scholarly journals Anastrozole-induced liver injury after a prolonged latency: a very rare complication of a commonly prescribed medication

2019 ◽  
Vol 12 (11) ◽  
pp. e231741 ◽  
Author(s):  
Chencheng Xie ◽  
Hafez Mohammad Ammar Abdullah ◽  
Mohamed Abdallah ◽  
Erin Quist ◽  
Mumtaz Niazi
Keyword(s):  
Liver Injury ◽  
Liver Enzymes ◽  
Rare Complication ◽  
Assessment Method ◽  
Drug Induced ◽  
Serious Adverse Events ◽  
Drug Induced Liver Injury ◽  
Elevated Liver Enzymes ◽  
Safe Side ◽  
Prolonged Latency

Anastrozole is an aromatase inhibitor that has been used more frequently over the last decade especially for oestrogen receptor-positive breast cancer. It has a relatively safe side effect profile. However, occasionally it has been associated with serious adverse events. Here, we present the case of a 58-year-old woman who presented with significantly elevated liver enzymes 4 years after starting anastrozole. She was not taking any other medications and an extensive workup did not reveal any other cause for her liver injury. The patient’s liver enzymes normalised after discounting the anastrozole. She scored 4 on the updated Roussel Uclaf Causality Assessment Method grading system which was possible for drug-induced liver injury. A review of the literature revealed six prior cases of anastrozole-related liver injury. Anastrozole should be considered as a possible culprit in patients who develop an unexplained acute liver injury.

scholarly journals A possible increase in liver enzymes due to amlodipine: A case report

2020 ◽  
Vol 8 ◽  
pp. 2050313X2091782
Author(s):  
Ginny Varghese ◽  
Lama Madi ◽  
Muna Ghannam ◽  
Rafaat Saad
Keyword(s):  
Liver Injury ◽  
Liver Enzymes ◽  
Case Reports ◽  
Assessment Method ◽  
Probability Scale ◽  
Antihypertensive Medications ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Elevated Liver Enzymes ◽  
Liver Transaminases

Amlodipine is a commonly prescribed antihypertensive drug, well tolerated and has rarely been attributed as a cause for elevated liver enzymes. Here, we present a 47-year-old male patient known to be hypertensive and admitted to our rehabilitation facility after an acute stroke. During his stay, amlodipine was started in addition to other antihypertensive medications to control his blood pressure. His liver transaminases after 4 days (notably alanine aminotransferase) were found to be markedly elevated. After reviewing the medications and investigating probable causes, amlodipine was suspended. After 5 days of suspending amlodipine, the transaminases started to trend downward. The Naranjo Adverse Drug Reaction Probability Scale and the Roussel Uclaf Causality Assessment Method were performed to assess causality in this suspected idiosyncratic drug-induced liver injury case. Both the scores denoted a probable amlodipine-induced liver injury. Previous case reports related to amlodipine-induced liver injury are mentioned and presented in the table below. In conclusion, amlodipine, though not well known to be hepatotoxic, can induce liver enzyme elevations in an idiosyncratic manner.

scholarly journals Recurrence and Severe Worsening of Hepatotoxicity After Reintroduction of Atorvastatin in Combination With Ezetimibe

2017 ◽  
Vol 10 ◽  
pp. 117954761773137 ◽  
Author(s):  
Silje Bergland Ellingsen ◽  
Elisabet Nordmo ◽  
Knut Tore Lappegård
Keyword(s):  
Liver Injury ◽  
Liver Enzymes ◽  
Current Data ◽  
Class Effect ◽  
Drug Induced ◽  
Good Tolerance ◽  
Drug Induced Liver Injury ◽  
Severe Hepatotoxicity ◽  
Elevated Liver Enzymes ◽  
History Of

Severe hepatotoxicity is a rare but well-known adverse reaction to statins. However, despite the widespread use of statins, only a few cases describing statin reexposure or switch to another statin after liver injury have been published. The literature on hepatotoxicity with ezetimibe alone or in combination with statins is also scarce. We report a case where a patient with a history of elevated liver enzymes while using atorvastatin, but prior and subsequent good tolerance to simvastatin and pravastatin, developed drug-induced liver injury on reexposure to a combination of atorvastatin and ezetimibe. The hepatotoxicity in our patient was most likely caused by reexposure to atorvastatin, although we cannot exclude ezetimibe as a contributing factor. This case highlights the risk of hepatotoxicity recurrence on rechallenge with the same statin. The tolerance to other statins in this case also strengthens the suspicion that statin-induced liver injury may not be a class effect, although the current data are too scarce to draw any definite conclusions.

