Severe Drug-Induced Liver Injury as an Adverse Drug Event of Antibiotics: A Case Report and Review of the Literature

Chemotherapy ◽  
2017 ◽  
Vol 62 (6) ◽  
pp. 367-373 ◽  
Author(s):  
Martin Munz ◽  
Hans Grummich ◽  
Josef Birkmann ◽  
Martin Wilhelm ◽  
Ulrike Holzgrabe ◽  
...  
Keyword(s):  
Case Report ◽  
Liver Injury ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Adverse Drug Event ◽  
Drug Event ◽  
Review Of The Literature ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Life Threatening

Drug-induced liver injury is one of the main reasons for acute liver failure. We report the case of a young patient who experienced a drug-induced liver injury resulting in life-threatening acute liver failure after treatment with different antibiotics (amoxicillin, ciprofloxacin, cefazolin, clindamycin) and acetaminophen, or a combination of these drugs. Moreover, we provide an overview of the hepatotoxic potential of these drugs.

scholarly journals Sunitinib-Induced Acute Liver Failure

2021 ◽  
pp. 17-21
Author(s):  
Anum Aqsa ◽  
Sami Droubi ◽  
Shivantha Amarnath ◽  
Hassan Al-Moussawi ◽  
Jeffrey Abergel
Keyword(s):  
Liver Injury ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Kinase Inhibitor ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Therapy Initiation ◽  
Pancreatic Neuroendocrine Carcinoma ◽  
Life Threatening ◽  
Transient Elevation

Drug-induced liver injury is an uncommon but life-threatening entity. Sunitinib is a tyrosine kinase inhibitor used for advanced and imatinib-refractory gastrointestinal stromal tumors. It causes transient elevation in liver enzymes. The incidence of fatal acute liver failure is rare. Five cases of sunitinib-induced acute liver injury have been reported in the literature thus far. We present a case of fatal acute liver failure and cardiomyopathy within 2 weeks of sunitinib therapy initiation for advanced pancreatic neuroendocrine carcinoma. We believe our case is unique due to the rarity of its presentation. It highlights hepatotoxicity as a potentially fatal side effect of sunitinib therapy.

scholarly journals PP025—Improving hy’s law definition to better predict the risk of developing acute liver failure in drug-induced liver injury (DILI)

2013 ◽  
Vol 35 (8) ◽  
pp. e25
Author(s):  
M. Robles-Díaz ◽  
C. Stephens ◽  
I. Medina-Cáliz ◽  
A.F. González ◽  
A. González-Jiménez ◽  
...  
Keyword(s):  
Liver Injury ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Hy’S Law

scholarly journals Correction: Cytokine profiles in acute liver injury—Results from the US Drug-Induced Liver Injury Network (DILIN) and the Acute Liver Failure Study Group

PLoS ONE ◽  
2019 ◽  
Vol 14 (2) ◽  
pp. e0212394 ◽  
Author(s):  
Herbert L. Bonkovsky ◽  
Huiman X. Barnhart ◽  
David M. Foureau ◽  
Nury Steuerwald ◽  
William M. Lee ◽  
...  
Keyword(s):  
Liver Injury ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Acute Liver Injury ◽  
Study Group ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Cytokine Profiles ◽  
The Us

Use of Hy's Law and a New Composite Algorithm to Predict Acute Liver Failure in Patients With Drug-Induced Liver Injury

2014 ◽  
Vol 147 (1) ◽  
pp. 109-118.e5 ◽  
Author(s):  
Mercedes Robles–Diaz ◽  
M. Isabel Lucena ◽  
Neil Kaplowitz ◽  
Camilla Stephens ◽  
Inmaculada Medina–Cáliz ◽  
...  
Keyword(s):  
Liver Injury ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Hy’S Law

scholarly journals Necrotic cell death and suppression of T-cell immunity characterized acute liver failure due to drug-induced liver injury

Cytokine ◽  
2016 ◽  
Vol 86 ◽  
pp. 21-28 ◽  
Author(s):  
Keisuke Kakisaka ◽  
Kojiro Kataoka ◽  
Yuji Suzuki ◽  
Yohei Okada ◽  
Yuichi Yoshida ◽  
...  
Keyword(s):  
Cell Death ◽  
Liver Injury ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
T Cell Immunity ◽  
Necrotic Cell Death ◽  
Necrotic Cell ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Cell Immunity

