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Relevant bibliographies by topics / Amiodarone induced liver injury

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Academic literature on the topic 'Amiodarone induced liver injury'

Author: Grafiati

Published: 4 June 2025

Last updated: 23 June 2025

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Journal articles on the topic "Amiodarone induced liver injury"

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Essrani, Rajesh, Shehriyar Mehershahi, Rajesh Kumar Essrani, et al. "Amiodarone-Induced Acute Liver Injury." Case Reports in Gastroenterology 14, no. 1 (2020): 87–90. http://dx.doi.org/10.1159/000506184.

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Amiodarone is a lipophilic structure with a half-life of 25–100 days. Long-term oral amiodarone is associated with photosensitivity, thyroid dysfunction, and pulmonary and hepatic toxicity. Intravenous amiodarone can lead to sweating, heating sensation, nausea, phlebitis at the injection site, and rarely acute hepatitis. This is a compelling case of a 60-year-old male who developed acute liver injury 24–36 h after starting amiodarone. All the possible causes of acute liver injury were ruled out, and his liver enzymes improved after discontinuing amiodarone.

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Wandrer, Franziska, Živa Frangež, Stephanie Liebig, et al. "Autophagy alleviates amiodarone-induced hepatotoxicity." Archives of Toxicology 94, no. 10 (2020): 3527–39. http://dx.doi.org/10.1007/s00204-020-02837-9.

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Abstract Amiodarone is a widely used antiarrhythmic drug that can cause the development of steatohepatitis as well as liver fibrosis and cirrhosis. The molecular mechanisms of amiodarone-mediated liver injury remain largely unknown. We therefore analyzed amiodarone-mediated hepatocellular injury in patients with chronic heart failure, in primary hepatocytes and HepG2 cells. We found that amiodarone-treated patients with chronic heart failure revealed significantly higher serum levels of caspase-cleaved keratin-18, an apoptosis biomarker, compared to healthy individuals or patients not receiving amiodarone. Furthermore, amiodarone treatment of hepatocytes resulted in apoptosis associated with lipid accumulation and ER-stress induction. Liver cell steatosis was accompanied by enhanced de novo lipogenesis which, after reaching peak levels, declined together with decreased activation of ER stress. The decline of amiodarone-mediated lipotoxicity was associated with protective autophagy induction. In contrast, in hepatocytes treated with the autophagy inhibitor chloroquine as well as in autophagy gene (ATG5 or ATG7)-deficient hepatocytes, amiodarone-triggered toxicity was increased. In conclusion, we demonstrate that amiodarone induces lipid accumulation associated with ER stress and apoptosis in hepatocytes, which is mirrored by increased keratin-18 fragment serum levels in amiodarone-treated patients. Autophagy reduces amiodarone-mediated lipotoxicity and could provide a therapeutic strategy for protection from drug-induced liver injury.

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Buggey, Jonathan, Matthew Kappus, Anand S. Lagoo, and Carla W. Brady. "Amiodarone-Induced Liver Injury and Cirrhosis." ACG Case Reports Journal 2, no. 2 (2015): 116–18. http://dx.doi.org/10.14309/crj.2015.23.

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Essrani, Rajesh, Shehriyar Mehershahi, Rajesh Essrani, Sajeer Bhura, and Asif Mehmood. "2383 Amiodarone-Induced Acute Liver Injury." American Journal of Gastroenterology 114, no. 1 (2019): S1324—S1325. http://dx.doi.org/10.14309/01.ajg.0000599064.75682.73.

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Diab, O. A., John Kamel, and Ahmed Adel Abd-Elhamid. "Predictors of intravenous amiodarone induced liver injury." Egyptian Heart Journal 69, no. 1 (2017): 45–54. http://dx.doi.org/10.1016/j.ehj.2016.05.001.

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Chang, Chung-Che, Mary Petrelli, Joseph F. Tomashefski, and Arthur J. McCullough. "Severe Intrahepatic Cholestasis Caused by Amiodarone Toxicity After Withdrawal of the Drug." Archives of Pathology & Laboratory Medicine 123, no. 3 (1999): 251–56. http://dx.doi.org/10.5858/1999-123-0251-siccba.