scholarly journals Drug-Induced Liver Injury: A Unique Presentation of Single-Dose Administration of Propylthiouracil

2020 ◽  
Vol 8 ◽  
pp. 232470962095132
Author(s):  
Simcha Weissman ◽  
Nishan G. Rajaratnam ◽  
Nabeel Qureshi ◽  
Faisal Inayat ◽  
Sameh Elias
Keyword(s):  
Single Dose ◽  
Liver Injury ◽  
Liver Enzymes ◽  
Antithyroid Drug ◽  
Thyroid Storm ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Elevated Liver Enzymes ◽  
Pharmacologic Agents

Antithyroid drug-induced severe liver injury is an uncommon but serious complication. We hereby delineate the case of a 38-year-old female who presented to the emergency department for an impending thyroid storm. After initiation of a single dose of propylthiouracil, her liver enzymes went into the thousands. She was subsequently admitted to the intensive care unit. Propylthiouracil was discontinued and corticosteroids were initiated with the resolution of her elevated liver enzymes. On follow-up, her liver function was at its baseline and thyroid hormone levels were under control. We hope this report will encourage clinicians to cast a broad differential diagnosis in patients presenting with liver injury in the acute setting. Furthermore, it is imperative to raise awareness regarding the ever-increasing list of pharmacologic agents that can perpetuate drug-induced hepatotoxicity.

scholarly journals Meropenem-induced liver injury and beta-lactam cross-reactivity

2018 ◽  
Vol 11 (1) ◽  
pp. e227124 ◽  
Author(s):  
Timothy Tattersall ◽  
Hugh Wright ◽  
Andrew Redmond
Keyword(s):  
Liver Injury ◽  
Liver Enzymes ◽  
Early Recognition ◽  
Cross Reactivity ◽  
Beta Lactam ◽  
Severe Liver ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Rehabilitation Facility ◽  
Elevated Liver Enzymes

A 63-year-old man admitted to hospital for the management of a frontal lobe abscess developed elevated liver enzymes within 48 hours of receiving meropenem. Liver enzymes reached a maximum at 5 days postadministration of meropenem, with alanine aminotransferase 1160 U/L, aspartate aminotransferase 787 U/L, alkaline phosphatase 297 U/L and gamma-glutamyltransferase 252 U/L. Meropenem was ceased and liver function normalised. Meropenem was administered for a second time later in the patient’s admission and again the patient developed rapidly increasing liver enzymes, with a mixed hepatocellular/cholestatic pattern. Other possible causes of liver injury were excluded following extensive investigations, and the patient’s liver enzymes continued to normalise following meropenem discontinuation. The patient was asymptomatic during the admission and was transferred to a rehabilitation facility. This case demonstrates that meropenem can cause severe liver injury and that early recognition of drug-induced liver injury is important.

scholarly journals Circulatory Inflammatory Mediators in the Prediction of Anti-Tuberculous Drug-Induced Liver Injury Using RUCAM for Causality Assessment

Biomedicines ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 891
Author(s):  
Cheng-Maw Ho ◽  
Chi-Ling Chen ◽  
Chia-Hao Chang ◽  
Meng-Rui Lee ◽  
Jann-Yuan Wang ◽  
...  
Keyword(s):  
Liver Injury ◽  
Inflammatory Mediators ◽  
Cox Regression ◽  
Causality Assessment ◽  
Area Under The Curve ◽  
Assessment Method ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Tb Treatment ◽  
Pre Treatment

Background: Anti-tuberculous (TB) medications are common causes of drug-induced liver injury (DILI). Limited data are available on systemic inflammatory mediators as biomarkers for predicting DILI before treatment. We aimed to select predictive markers among potential candidates and to formulate a predictive model of DILI for TB patients. Methods: Adult active TB patients from a prospective cohort were enrolled, and all participants received standard anti-tuberculous treatment. Development of DILI, defined as ≥5× ULN for alanine transaminase or ≥2.6× ULN of total bilirubin with causality assessment (RUCAM, Roussel Uclaf causality assessment method), was regularly monitored. Pre-treatment plasma was assayed for 15 candidates, and a set of risk prediction scores was established using Cox regression and receiver-operating characteristic analyses. Results: A total of 19 (7.9%) in 240 patients developed DILI (including six carriers of hepatitis B virus) following anti-TB treatment. Interleukin (IL)-22 binding protein (BP), interferon gamma-induced protein 1 (IP-10), soluble CD163 (sCD163), IL-6, and CD206 were significant univariable factors associated with DILI development, and the former three were backward selected as multivariable factors, with adjusted hazards of 0.20 (0.07–0.58), 3.71 (1.35–10.21), and 3.28 (1.07–10.06), respectively. A score set composed of IL-22BP, IP-10, and sCD163 had an improved area under the curve of 0.744 (p < 0.001). Conclusions: Pre-treatment IL-22BP was a protective biomarker against DILI development under anti-TB treatment, and a score set by additional risk factors of IP-10 and sCD163 employed an adequate DILI prediction.

