Corrigendum to “Drug-induced liver injury after switching from tamoxifen to anastrozole in a patient with a history of breast cancer being treated for hypertension and diabetes”

Anastrozole is a selective non-steroidal aromatase inhibitor that blocks the conversion of androgens to estrogens in peripheral tissues. It is used as adjuvant therapy for early-stage hormone-sensitive breast cancer in postmenopausal women. Significant side effects of anastrozole include osteoporosis and increased levels of cholesterol. To date, seven case reports on anastrozole hepatotoxicity have been published. We report the case of an 81-year-old woman with a history of breast cancer, arterial hypertension, type 2 diabetes mellitus, hyperlipidemia, and chronic renal insufficiency. Four days after switching hormone therapy from tamoxifen to anastrozole, icterus developed along with a significant increase in liver enzymes (measured in the blood). The patient was admitted to hospital, where a differential diagnosis of jaundice was made and anastrozole was withdrawn. Subsequently, hepatic functions quickly normalized. The observed liver injury was attributed to anastrozole since other possible causes of jaundice were excluded. However, concomitant pharmacotherapy could have contributed to the development of jaundice and hepatotoxicity, after switching from tamoxifen to anastrozole since several the patient’s medications were capable of inhibiting hepatobiliary transport of bilirubin, bile acids, and metabolized drugs through inhibition of ATP-binding cassette proteins. Telmisartan, tamoxifen, and metformin all block bile salt efflux pumps. The efflux function of multidrug resistance protein 2 is known to be reduced by telmisartan and tamoxifen and breast cancer resistance protein is known to be inhibited by telmisartan and amlodipine. Moreover, the activity of P-glycoprotein transporters are known to be decreased by telmisartan, amlodipine, gliquidone, as well as the previously administered tamoxifen. Finally, the role of genetic polymorphisms of cytochrome P450 enzymes and/or drug transporters cannot be ruled out since the patient was not tested for polymorphisms.

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Diphenhydramine as a Cause of Drug-Induced Liver Injury

Case Reports in Hepatology ◽

10.1155/2017/3864236 ◽

2017 ◽

Vol 2017 ◽

pp. 1-4 ◽

Cited By ~ 2

Author(s):

Yunseok Namn ◽

Yecheskel Schneider ◽

Isabelle H. Cui ◽

Arun Jesudian

Keyword(s):

Liver Injury ◽

Acute Liver Injury ◽

Chromosomal Translocation ◽

Altered Mental Status ◽

Drug Induced ◽

Drug Induced Liver Injury ◽

Patient Reported ◽

History Of ◽

Concomitant Medications ◽

Unites States

Drug-induced liver injury (DILI) is the most common cause of acute liver failure in the Unites States and accounts for 10% of acute hepatitis cases. We report the only known case of diphenhydramine-induced acute liver injury in the absence of concomitant medications. A 28-year-old man with history of 13/14-chromosomal translocation presented with fevers, vomiting, and jaundice. Aspartate-aminotransferase and alanine-aminotransferase levels peaked above 20,000 IU/L and 5,000 IU/L, respectively. He developed coagulopathy but without altered mental status. Patient reported taking up to 400 mg diphenhydramine nightly, without concomitant acetaminophen, for insomnia. He denied taking other medications, supplements, antibiotics, and herbals. A thorough workup of liver injury ruled out viral hepatitis (including A, B, C, and E), autoimmune, toxic, ischemic, and metabolic etiologies including Wilson’s disease. A liver biopsy was consistent with DILI without evidence of iron or copper deposition. Diphenhydramine was determined to be the likely culprit. This is the first reported case of diphenhydramine-induced liver injury without concomitant use of acetaminophen.

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Clinical Features, Diagnosis, and Natural History of Drug-Induced Liver Injury

Seminars in Liver Disease ◽

10.1055/s-0034-1375955 ◽

2014 ◽

Vol 34 (02) ◽

pp. 134-144 ◽

Cited By ~ 27

Author(s):

Robert Fontana ◽

Paul Hayashi

Keyword(s):

Liver Injury ◽

Natural History ◽

Clinical Features ◽

Drug Induced ◽

Drug Induced Liver Injury ◽

History Of

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A Time to Pause and Reflect: When a Patient with Autoimmune Hepatitis Stops Responding to Corticosteroids

Case Reports in Gastrointestinal Medicine ◽

10.1155/2016/7092434 ◽

2016 ◽

Vol 2016 ◽

pp. 1-3

Author(s):

Lewis Tsang ◽

Mitali Fadia ◽

Shivakumar Chitturi

Keyword(s):

Liver Injury ◽

Autoimmune Hepatitis ◽

Biochemical Relapse ◽

Drug Induced ◽

Drug Induced Liver Injury ◽

History Of ◽

Histological Characteristics ◽

Prompt Response

Drug-induced liver injury (DILI) with features of autoimmunity (AI) is a challenging diagnosis to make particularly due to its apparent corticosteroid responsiveness. We present the case of a 74-year-old woman who presented with a 2-week history of jaundice and fatigue. She was initially diagnosed with autoimmune hepatitis (AIH) based on biochemical and histological characteristics and prompt response with budesonide but a biochemical relapse occurred soon after inadvertent rechallenge with irbesartan, a drug that she had discontinued prior to her presentation but was not initially considered to be a cause of her symptoms.

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A natural history of efavirenz drug-induced liver injury

South African Medical Journal ◽

10.7196/samj.2021.v111i12.14584 ◽

2021 ◽

Vol 111 (12) ◽

pp. 1190

Author(s):

D Maughan ◽

M Sonderup ◽

N Gogela ◽

M Locketz ◽

H Wainwright ◽

...

