive, negative predictive values, sensitivity, specificity) are reviewed. The role of radiological imaging is also discussed. Although the non-invasive methods discussed in this article are useful to assess liver steatosis, further studies are needed to validate to follow progression of the diseases and to control therapeutic response. Orv. Hetil., 2015, 156(14), 543–551.
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Gordeeva, A. E., E. A. Kurganova, and V. I. Novoselov. "Use of peroxiredoxin 6 to prevent liver dysfunction in acute kidney injury." Биофизика 68, no. 4 (August 15, 2023): 770–79. http://dx.doi.org/10.31857/s000630292304018x.
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Acute kidney injury causes deterioration of liver function, that is a confounding factor affecting treatment outcomes. In this work, renal ischemia reperfusion injury was used as a model. Taking into account that hyperproduction of reactive oxygen species is the major risk factor for kidney damage, the exogenous antioxidant enzyme peroxiredoxin 6, able to neutralize reactive oxygen species, has been used to prevent liver damage when kidneys are damaged. Kidney injury was initiated by a 45-minute ischemia simultaneously with a left-sided donor nephrectomy without manipulations of the liver. Peroxiredoxin 6 was administered intravenously 15 minutes before ischemia. The functional state of the liver was assessed after 2, 5 and 24 hours of reperfusion using histological and biochemical analysis. The signs of liver damage were detected in the best possible way after 5 hours of kidney reperfusion. It was found that peroxiredoxin 6 helps reduce the severity of the vascular reaction and leukocyte infiltration in the liver; lower the level of dystrophy and apoptosis of hepatocytes; keep the concentration of TBA-reactive products even and stabilize the level of cytokines, IL-6 and IL-10, in the liver tissue, as well as normalize the activity of intracellular transferases in the blood at the onset of reperfusion. The protective effect of peroxiredoxin 6 is associated primarily with its antioxidant properties, due to which hyperproduction of reactive oxygen species can be neutralized in the early phase of kidney reperfusion, but the signal-regulatory function of the protein can also contribute to a protective role peroxiredoxin 6.
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de Oliveira, Felipe Leite, Nadia Panera, Cristiano De Stefanis, Antonella Mosca, Valentina D’Oria, Annalisa Crudele, Rita De Vito, Valerio Nobili, and Anna Alisi. "The Number of Liver Galectin-3 Positive Cells Is Dually Correlated with NAFLD Severity in Children." International Journal of Molecular Sciences 20, no. 14 (July 14, 2019): 3460. http://dx.doi.org/10.3390/ijms20143460.
Full textAbstract:
Non-alcoholic fatty liver disease (NAFLD) is a complex disease ranging from steatosis to non-alcoholic steatohepatitis (NASH). Galectin-3 (Gal-3), which is a β-galactoside binding protein, has been associated with liver fibrosis, but its role in NAFLD remains elusive. We investigated the expression of Gal-3 in liver resident cells and its potential association with liver damage in 40 children with biopsy-proven NAFLD. We found that several liver cells expressed Gal-3. The number of total Gal-3 positive cells decreased with the severity of disease and the cells were correlated with the presence of steatosis and the diagnosis of NASH. CD68 macrophages expressed Gal-3 but the number CD68/Gal-3 positive cells was significantly reduced in patients diagnosed with steatosis and NASH. Triple CD68/CD206/Gal-3, which represented the subpopulation of M2 macrophages, were mainly present in patients without NASH, and clearly reduced in patients with steatosis and NASH. On the contrary, the number of α-smooth muscle actin (SMA)/Gal-3 positive cells increased with the severity of fibrosis in children with NAFLD. Our data demonstrated that the number of Gal-3 positive cells was associated with tissue damage in different ways, which suggests a dual role of this protein in the pathogenesis of pediatric NAFLD, even if the role of Gal-3 deserves further studies.
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Vlassaks, E., M. Nikiforou, E. Strackx, M. Hütten, O. Bekers, D. Gazzolo, G. Li Volti, P. Martinez-Martinez, B. W. Kramer, and A. W. D. Gavilanes. "Acute and chronic immunomodulatory changes in rat liver after fetal and perinatal asphyxia." Journal of Developmental Origins of Health and Disease 5, no. 2 (January 22, 2014): 98–108. http://dx.doi.org/10.1017/s2040174413000561.