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Abstract Cholestasis has been reported as a rare presentation among patients with severe liver injury secondary to amiodarone hepatic toxicity. We report an unusual case of amiodarone-induced cholestatic hepatotoxicity occurring after amiodarone had been discontinued and the initial abnormal liver function findings had improved. The patient, without jaundice at the initial presentation, developed severe jaundice about 4 months after withdrawal of amiodarone. Light and transmission electron microscopic examination of a specimen secured by computed tomographically guided liver biopsy was consistent with amiodarone hepatic toxicity as the cause of intrahepatic cholestasis. An abdominal ultrasound, endoscopic retrograde cholangiography, and dimethyl iminodiacetic acid and computed tomographic scans of the abdomen all failed to demonstrate any other causes for jaundice other than amiodarone toxicity. Thus, amiodarone hepatic toxicity may occur after drug withdrawal even if results of liver function tests improve. Histopathologic examination of a liver biopsy specimen is of value for diagnosis and prognosis. The liver biopsy findings, clinical course, and liver function test results are discussed, and the English-language literature on amiodarone cholestatic hepatotoxicity is reviewed.

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Mudalel, Matthew L. "N-acetylcysteine treats intravenous amiodarone induced liver injury." World Journal of Gastroenterology 21, no. 9 (2015): 2816. http://dx.doi.org/10.3748/wjg.v21.i9.2816.

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Okayama, Chihiro, Hiroo Mizuta, Takehide Fujimoto, et al. "Two Cases of Amiodarone-induced Liver Injury and Cirrhosis." Nihon Naika Gakkai Zasshi 106, no. 6 (2017): 1199–205. http://dx.doi.org/10.2169/naika.106.1199.

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Avula, Sreekanth, Sujithraj Dommaraju, Purveshkumar Patel, et al. "S3668 Wonderful Drug Yet Dangerous: Amiodarone-Induced Acute Liver Injury." American Journal of Gastroenterology 116, no. 1 (2021): S1498. http://dx.doi.org/10.14309/01.ajg.0000788204.65970.62.

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Gubergrits, N. B., N. V. Byelyayeva, A. Ye Klochkov, G. M. Lukashevich, and P. G. Fomenko. "Drug-induced liver injury: from pathogenesis to treatment." Herald of Pancreatic Club 46, no. 1 (2020): 72–80. http://dx.doi.org/10.33149/vkp.2020.01.10.

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The article presents data on classification, pathogenesis, clinical picture, diagnosis and differentiated treatment tactics, as well as practical algorithm for recognizing and preventing the development of drug-induced liver injury. Pathogenesis of drug-induced liver injury is analyzed, mechanisms of drug metabolism are explained, metabolism phases are described. Four main mechanisms of the pathological effect of drugs on the liver are identified: direct toxic effect on hepatocytes; toxic effect of drug metabolites; immunoallergic liver injury; idiosyncrasy. Peculiar attention is paid to the pathogenesis of drug-induced cholestasis. Direct hepatotoxic reactions develop according to the cytolytic (hepatocellular, parenchymal), cholestatic or mixed option. The most commonly diagnosed clinical variant of drug-induced liver injury is drug-induced hepatitis. Five forms of hepatitis induced by the use of pharmacological agents are distinguished: drug-induced hepatitis with an isolated increase in transaminases (anti-TB drugs, methyldopa, amiodarone, statins); acute hepatitis with jaundice; pseudo-surgical form of acute hepatitis: abdominal pain, fever, jaundice, enlarged gall bladder (cytostatics, antidepressants, antiarrhythmic drugs); severe forms of acute hepatitis with liver failure; chronic drug hepatitis. International diagnostic criteria, basic data on morphological liver changes are presented. Action of ursodeoxycholic acid is explained. It has a litholytic, anticholestatic, cytoprotective, immunomodulating, anti-inflammatory, antitoxic, hypocholesterolemic effect, modulates apoptosis, has a differentiated effect on the regeneration of hepatocytes.

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Dissertations / Theses on the topic "Amiodarone induced liver injury"

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Cohen, Jessica I. "Ethanol-induced liver injury preventing apoptosis /." Cleveland, Ohio : Case Western Reserve University, 2010. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1259859785.

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Alshabeeb, Mohammad. "Genetic factors affecting antimicrobial-induced liver injury." Thesis, University of Newcastle upon Tyne, 2014. http://hdl.handle.net/10443/2601.

