Drug-induced liver injury (DILI) is now a serious public health problem. Simple, objective and specific diagnostic indexes and treatment methods are still missing for DILI due to its complex pathogenesis. 

In managing DILI, discontinuation of suspicious drug or medicine serve as the initial step, but treatments including drugs and supporting approaches are required. Considering clinical patterns and disease severity grades of DILI, the treatment drugs were deemed to summarize into hepatoprotective drugs (N-acetylcysteine and Glutathione, Glycyrrhizin acid preparation, Polyene phosphatidylcholine, Bicyclol, Silymarin), anticholestatic drug (Ursodeoxycholic acid, S-adenosylmethionine, Cholestyramine), immunosuppressants (Glucocorticoids) and specific treatment agents (L-carnitine, Anticoagulants). 

Pharmacological therapy of DILI lacks normative guidance or guidelines. There is usually a complete or near-complete resolution of DILI within some days to weeks after offending drug withdrawal. The initiating point of protective drugs intervention remains difficult to choose. Hence, active monitoring of liver biochemical parameters is recommended by all clinical practice guidelines. According to the type of target cells injured, patients reveal different clinical phenotypes of DILI with a distinction in liver biochemical indicators. 

 NAC, MgIG, PPC, bicyclol, silymarin are conceivable hepatoprotective drugs for DILI. Among anticholestatic drugs, UDCA, SAMe, cholestyramine have shown therapeutic value for DILI. LC is advised for liver injury caused by VPA. GCs is suited for patients with apparent hypersensitivity or autoimmune symptoms and no noticeable improvement in liver biochemical indicators after withdrawal. Anticoagulants, like low-molecular-weight heparins and defibrotide, have key roles in some particular types of DILI (eg. PA-HSOS, etc.). They could furnish a reference for the selection and mixed application of protective drugs for different clinical phenotypes of DILI. However, the definite therapeutic effects of these drugs still need to be proven by prospective randomized and controlled studies.

The commencement of DILI is a complex process, and its pathogenesis has become a topic of research interest in recent years. Arising therapeutic interventions for DILI enclose gene therapy, nano-therapy, structural modification of toxic drugs, etc like the crucial effect of C-X-C motif chemokine ligand-9 (CXCL9) in APAP-induced liver injury was documented recently. 

Delivering inhibitors of inflammatory cytokines, apoptosis and other cellular events leading to liver cell necrosis and death directly to hepatocytes or other substructures to prevent DILI is an appealing option for the future.

SOURCE- Front Pharmacol. 2022;12:806249. Published 2022 Jan 5. doi:10.3389/fphar.2021.806249