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Hypoxic-ischemic encephalopathy (HIE) caused by fetal and perinatal asphyxia is an important cause of mortality in the neonatal period. Not only will asphyxia affect the brain but also other organs such as the liver and kidneys. Interestingly, it has been shown that liver damage is proportional to the severity of the asphyctic insult, implying an association between liver impairment and HIE. Accordingly, we investigated in an established rat model the acute and chronic hepatic response to both fetal (FA) and perinatal asphyxia (PA). In addition, we assessed whether fetal asphyctic preconditioning (PC) would have any beneficial effect on the liver. Inflammation, ceramide signaling and hepatocellular damage were analyzed in the livers of newborn and adult rats at several short- and long-term time points after both FA and PA. We found that although FA induced an acute inflammatory response, apoptotic mRNA levels and oxidative DNA damage were decreased at 96 h post FA. Whereas increased IL-6 and IL-10 mRNA levels were observed after PA, the combination of FA and PA (PC) attenuated the inflammatory response. Moreover, 6 h after PA anti-apoptotic genes were downregulated and associated with less lipid peroxidation, while preconditioned animals were comparable to controls. In summary, asphyctic PC seems to have an acute protective effect on the liver by modulating the inflammatory, apoptotic and anti-oxidative response. More insight into the hepatic response to asphyxia is necessary, as disturbed hepatic function is associated with metabolic diseases in later life.
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Filho, Irami. "COVID-19 and Liver injury: hepatology perspectives." Clinical Medical Reviews and Reports 2, no. 3 (June 22, 2020): 01–04. http://dx.doi.org/10.31579/2690-8794/020.
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SARS-CoV-2, a severe acute respiratory syndrome caused by Coronavirus 2, discovered in 2019 in China, is responsible for the current pandemic declared by the WHO since March 2020. The clinical syndrome caused by Covid-19 has a broad spectrum of severity. The most common clinical manifestations are fever, dry cough, dyspnea, fatigue, and anosmia. The virus binds to receptors for angiotensin-converting enzyme 2 (ECA2) and serine protease TMPRSS2 for protein S initiation, which are expressed not only in the lungs but also in the liver, colonic, esophageal and biliary epithelial cells. In this context, the liver is a potential target for COVID-19 infection. Liver damage occurs during the course and treatment of viral infection in patients with or without previous liver disease. Therefore, the characteristics of liver injury associated with COVID-19 were reviewed based on research related, in the context of the pandemic.
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Wallace, Karen, Alastair D. Burt, and Matthew C. Wright. "Liver fibrosis." Biochemical Journal 411, no. 1 (March 13, 2008): 1–18. http://dx.doi.org/10.1042/bj20071570.
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Liver damage leads to an inflammatory response and to the activation and proliferation of mesenchymal cell populations within the liver which remodel the extracellular matrix as part of an orchestrated wound-healing response. Chronic damage results in a progressive accumulation of scarring proteins (fibrosis) that, with increasing severity, alters tissue structure and function, leading to cirrhosis and liver failure. Efforts to modulate the fibrogenesis process have focused on understanding the biology of the heterogeneous liver fibroblast populations. The fibroblasts are derived from sources within and outwith the liver. Fibroblasts expressing α-smooth muscle actin (myofibroblasts) may be derived from the transdifferentiation of quiescent hepatic stellate cells. Other fibroblasts emerge from the portal tracts within the liver. At least a proportion of these cells in diseased liver originate from the bone marrow. In addition, fibrogenic fibroblasts may also be generated through liver epithelial (hepatocyte and biliary epithelial cell)–mesenchymal transition. Whatever their origin, it is clear that fibrogenic fibroblast activity is sensitive to (and may be active in) the cytokine and chemokine profiles of liver-resident leucocytes such as macrophages. They may also be a component driving the regeneration of tissue. Understanding the complex intercellular interactions regulating liver fibrogenesis is of increasing importance in view of predicted increases in chronic liver disease and the current paucity of effective therapies.
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Habib, Shahid, Khalid Khan, Chiu-Hsieh Hsu, Edward Meister, Abbas Rana, and Thomas Boyer. "Differential Simultaneous Liver and Kidney Transplant Benefit Based on Severity of Liver Damage at the Time of Transplantation." Gastroenterology Research 10, no. 2 (2017): 106–15. http://dx.doi.org/10.14740/gr803w.
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