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Flucloxacillin and co-amoxiclav are both associated with drug-induced liver injury (DILI). HLA genotype is an important predictor of DILI susceptibility but it is likely that non-HLA risk factors also contribute. This study aimed to characterise non-HLA risk factors in larger cohorts (155 flucloxacillin and 165 co-amoxiclav adjudicated cases) than previously. Drug causality of the cases was assessed using the RUCAM method which showed 88.1% of the cases were either highly probable or probable but 11.9% of them indicated a possible causality for the drug. Variants showing associations in previous candidate gene, genome-wide association and exome sequencing studies were genotyped to extend these findings. A SNP (rs2476601) in PTPN22, which encodes a protein involved in T-cell-receptor signalling had already been shown to be a risk factor for co-amoxiclav DILI. This was confirmed by genotyping co-amoxiclav DILI cases (n=99) (OR=2.74, 95% CI=1.58–4.77; P=4.1x10-4). There was also a significant effect for flucloxacillin DILI (OR=1.9, 95% CI=1.1–3.1; P=0.02). Exome sequencing performed previously on 66 UK co-amoxiclav DILI cases reported significant associations for several variants, including rs117511121 in IL12RB1 and rs145855109 in TPH1. Additional cases (n=99) were genotyped for rs117511121, confirming the association (OR 6.5, 95% CI=1.5-27.8; P=0.012). No association with IL12RB1 genotype was seen for flucloxacillin DILI. Functional analysis of IL12RB1 using reporter gene constructs revealed significantly lower luciferase activity for the variant constructs. The TPH1 variant was confirmed to be associated with co-amoxiclav DILI (n=99) (OR=14.73, 95% CI=2.94–73.92; P=0.013). Polymorphisms in the following genes showed no significant association with DILI due to either drug: FMO5, GPX1, GSTM1, GSTT1, HFE, KCNJ1, SHMT1, SLCO1B1, SOD2, ST6GAL1 and UGT1A1. The findings for PTPN22 and IL12RB1 confirm the relevance of T cell responses to co-amoxiclav DILI. Odds ratios of 17 for DILI risk can be calculated for individuals with the at risk HLA alleles (A*02:01 and DRB1*15:01) and the PTPN22 and IL12RB1 variants, assuming an additive model. PTPN22 is also relevant to flucloxacillin DILI but, though biologically plausible as a risk factor, appears minor compared with HLA-B*57:01.

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Badger, Andrew Ashley 1970. "Alterations in chemically-induced liver injury by immunomodulators." Diss., The University of Arizona, 1998. http://hdl.handle.net/10150/282642.

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Studies presented in this dissertation determined biochemical mechanisms underlying the modulation of chemical-induced liver injury by retinol and GdC₃ The first objective was to determine the role of inflammatory cells in the retinol potentiation of CCl₄-induced liver injury. Plasma alanine aminotranferase activities and histological analysis of liver sections both illustrated significant potentiation of CCl₄ hepatotoxicity by a single dose of retinol. The mechanism for this potentiation involves priming of Kupffer cells (KC) (i.e. by enhancing their response to toxic stimuli) as established by chemical inhibitors of KC, isolated KC, and immunohistochemical analysis of liver sections. Additional studies estimated the effect of retinol on non-inflammatory processes (i.e. cytochrome P450 (P450) activity). While total P450 content was not increased, the activity and concentration of CYP 2E1 were both significantly elevated following treatment with a single dose of retinol. These findings suggest that a single pretreatment with retinol potentiates CCl₄ hepatotoxicity by multiple mechanisms that involve increased biotransformation and inflammatory cell activities. Based on the findings with retinol, another immunomodulating agent, GdCl₃ might also alter the activity of hepatic biotransforming enzymes. Having established that GdCl₃ inhibits the activity of KC, the purpose of these studies was to determine the effect of GdCl₃ on the content and activity of hepatic P450. GdCl₃ treatment reduced total hepatic microsomal P450 as well as aniline hydroxylase activity by 30% in male and 20% in female rats. Hepatocytes isolated from rats pretreated with GdCl₃ were less susceptible to toxicity caused by CCl₄ but not cadmium, a hepatotoxic chemical not bioactivated by P450. Thus GdCl₃-mediated protection from toxicity in vivo might involve decreased biotransformation and inflammatory cell activities. Data presented in this dissertation suggest that, in addition to altering the inflammatory response to toxicants, retinol and GdCl₃ may modulate liver injury by altering the P450-mediated bioactivation of chemicals. Considering the multiple effects described here for each of these compounds, investigators should be cautious in the interpretation of data utilizing retinol or GdCl₃ to implicate KC as the sole contributor to toxicological mechanisms. This is especially important in models of chemical-induced injury in which bioactivation is a key feature.

