Primary prevention
As paracetamol hepatotoxicity is one of the leading causes of ALF, efforts to prevent unintentional overdose may translate into reductions in cases of ALF. Actions that could prevent ALF include patient, pharmacy, and physician education to avoid prescribing multiple paracetamol-containing preparations and to avoid exceeding maximum daily recommended dosing of paracetamol. Methods to restrict access to paracetamol have been used in Europe with significant reductions of hospital admissions, liver transplants, and deaths associated with paracetamol overdose.[14]
Immunisation for hepatitis A and B is currently recommended for all infants in the US.[47] Immunisation strategies for patients with chronic liver diseases to receive hepatitis A and B vaccines may prevent acute superinfection with these viruses and risk of an acute fulminant course.
Secondary prevention
Guidelines from the American Association for the Study of Liver Diseases (AASLD) emphasise that early detection may prevent drug-induced liver injury (DILI) from becoming symptomatic or severe.[30] Monitoring protocols for drugs with a high likelihood of causing hepatotoxicity (e.g., isoniazid, methotrexate, cancer immunotherapies) should be followed. Patients should be encouraged to report possible symptoms of DILI to their healthcare provider. Further information for healthcare providers, including drug surveillance recommendations and relative likelihood of causing DILI, is available at LiverTox and DILIrank Dataset (Food and Drug Administration). NIH: LiverTox Opens in new window FDA: Drug induced liver injury rank (DILIrank) dataset Opens in new window Prompt initiation of treatment for paracetamol overdose, including administration of acetylcysteine therapy, significantly reduced the risk of DILI.[30] The AASLD also emphasises on recognition of ALF due to Wilson's disease so that other first‐degree relatives may then be screened for this disorder, thus preventing liver failure or death from Wilson's disease in these individuals.[43]
In hepatitis B surface antigen carriers with surface antigen positivity who undergo treatment with cancer chemotherapy, B-cell depleting agents such as rituximab, long-term corticosteroids, tumour necrosis factor-alpha inhibitors, or other forms of immunosuppression, prophylactic antiviral therapy should be initiated at the onset of pharmacotherapy and continued for at least 6 months following completion to prevent acute reactivation of hepatitis B and a potential risk of ALF.[142][143] Antiviral prophylaxis may also be considered in those with resolved infection, characterised by a positive antibody to hepatitis B core antigen and negative hepatitis B surface antigen, in which the risk of reactivation exists with increasing levels of immunosuppression.[144] Nearly 20% of hepatitis B virus (HBV)-associated ALF cases enrolled in the US Acute Liver Failure Study Group from 1998 to 2015 occurred in the setting of HBV reactivation following immunosuppressive therapy.[41]
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