Drug-induced liver injury (DILI) is an adverse reaction to drugs or other xenobiotics that occurs either as a predictable event when an individual is exposed to toxic doses of some compounds or as an unpredictable event with many drugs in common use. Drugs can be harmful to the liver in susceptible individuals owing to genetic and environmental risk factors. These risk factors modify hepatic metabolism and excretion of the DILI-causative agent leading to cellular stress, cell death, activation of an adaptive immune response and a failure to adapt, with progression to overt liver injury. Idiosyncratic DILI is a relative rare hepatic disorder but can be severe and, in some cases, fatal, presenting with a variety of phenotypes, which mimic other hepatic diseases. The diagnosis of DILI relies on the exclusion of other aetiologies of liver disease as specific biomarkers are still lacking. Clinical scales such as CIOMS/RUCAM can support the diagnostic process but need refinement. A number of clinical variables, validated in prospective cohorts, can be used to predict a more severe DILI outcome. Although no pharmacological therapy has been adequately tested in randomized clinical trials, corticosteroids can be useful, particularly in the emergent form of DILI related to immune-checkpoint inhibitors in patients with cancer.

/pdf/drug-induced-liver-injury-3n62mwaml0.pdf

Drug-induced liver injury

Drug-induced liver disease can result from dosage-dependent hepatotoxicity or from adverse reactions to drugs used in therapeutic dosage. The latter idiosyncratic hepatotoxins can cause clinical syndromes that mimic all known liver diseases, so that drugs must be considered as the possible causal agent for all unexplained cases of liver disease.


The only specific antidote for dosage-dependent hepatotoxicity is N-acetylcysteine (and some other sulfhydryl donors), which is highly effective for the prevention of significant hepatotoxicity after acetaminophen overdose.


Early diagnosis and prompt withdrawal of the offending drug is the key to successful management of most drug-induced liver diseases.


The mainstay of treatment is supportive care, with careful monitoring for signs of acute liver failure or progression to chronic liver disease.


In cases of liver failure, close liaison with a liver transplant center is crucial; referral for liver transplantation should be considered if standard transplant criteria are fulfilled.


Pruritus is a major symptom of drug-induced cholestasis; protracted cases may respond to ursodeoxycholic acid.


Corticosteroids can be considered for cases of drug-induced hepatitis, especially those with evidence of immune hypersensitivity, if no improvement is seen in 8 to 12 weeks. Although there are no controlled trials, some patients may respond favorably.

Drug-Induced Liver Disease

Thiopurine-induced liver injury in patients with inflammatory bowel disease: a systematic review.

Drug-induced liver injury (DILI) is common and nearly all classes of medications can cause liver disease. Most cases of DILI are benign, and improve after drug withdrawal. It is important to recognize and remove the offending agent as quickly as possible to prevent the progression to chronic liver disease and/or acute liver failure. There are no definite risk factors for DILI, but pre-existing liver disease and genetic susceptibility may predispose certain individuals. Although most patients have clinical symptoms that are identical to other liver diseases, some patients may present with symptoms of systemic hypersensitivity. Treatment of drug and herbal-induced liver injury consists of rapid drug discontinuation and supportive care targeted to alleviate unwanted symptoms.

Drug-induced Liver Injury.

Nodular regenerative hyperplasia of the liver graft after liver transplantation

Azathioprine hepatotoxicity has been described mainly in renal transplant recipients. Most reported cases are related to lesions of the venous system of the liver: peliosis hepatis, veno-occlusive disease of the liver, perisinusoidal fibrosis, and nodular regenerative hyperplasia of the liver. The most common clinical manifestation of these hepatic vascular lesions is portal hypertension. We present a case of nodular regenerative hyperplasia and perivenous fibrosis in a patient receiving azathioprine for multiple sclerosis. Histological abnormalities were similar to those described in renal transplant patients, and azathioprine was the only potential hepatotoxic agent present.

https://gut.bmj.com/content/gutjnl/32/6/715.full.pdf

Azathioprine induced liver disease: nodular regenerative hyperplasia of the liver and perivenous fibrosis in a patient treated for multiple sclerosis.

[Acute drug-induced hepatitis: a case of acute cytolysis after ingestion of fipexide].

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Azathioprine induced liver disease: nodular regenerative hyperplasia of the liver and perivenous fibrosis in a patient treated for multiple sclerosis.

[Acute drug-induced hepatitis: a case of acute cytolysis after ingestion of fipexide].