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Poli, G. "Biochemical studies on CC14Ì²-induced liver injury using isolated rat liver cells." Thesis, Brunel University, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.379250.

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Teng, Shuzhi, and 滕曙智. "Hepatocellular injury induced by endotoxin and galactosamine." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31241037.

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Hornby, R. "Intracellular and extracellular biomarkers of drug-induced liver injury." Thesis, University of Liverpool, 2016. http://livrepository.liverpool.ac.uk/3001312/.

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Drug-induced liver injury (DILI) is a common form of adverse drug reaction (ADR) seen within the clinic. Sensitive and specific circulating biomarkers would aid in the prediction of DILI early in its course. However, the current biomarkers of DILI, such as alanine transaminase (ALT) suffer from a lack of specificity and sensitivity. Because of this, we have examined both intracellular and extracellular biomarkers of DILI in order to validate and identify novel biomarkers of DILI. Protein tyrosine nitration (PTN), an intracellular marker of oxidative stress, has been shown to be present in paracetamol-DILI, and it is thought that the causative factor for its occurrence is mitochondrial damage. In order to test this, we used Furosemide (FS), a hepatotoxin not thought to cause mitochondrial injury or glutathione (GSH) depletion with the hypothesis that this compound would not generate PTN. First, we tested the role of GSH in protecting from PTN through depleting GSH in a mouse hepatoma cell line, followed by incubation with peroxynitrite. We found that GSH depletion was required in order to elicit PTN. Following this, we compared the ability of toxic doses of FS and paracetamol to cause PTN in mice. Interestingly, we found both compounds lead to PTN, suggesting that there is a pathway independent of GSH-depletion and mitochondrial injury which may lead to PTN. MicroRNA-122 (miR-122) a potential novel extracellular biomarker of DILI, has been demonstrated to be elevated in the circulation earlier in the course of injury than current DILI biomarkers. We examined the potential for miR-122 to be released actively in exosomes during paracetamol-DILI in rats and multiple forms of DILI in humans. Our findings suggested that in both human and rodent’s, miR-122 is released in a similar profile throughout the course of DILI in exosomes, and in an exosome-free (protein-rich fraction) form. We also examined whether miR-122 is selectively released in exosomes during hepatocellular, mixed and cholestatic DILI in humans which had been prescribed a number of hepatotoxic compounds. Our study suggested that, similar to our rodent model, there is no specific pattern of exosomal release of miR-122 in any of these forms of injury. We then looked at new and relatively unexplored aspects of microRNAs, in order to evaluate how they may be used to look at damage to different zones of the liver, and damage to cells other than hepatocytes. Hepatocytes are heterogeneous, with their phenotype depending on their localisation along the porto- central axis, which has resulted in certain drugs causing zone-specific hepatotoxicity. None of the current biomarkers is able to identify zone-specific injury. We examined zonal profiles of microRNA expression within the liver of rats under basal conditions and following paracetamol. Our analysis demonstrated that 45 miRNAs are significantly differentially expressed between zone I and zone III, with three species being expressed in only one zone. Of these differentially expressed miRNAs we found that 9 species were involved in regulating 109 members Wnt/β-Catenin pathway, the molecular driver of liver zonation. We also examined changes in zonal miRNA expression following a toxic dose of paracetamol in rats. Our study was able to demonstrate that paracetamol was able to cause significant changes in the profiles of 42 and 43 miRNAs in zone I and zone III respectively. Importantly, miRNAs were both up and down regulated in both zones, suggesting that not only a loss of miRNAs is occurring during liver injury in each zone. Biliary epithelial cells (BEC) can be damaged by a plethora of different compounds, leading to vanishing bile duct syndrome, or bile duct hyperplasia. Current biomarkers for the diagnosis of BEC- injury lack in specificity, and are prone to false-positives. We developed a method to isolate BEC from the mouse liver and performed a global miRNA profile comparison of hepatocytes and BEC. As in previous studies we found miR-122-5p to be the most enriched miRNA in hepatocytes and miR-1224- 5p in BEC. On comparison of the profiles we found that 83 miRNAs were detectable in BEC but not in Hepatocytes, however further work will be required to validate any of these as markers of BEC injury.

