Acute cholestatic hepatitis caused by amoxicillin/clavulanate

Beraldo, Daniel Oliveira; Melo, Joanderson Fernandes; Bonfim, Alexandre Vidal; Teixeira, Anderson; Teixeira, Ricardo Alkmim; Duarte, André Loyola

doi:10.3748/wjg.v19.i46.8789

Cited by 15 publications

(25 citation statements)

References 14 publications

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“…For example, amoxicillin-clavulanate usually results in a cholestatic injury but less frequently has also been associated with ALF. 17,18 Another way to classify idiosyncratic DILI is as immunemediated (allergic) or non-immune mediated (nonallergic). 19 If immune-mediated, the latency is shorter (1-6 weeks) compared with non-immune mediated reactions (1 month to 1 year).…”

Section: Epidemiologymentioning

confidence: 99%

Drug-induced liver injury

2016

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Drug-induced liver injury (DILI) remains the most common cause of acute liver failure (ALF) in the western world. Excluding paracetamol overdose, nearly all DILI encountered in the clinical setting is idiosyncratic in nature because affected individuals represent only a small proportion of those treated with such drugs. In many cases, the mechanism for idiosyncrasy is immune-mediation and is often identifi ed by genetic risk determined by human leukocyte antigen variants. In the absence of diagnostic tests and/or biomarkers, the diagnosis of DILI requires a high index of suspicion after diligently excluding other causes of abnormal liver tests. Antibiotics are the class of drugs most frequently associated with idiosyncratic DILI, although recent studies indicate that herbal and dietary supplements are an increasingly recognised cause. It is imperative that upon development of DILI the culprit drug be discontinued, especially in the presence of elevated transaminases (aspartate aminotransferase/alanine aminotransferase ratio ≥5 times the upper limit of normal) and/or jaundice. Risk factors for the development ALF include hepatocellular DILI and female gender, the treatment being supportive with some benefi t of N-acetylcysteine in the early stages. In view of the poor transplant-free survival in idiosyncratic DILI, early consideration for liver transplant is mandatory. KEYWORDS : Autoimmune hepatitis , cholestasis , drug-induced acute liver failure , herbal and dietary supplements , hepatocellular DILI , hepatotoxicity IntroductionAt a regulatory level, drug-induced liver injury (DILI) is the commonest reason for withdrawing drugs from the market and/or issuing warnings and modification of use.1 DILI is classified as either predictable or unpredictable (idiosyncratic). 2The former tends to be dose-related, has a short latency (days), is due to direct toxicity of the drug or its metabolite, and is ABSTRACT Drug-induced liver injuryreproducible in animal models (eg paracetamol overdose). 3The vast majority of DILI, however, is idiosyncratic or unpredictable -it is unexpected based on the pharmacological actions of the drug and in most cases routine animal toxicology fails to identify the risk of subsequent clinical toxicity. 4 This review shall largely focus on idiosyncratic DILI .

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Section: Epidemiologymentioning

confidence: 99%

Drug-induced liver injury

2016

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“…3,4 Many different classes of drugs may cause iDILI, but the most common are antibiotics and nonsteroidal anti-inflammatories, namely co-amoxiclav, flucloxacillin, diclofenac and isoniazid. [5][6][7][8][9] It therefore seems unlikely, given the mixed clinical picture and the different classes of drugs involved, that a single mechanism is responsible for iDILI. 10,11 Moreover, similar symptoms may be the result of different mechanisms even within the same class of drugs.…”

Section: What Is Idili?mentioning

confidence: 99%

The chemical, genetic and immunological basis of idiosyncratic drug–induced liver injury

et al. 2015

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Idiosyncratic drug reactions can be extremely severe and are not accounted for by the regular pharmacology of a drug. Thus, the mechanism of idiosyncratic drug–induced liver injury (iDILI), a phenomenon that occurs with many drugs including β-lactams, anti-tuberculosis drugs and non-steroidal anti-inflammatories, has been difficult to determine and remains a pressing issue for patients and drug companies. Evidence has shown that iDILI is multifactorial and multifaceted, which suggests that multiple cellular mechanisms may be involved. However, a common initiating event has been proposed to be the formation of reactive drug metabolites and covalently bound adducts. Although the fate of these metabolites are unclear, recent evidence has shown a possible link between iDILI and the adaptive immune system. This review highlights the role of reactive metabolites, the recent genetic innovations which have provided molecular targets for iDILI, and the current literature which suggests an immunological basis for iDILI.

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“…In 1984, amoxicillin-clavulanate was commercialized for the first time. The first-ever reported case of toxic hepatitis related to this antibiotic was from The Netherlands in 1988 [5,12]. Amoxicillin-clavulanate is generally a well-tolerated antibiotic used for mild to moderate respiratory and cutaneous bacterial infections [12].…”

Section: Discussionmentioning

confidence: 99%

Delayed Presentation of Drug-Induced Hepatic Injury

Ahmed¹,

Onteddu²,

Jabur³

et al. 2020

Cureus

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Drug-induced hepatotoxicity is a major cause of acute liver failure (ALF) in the United States. There are many offending agents like prescription drugs and herbal remedies. However, the most common prescription medication involved worldwide is amoxicillin-clavulanate. We report an unusually delayed presentation of severe cholestatic hepatitis caused by amoxicillinclavulanate in a 20-year-old female with worsening hyperbilirubinemia that was successfully treated with corticosteroids and ursodeoxycholic acid (UDCA).

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Acute cholestatic hepatitis caused by amoxicillin/clavulanate

Cited by 15 publications

References 14 publications

Drug-induced liver injury

Drug-induced liver injury

The chemical, genetic and immunological basis of idiosyncratic drug–induced liver injury

Delayed Presentation of Drug-Induced Hepatic Injury

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