scholarly journals Causality assessment in drug-induced liver injury using a structured expert opinion process: Comparison to the Roussel-Uclaf causality assessment method

Hepatology ◽  
2010 ◽  
Vol 51 (6) ◽  
pp. 2117-2126 ◽  
Author(s):  
Don C. Rockey ◽  
Leonard B. Seeff ◽  
James Rochon ◽  
James Freston ◽  
Naga Chalasani ◽  
...  
Keyword(s):  
Liver Injury ◽  
Expert Opinion ◽  
Causality Assessment ◽  
Assessment Method ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Process Comparison

scholarly journals A case report of a drug‐induced liver injury (DILI) caused by multiple antidepressants with causality established by the updated Roussel Uclaf causality assessment method (RUCAM) and in vitro testing

2020 ◽  
Vol 8 (12) ◽  
pp. 3105-3109
Author(s):  
Miguel González‐Muñoz ◽  
Jaime Monserrat Villatoro ◽  
Eva Marín‐Serrano ◽  
Stefan Stewart ◽  
Belén Bardón Rivera ◽  
...  
Keyword(s):  
Case Report ◽  
Liver Injury ◽  
Causality Assessment ◽  
Assessment Method ◽  
In Vitro Testing ◽  
Drug Induced ◽  
Drug Induced Liver Injury

scholarly journals Potentially hepatotoxic drugs are still being prescribed to liver disease patients under tertiary care: it is time to say enough

2021 ◽  
Vol 5 (4) ◽  
pp. 279-286
Author(s):  
Rodrigo Dorelo ◽  
Samantha T.A. Barcelos ◽  
Magela Barros ◽  
Valeria Elustondo ◽  
Ysela Y.P. Pérez ◽  
...  
Keyword(s):  
Liver Disease ◽  
Hepatitis C ◽  
Liver Enzymes ◽  
Tertiary Care ◽  
University Hospital ◽  
Decompensated Cirrhosis ◽  
Drug Induced ◽  
Alcoholic Fatty Liver ◽  
Drug Induced Liver Injury ◽  
Elevated Liver Enzymes

Introduction and aim: Drug-induced liver injury (DILI) manifests as a spectrum of clinical presentations that carries morbidity and mortality. Patients with chronic liver disease (CLD), particularly hospitalized, are at high risk for developing DILI. We aimed to investigate the use of potentially hepatotoxic drugs (PHD) in patients with CLD in a tertiary university hospital. Materials and methods: Adult (≥ 18 years-old) with CLD admitted to the hospital from January 2016 to December 2018 were evaluated regarding PHD, assessing the risk of DILI and liver enzymes behavior after exposure. Results: From 931 hospitalized patients with CLD, 291 (31.3%) were exposed to hepatotoxic drugs during their hospitalization. Of those, 244 (83.8%) were cirrhotic. The most frequent causes of liver disease were hepatitis C (41.2%), followed by alcohol (13.2%), hepatitis C/alcohol (11.7%) and non-alcoholic fatty liver disease (5.8%). Decompensated cirrhosis (46.7%) was the main reason for hospital admission. The most often prescribed PHD were antibiotics (67.7%), cardiovascular drugs (34.4%), neuromodulators (26.1%) and anesthetics (19.9%). After exposure, 113 patients (38.8%) presented significant elevated liver enzymes. Surprisingly, PHD were more often prescribed in GI/Liver unit (48.8%) followed by emergency/intensive care unit (28.5%). A total of 65 patients (22%) died, however in neither case was it possible to safely infer causal relationship among PHD, liver enzymes and death. Conclusion: PHD prescription is frequent in patients with CLD even in a tertiary university hospital and in the gastroenterology and hepatology department, exposing these patients to an additional risk.

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