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Wilson, Garrick Kenardo. "Mechanism(s) of hepatitis C virus induced liver injury." Thesis, University of Birmingham, 2012. http://etheses.bham.ac.uk//id/eprint/3530/.

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Hepatitis C virus (HCV) infects hepatocytes of the liver causing progressive liver disease including; fibrosis, cirrhosis and hepatocellular carcinoma. However, the precise mechanism(s) underlying HCV induced liver injury are poorly understood. Hepatocytes are highly polarized with distinct apical and basolateral membranes separated by tight junctions that maintain a normal liver physiology. We studied the role of HCV infection in driving hepatic injury. Our studies show that HCV infection induces hepatocellular reprogramming via hypoxia inducible factor-1α (HIF-1α) stabilization and increased glucocorticoid receptor (GR) signaling. HIF-1α stabilization promoted epithelial to mesenchymal transition accompanied by reduced polarity and cell adhesion. Whereas GR signaling increased cholesterol synthesis and altered HCV receptor expression. Alterations in hepatocellular biology induced a cellular state conducive for virus entry and replication. Consequently, cells de-differentiate to acquire a malignant phenotype via HIF-1α target genes including vascular endothelial growth factor (VEGF) and transforming growth factor-beta (TGF). In addition, GR transcription induced by glucocorticoid treatment or HCV infection enhanced virus uptake, highlighting the caveat for glucocorticoid immunosuppression post liver transplantation. Importantly, HIF-1α inhibitors and GR antagonist reversed the effects of both transcription factors on virus infection and hepatocellular biology. These findings suggest that HCV potentiate liver injury via indirect mechanisms.

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Dalakas, Evangelos. "Haematopoietic stem cell response in alcohol induced liver injury." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/29723.

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Aims: 1) To investigate the mobilisation and hepatic recruitment of HSCs in patients with alcohol induced liver injury and define their contribution to parenchymal and nonparenchymal liver cell lineages. 2) To establish that mobilised HSCs in alcohol induced liver injury are functional and demonstrate pluripotent stem cell properties. 3) To study the role of inflammatory cytokines and chemokine axes in regulating the mobilisation and hepatic recruitment of HSCs in alcohol induced liver injury. Methods: Liver biopsies from alcoholic hepatitis (AH) patients and male patients who had received a female liver transplant (and who subsequently developed AH) were analysed for HSC content using immunohistochemical and flurorescent <i>in situ</i> hybridisation techniques (FISH). FISH for Y-chromosome was performed on liver tissue, along with co-staining for hepatocyte, biliary, myofibroblasts (α-SMA) and hepatic parenchymal cells proliferation markers. Peripheral blood HSC (CS34<sup>+</sup>) levels were quantified in AH patients and normal controls (NC) using flow cytometry and CD34<sup>+</sup>/CD45<sup>+</sup> HSCs were collected and cultured in colony forming unit (CFU) assays. CXCR3/CXCR4 receptor cell expression on mobilised CD34<sup>+</sup> HSCs were quantified in AH patients using flow cytometry. Conclusions: Alcohol induced liver injury mobilises CD34<sup>+</sup> stem cells into the peripheral circulation and recruits them into the liver. These bone marrow derived stem cells contribute to the hepatic myofibroblasts population but not to parenchymal lineages and their presence within the liver does not promote hepatocyte repair. Mobilised HSCs from AH patients were functional and displayed true stem cell potential at a level higher than control HSCs. Serum SDF-1, MMP-9 and G-CSF rather than chemokine receptor expression, plays a central role in regulating the mobilisation of CD34<sup>+</sup> stem cells in alcohol induced liver injury.

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Maughan, Deborah. "The natural history of Efavirenz Drug Induced liver injury." Master's thesis, Faculty of Health Sciences, 2021. http://hdl.handle.net/11427/32832.