Keyword(s):

Liver Injury ◽

Natural History ◽

Drug Induced ◽

Drug Induced Liver Injury ◽

History Of

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Case of cholestatic drug-induced liver injury (DILI) associated with black cohosh

BMJ Case Reports ◽

10.1136/bcr-2020-240408 ◽

2021 ◽

Vol 14 (5) ◽

pp. e240408

Author(s):

Himmat Singh Brar ◽

Rachana Marathi

Keyword(s):

Liver Injury ◽

Liver Enzymes ◽

American Woman ◽

Black Cohosh ◽

Herbal Supplement ◽

Drug Induced ◽

Drug Induced Liver Injury ◽

Postmenopausal Symptoms ◽

Autoimmune Pathology ◽

History Of

Drug-induced liver injury is an uncommon yet fatal cause of liver injury. Black cohosh is a herbal supplement that is derived from Actaea racemosa. It has been used for vasomotor symptoms in postmenopausal women, but it can cause liver injury. A 50-year-old Afro-American woman presented with a 2-month history of malaise, itching and severe jaundice. The labs showed elevation of bilirubin and alkaline phosphatase. The patient had a history of black cohosh use for postmenopausal symptoms before she developed her current symptoms. The extensive workup for infective and autoimmune pathology was negative. Black cohosh was discontinued. The patient improved clinically, and her liver enzymes normalised 6 months after the discontinuation of black cohosh. This report emphasises the need to recognise black cohosh as a potential hepatotoxic agent and to monitor the liver enzymes for a patient on black cohosh.

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

Clinical Medicine Insights Case Reports ◽

10.1177/1179547617731375 ◽

2017 ◽

Vol 10 ◽

pp. 117954761773137 ◽

Cited By ~ 4

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.

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Fatal Isoniazid Hepatotoxicity in the Deployed Environment

Military Medicine ◽

10.1093/milmed/usaa414 ◽

2020 ◽

Author(s):

Daniel J Cybulski ◽

Brian K White

Keyword(s):

Liver Injury ◽

Latent Tuberculosis Infection ◽

Latent Tuberculosis ◽

Tuberculosis Infection ◽

Medical Decision ◽

Drug Induced ◽

Drug Induced Liver Injury ◽

Medical Needs ◽

Medical Standards ◽

History Of

Abstract Deployed clinicians have limited resources at their disposal to augment medical decision-making and management. All deploying personnel undergo predeployment medical assessment to evaluate their fitness for deployment. The purpose of predeployment screening is to allow for anticipation of medical needs that may arise which could challenge the available medical resources in an expeditionary environment. Medical standards for deployment are published, identifying disqualifying conditions and medications. A history of latent tuberculosis infection is not disqualifying for deployment. Isoniazid is not specifically mentioned as a disqualifying medication, though it is well known to have the potential of causing drug-induced liver injury. Here, a case of fatal isoniazid-induced drug-induced liver injury in a deployed setting is presented with a review of current latent tuberculosis infection literature. Our goal is for the reader to form their own opinion whether or not isoniazid should be used in the forward environment.

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Albendazole-induced liver injury: a case report

Colombia Medica ◽

10.25100/cm.v44i2.1021 ◽

2013 ◽

pp. 118-120 ◽

Cited By ~ 7

Author(s):

David Ríos ◽

Juan Carlos Restrepo

Keyword(s):

Case Report ◽

Liver Injury ◽

Drug Toxicity ◽

Laboratory Tests ◽

Clinical Record ◽

Drug Induced ◽

Drug Induced Liver Injury ◽

Hepatic Hydatidosis ◽

Hepatocellular Damage ◽

History Of

We report a case of a 47-year-old male, who was referred to the clinical hepatology services at Pablo Tobón Uribe Hospital for evaluation of a jaundice syndrome. After undergoing several exams, we diagnosed hepatic hydatidosis and the patient was treated with albendazole; however, after five months of uninterrupted treatment the patient again consulted and his liver test showed marked hepatocellular damage. This time, the patient was diagnosed with drug-induced liver injury due to albendazole, based on information from the clinical record, history of drug consumption, clinical and laboratory tests improved after discontinuing the medication and after discarding other possible causes; this diagnosis was supported by the CIOMS/RUCAM scale, which showed a “likely” correlation between hepatocellular damage and drug toxicity etiology.

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Albendazole-induced liver injury of a 11-year-old girl

Experimental and Clinical Gastroenterology ◽

10.31146/1682-8658-ecg-171-11-83-88 ◽

2019 ◽

pp. 83-88

Author(s):

S. N. Borzakova ◽

L. A. Kharitonova ◽

M. N. Ermakova ◽

I. M. Osmanov ◽

E. V. Rudikova

Keyword(s):

Risk Factors ◽

Liver Injury ◽

Fat Metabolism ◽

Female Gender ◽

The Self ◽

Drug Induced ◽

Drug Induced Liver Injury ◽

Antiparasitic Drug ◽

Pathogenetic Therapy ◽

History Of

A case of the drug-induced liver injury (DILI) development is presented on the background of the self-treatment with an antiparasitic drug Albendazole in an 11 years-old girl with several risk factors for the drug-induced liver injury (history of a drug reaction, carbohydrate and fat metabolism disturbance, female gender, and adolescence). The disease was diagnosed using the the CIOMS/RUCAM scale. The drug was withdrawn and the pathogenetic therapy was established (fluids, hepatoprotective drugs) with the resolution of the drug-induced hepatitis.

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