Drug-Drug Combinations Can Enhance Toxicity as Shown by Monocyte-Derived Hepatocyte-like Cells From Patients With Idiosyncratic Drug-Induced Liver Injury

2019 ◽  
Vol 171 (2) ◽  
pp. 296-302 ◽  
Author(s):  
Andreas Benesic ◽  
Kowcee Jalal ◽  
Alexander L Gerbes
Keyword(s):  
Liver Injury ◽  
Liver Failure ◽  
Drug Interactions ◽  
Acute Liver Failure ◽  
Causality Assessment ◽  
Drug Combinations ◽  
Positive Interactions ◽  
In Vitro Test ◽  
Drug Induced ◽  
Drug Induced Liver Injury

Abstract Drug-induced liver injury (DILI) is a major cause for acute liver failure and regulatory actions on novel drugs. Individual patient characteristics are the main determinant of idiosyncratic DILI, making idiosyncratic DILI (iDILI) one of the most challenging diagnoses in hepatology. Individual drug-drug interactions might play a role in iDILI. However, the current approaches to iDILI diagnosis are focused on single drugs as causative agents. For the present analysis, 48 patients with acute liver injury who took 2 drugs and who were diagnosed as iDILI were investigated. A novel in vitro test was employed using monocyte-derived hepatocyte-like cells (MH cells) generated from these patients. iDILI diagnosis and causality were evaluated using clinical causality assessment supported by Roussel-Uclaf Causality Assessment Method. In 13 of these 48 patients (27%), combinations of drugs increased toxicity in the MH test when compared with the single drugs. Interestingly, whereas in 24 cases (50%) drug-drug combinations did not enhance toxicity, in 11 cases (23%) only the combinations caused toxicity. The incidence of severe cases fulfilling Hy’s law was higher in patients with positive interactions (57% vs 43%; p = .04), with acute liver failure occurring in 40% versus 8% (p = .01). The most common drug combinations causing increased toxicity were amoxicillin/clavulanate (8 of 9 cases) and diclofenac in combination with steroid hormones (4 of 9 cases). Drug-drug interactions may influence the incidence and/or the severity of idiosyncratic DILI. MH cell testing can identify relevant drug-drug interactions. The data generated by this approach may improve patient safety. Study identifier ClinicalTrials.gov NCT 02353455.

Drug Hepatotoxicity

2018 ◽  
Author(s):  
Fernando Bessone ◽  
Raúl J Andrade
Keyword(s):  
Immune System ◽  
Liver Injury ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Causality Assessment ◽  
Adaptive Immune System ◽  
Genome Wide Association Studies ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Adaptive Immune

Idiosyncratic drug-induced liver injury (DILI) caused by xenobiotics (drugs, herbals, and dietary supplements) is an elusive liver disease presenting with a range of phenotypes and severity, including acute hepatitis that is indistinguishable from viral hepatitis, autoimmune hepatitis, steatosis, fibrosis or rare chronic vascular syndromes, asymptomatic liver test abnormalities,and acute liver failure. Case definition and characterization using liver biochemistry and histology are crucial for appropriate phenotyping. The incidence of DILI is probably higher than expected by the cases that are identified in clinical practice because of misdiagnosis and underreporting.The pathogenesis of DILI is complex, depending on the interaction of a drug’s physicochemical properties and host factors. Genome-wide association studies have identified several alleles from the major histocompatibility complex system, indicating a fundamental role of the adaptive immune system in DILI pathogenesis. As specific biomarkers for hepatotoxicity are still not available, the diagnosis of DILI remains one of exclusion of the alternative causes of liver damage. Structured causality assessment using the Roussel Uclaf Causality Assessment Method (RUCAM) or previously Council for International Organizations of Medical Sciences (CIOMS) instrument adds consistency to the diagnostic process, although there is room for improvement in the scale domains and score weighting. The therapy for idiosyncratic hepatotoxicity is supportive and relies on the prompt withdrawal of the offending agent. Corticosteroid therapy for hypersensitivity reactions or ursodeoxycholicacid for prolonged cholestasis is empirically used, although the degree of evidence is low. Existing databases have enabled a better prediction of immediate and long-term DILI prognosis. Multivariate models have identified clinical and analytical variables as predictive of acute liver failure and mortality as well as of chronic DILI. This review contains 2 figures, 5 tables, and 55 references Key Words: adaptive immune system; causality assessment; drug-induced liver injury; epidemiology; HLA alleles; pharmacogenetics; registries; risk factors

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