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Background Efavirenz (EFV), a non-nucleoside reverse transcriptase inhibitor (NNRTI), has been a component of first line antiretroviral treatment in the South African HIV/AIDS programme since 2004. Similarly, it is extensively used in ART programmes in other low and middle incomes countries. The natural history of the previously reported EFV drug induced liver injury (DILI), is unknown. Objectives To establish causality assessment for the drug-induced liver injury and elucidate the natural history of EFV DILI by observing a cohort of patients through documenting all the factors influencing the patterns of clinical and histological injury, the time to clinical and biochemical recovery, the associated mortality rate and to establish if any demographic or clinical factors predict poor outcomes. Methods Patients were prospectively included after establishing causality criteria for EFV DILI. Clinical, demographic and histological features were carefully documented from the time of presentation and through follow up. Prednisone at 0.25-0.5mg/kg was initiated at the discretion of the treating hepatologist. Risk factors for severe injury or death and time to event (full clinical recovery and full biochemical recovery) were analyzed. Results 50 patients were included in the analysis, median age 34 (IQR 29-39) years, men significantly older than women, p=0.014. Most (92%) were female gender, and of black African ethnicity (86%). The median duration on ART at time of presentation was 6.5 months with half of the women initiating ART during pregnancy at a median gestation of 24 weeks (IQR 11 – 36). Median CD4 nadir at ART treatment initiation was 517 cells/mm3, with no significant difference (p=NS) in CD4 nadir in those pregnant or not. Median RUCAM score was 7 and of the 66% of patients who had liver biopsies, 3 histological patterns were identified: submassive necrosis (57,5%), nonspecific hepatitis (36%) and mixed cholestatic hepatitis (6%). Multivariate analysis suggested predictors for the development of submassive necrosis included age >30 years [OR 0.86 (0.15-0.97), p=0.02], pregnancy [OR 6.9 (1.34 – 35.6), p=0.02]; CD4 >350 [OR, 7.1 (1.5-31.9), p=0.02] but not alcohol use [OR 1.17 (0.72-1.18); p=0.07]. For the non-specific hepatitis group, only pregnancy predicted [OR 8.7 (1.3- 58.2), p=0.03]. The mortality rate was 14%, median time from admission to death was 15 days with the median duration to initial hospital discharge 33 (IQR 24 -52) days. Biochemical recovery was prolonged necessitating a follow up period of more than a year at an outpatient specialist clinic. 86% initiated protease inhibitor based ART successfully. Conclusion EFV DILI is a severe injury with significant inpatient mortality and morbidity requiring prolonged hospitalization and outpatient follow up.

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Salamat, Julia. "The Role of CYP2A5 in Cadmium-Induced Liver Injury." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/etd/3498.

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Cadmium is present in food and groundwater. Tobacco smoking and occupational exposure are also major sources for cadmium. Cadmium is primarily accumulated in liver, a major organ metabolizing exogenous chemicals. Chemical metabolism may cause detoxification, but it can also cause bio-activation resulting in liver damage. Cytochrome P450s (CYP) are major liver metabolism enzymes, and cadmium chloride (CdCl2) can induce CYP2A5 in mice. We examined the effect of CYP2A5 on CdCl2-induced liver injury using CYP2A5-knockout (cyp2a5-/-) mice. The cyp2a5-/- mice and their control WT mice were injected CdCl2 intraperitoneally at 5 mg/kg body weight, respectively, to induce liver injury. The control group of cyp2a5-/- mice and WT mice were injected saline at the same volume. Twenty-four hours later, all the mice were sacrificed. As indicated by biochemical assays and pathological evaluation, CdCl2-treated WT mice exhibited more severe liver injury than CdCl2-treated cyp2a5-/- mice, suggesting that CYP2A5 contributes to Cd-induced liver injury.

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Books on the topic "Amiodarone induced liver injury"

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Poli, Giuseppe. Biochemical studies on CCl4-induced [tetrachloromethane-induced] liver injury using isolated rat liver cells. Brunel University, 1987.

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Neil, Kaplowitz, and DeLeve Laurie D. 1955-, eds. Drug-induced liver disease. 2nd ed. Informa Healthcare USA, 2007.

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Farrell, Geoffrey C. Drug-induced liver disease. Churchill Livingstone, 1994.

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Neil, Kaplowitz, and DeLeve Laurie D. 1955-, eds. Drug-induced liver disease. Marcel Dekker, 2003.

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Neil, Kaplowitz, and DeLeve Laurie D. 1955-, eds. Drug-induced liver disease. Marcel Dekker, 2003.

