Anti-tumour necrosis factor agent and liver injury: Literature review, recommendations for management

Abstract

Abnormalities in liver function tests, including transient and self-limiting hypertransaminasemia, cholestatic disease and hepatitis, can develop during treatment with anti-tumour-necrosis-factor (TNF) therapy. The optimal management of liver injury related to anti-TNF therapy is still a matter of debate. Although some authors recommend discontinuing treatment in case of both a rise of alanine aminotransferase more than 5 times the upper limit of normal, or the occurrence of jaundice, there are no standard guidelines for the management of anti-TNF-related liver injury. Bibliographical searches were performed in PubMed, using the following key words: inflammatory bowel disease (IBD); TNF inhibitors; hypertransaminasemia; drug-related liver injury; infliximab. According to published data, elevation of transaminases in patients with IBD treated with anti-TNF is a common finding, but resolution appears to be the usual outcome. Anti-TNF agents seem to be safe with a low risk of causing severe drug-related liver injury. According to our centre experience, we found that hypertransaminasemia was a common, mainly self-limiting finding in our IBD cohort and was not correlated to infliximab treatment on both univariate and multivariate analyses. An algorithm for the management of liver impairment occurring during anti-TNF treatment is also proposed and this highlights the need of a multidisciplinary approach and suggests liver biopsy as a key-point in the management decision in case of severe rise of transaminases. However, hepatic injury is generally self-limiting and drug withdrawal seems to be an exception.

Protective Effect of Infliximab, a Tumor Necrosis Factor-Alfa Inhibitor, on Bleomycin-Induced Lung Fibrosis in Rats

“…[24]. There is convincing evidence that ROS play a major role in mediating structural cell apoptosis, lipid peroxidation, and upregulating pro-inflammatory cytokine synthesis such as TNF-α and IL-6 [34] which in turn, increases pulmonary endothelial permeability, subsequently extravasation and cytotoxicity of inflammatory cells and tissue injury [35].…”

Potential Clinical Targets in Hepatopulmonary Syndrome: Lessons From Experimental Models

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Monitoring ankylosing spondylitis: clinically useful markers and prediction of clinical outcomes

“…In case of a suspicious TB infection, diagnostic work up according to local guidelines, for example, with tuberculin skin tests, IFN-g release assays or chest x-rays, sometimes microbiologic examination of bronchial fluids is mandatory. As anti-TNF therapy may cause liver injury (transient and self-limiting hypertransaminasemia, cholestatic disease or hepatitis, rarely severe liver injury) [97] or neutropenia [98], liver enzymes and a blood cell count should be measured regularly. One has to bear in mind that patients with low neutrophil counts at baseline and a history of neutropenia are at a higher risk for developing neutropenia under anti-TNF therapy [98] and should be monitored very carefully.…”