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S, Anuras, Cameron R. G. 1949-, Feuer George 1921-, and De la Iglesia, Felix A., 1939-, eds. Drug-induced hepatotoxicity. Springer, 1996.

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P, Spoelstra, ed. Drug-induced hepatic injury: A comprehensive survey of the literature on adverse drug reactions up to January 1985. Elsevier Science Publishers, 1985.

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C, Sahu Saura, ed. Hepatotoxicity: From genomics to in vitro and in vivo models. John Wiley & Sons, 2007.

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Hegarty, Rob, and Fevronia Kiparissi. Drug-induced liver injury. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198759928.003.0058.

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The chapter on drug-induced liver injury discusses the definition, clinical manifestations, and then management of this frequently challenging to diagnose situation. It also covers in more detail the management of paracetamol overdose.

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Beattie, R. Mark, Anil Dhawan, and John W.L. Puntis. Drug-induced liver injury. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569862.003.0052.

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Epidemiology 374Pathophysiology 374Herbal drugs and alternative medicines 377Risk factors 377Clinical features 378Investigation 379Management 380Drug induced liver injury (DILI) is a variable and complex diagnosis of exclusion, as it can present in different ways. Because of the liver's central role in drug metabolism, most prescribed drugs can cause liver injury. Liver damage can occur through drugs in a predictable, intrinsic dose-related way or in a unpredictable, idiosyncratic dose-unrelated fashion....

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Book chapters on the topic "Amiodarone induced liver injury"

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Vuppalanchi, Raj. "Drug-Induced Liver Injury." In Liver Disorders. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30103-7_25.

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Shung, Dennis L., and Joseph K. Lim. "Drug-Induced Liver Injury." In Liver Disease. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-98506-0_1.

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Nazer, Lama H., and Hisham M. Nazer. "Drug-Induced Liver Injury." In Textbook of Clinical Pediatrics. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-02202-9_219.

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Björnsson, Einar S., and Naga Chalasani. "Drug-Induced Liver Injury." In Practical Gastroenterology and Hepatology: Liver and Biliary Disease. Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444325249.ch23.

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Popper, Hans. "Drug-Induced Liver Injury." In Assessment and Management of Hepatobiliary Disease. Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-72631-6_19.

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Donepudi, Indira, Hatef Massoumi, T. S. Dharmarajan, et al. "Drug-Induced Liver Injury." In Geriatric Gastroenterology. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-1623-5_41.

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DiPaola, Frank W., and Robert J. Fontana. "Drug-Induced Liver Injury." In Sherlock's Diseases of the Liver and Biliary System. John Wiley & Sons, Ltd, 2018. http://dx.doi.org/10.1002/9781119237662.ch24.

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Ren, Bing, Arief A. Suriawinata, and Masaki Iwai. "Drug-Induced Liver Injury." In Diagnosis of Liver Disease. Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-6806-6_8.

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Dancygier, Henryk. "Drug-Induced Liver Injury." In Clinical Hepatology. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-04519-6_17.

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Israel, Y., and E. Rubin. "Alcohol-Induced Liver Injury." In Handbook of Experimental Pharmacology. Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61013-4_25.

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Conference papers on the topic "Amiodarone induced liver injury"

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Chetana Shanmukhappa, S., M. A. Malik, F. Shaukat, D. Ravi, and A. Malik. "Amiodarone Induced Acute Liver Failure: A Case Report." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a5313.

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Tropschuh, K., and J. Ettl. "Drug-induced liver injury durch Abemaciclib." In Wissenschaftliche Abstracts zur 40. Jahrestagung der Deutschen Gesellschaft für Senologie e.V. (DGS) Interdisziplinär. Kommunikativ. Digital. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1730233.

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Liu, Xingjian, Tapan Bhavsar, Ming Liu, Joseph Cerreta, and Jerome Cantor. "The Effect Of Eta Receptor Antagonism On Amiodarone- And Bleomycin-Induced Lung Injury." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a6055.

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Elfers, C., KM Schneider, A. Ghallab, et al. "Intestinal dysbiosis amplifies acetaminophen induced acute liver injury." In 36. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402103.

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Mehrl, Alexander, Petra Stöckert, Merlin Küchle, Martina Müller-Schilling, and Sophia Rusch. "Turmeric-induced acute liver failure – A case report of an idiosyncratic drug-induced liver injury (DILI)." In 40. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag, 2024. http://dx.doi.org/10.1055/s-0043-1777526.

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Choi, Geonyeong, Hyo Jung Cho, Soon Sun Kim, Ji Eun Han, Jae Youn Cheong, and Charmgil Hong. "Drug Induced Liver Injury Prediction with Injective Molecular Transformer." In 2023 IEEE EMBS International Conference on Biomedical and Health Informatics (BHI). IEEE, 2023. http://dx.doi.org/10.1109/bhi58575.2023.10313508.

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Wuehrl, Michael, Marc Ringelhan, Ursula Ehmer, and Carolin Mogler. "Methylprednisolone-induced liver injury – an emerging autoimmune-mediated disease." In 40. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag, 2024. http://dx.doi.org/10.1055/s-0043-1777522.

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Soto, Juan M., Fabio A. Aguilar Mora, Jose A. Rodrigo, et al. "Refractive index tomography for drug-induced liver injury analysis." In Advances in Microscopic Imaging, edited by Emmanuel Beaurepaire, Adela Ben-Yakar, and YongKeun Park. SPIE, 2021. http://dx.doi.org/10.1117/12.2615732.

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Simon Frances, B., B. Goldner, and E. S. M. Oweis. "Suspected Drug-induced Liver Injury From CFTR Modulatory Therapy." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a5852.

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Hammad, Seddik, Yoon Seok Jung, Kamalakannan Radhakrishnan та ін. "ERRγ-induced hepatokine, FGF23, regulates chronic alcohol-induced liver injury in mice". У 39. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag, 2023. http://dx.doi.org/10.1055/s-0042-1759929.

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Reports on the topic "Amiodarone induced liver injury"

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Li, Chengcheng, Xin Yang, Yuhang Quan, Yafang Lai, Yifang Wang, and Anhao Wu. Network meta-analysis of different liver protective drugs in the treatment of drug-induced liver injury. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2023. http://dx.doi.org/10.37766/inplasy2023.6.0039.

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Liu, Xiaopei, Dan Liu, and Cong’e Tan. Gut microbiome-based machine learning for diagnostic prediction of liver fibrosis and cirrhosis: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.5.0133.

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Abstract:

Review question / Objective: The invasive liver biopsy is the gold standard for the diagnosis of liver cirrhosis. Other non-invasive diagnostic approaches, have been used as alternatives to liver biopsy, however, these methods cannot identify the pathological grade of the lesion. Recently, studies have shown that gut microbiome-based machine learning can be used as a non-invasive diagnostic approach for liver cirrhosis or fibrosis, while it lacks evidence-based support. Therefore, we performed this systematic review and meta-analysis to evaluate its predictive diagnostic value in liver cirrhosis or fibrosis. Condition being studied: Liver fibrosis and cirrhosis. Liver fibrosis refers to excessive deposition of liver fibrous tissue caused by various pathogenic factors, such as hepatitis virus, alcohol, and drug-induced chemical injury. Continuous progression of liver fibrosis can lead to liver cirrhosis.

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Drug-Induced Liver Injury (DILI): Current status and future directions for drug development and the post-market setting. Council for International Organizations of Medical Sciences (CIOMS), 2020. http://dx.doi.org/10.56759/ojsg8296.

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Drug-induced liver injury (DILI) is a growing challenge because of the ever- increasing number of drugs used in medical care. DILI is rare but can be serious and is largely unpredictable. It is an important cause of mortality and liver transplantation, and a leading cause of attrition in drug development. Progress is under way in identifying genetic risk factors, exploring new mechanistic concepts of the complex underlying interactions, and developing new biomarkers that can predict or diagnose DILI. The pharmaceutical industry has a key role in advancing these initiatives, and prospective DILI registries must adopt standard procedures for biological sample collection and storing. There is a strong need for standard guidelines to support these efforts. The consensus report of the CIOMS DILI Working Group aims to provide a critical framework and essential set of tools to detect, diagnose and manage DILI during drug development and in the post-marketing setting. The report is intended for clinical and basic pharmaceutical industry investigators who capture, analyze and communicate liver safety data in drug development. It is also intended for regulatory scientists and expert consultants who comprehensively evaluate new products and emerging biomarkers for their association with DILI risk, and for health care professionals who monitor and manage patients treated with potentially hepatotoxic drugs in clinical practice.

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