Editor's Note: Drug-induced autoimmune hepatitis, as a new and complex disease phenotype, has received widespread attention in recent years. On May 25, 2024, at the "8th International Forum on Drug-induced Liver Injury" in Malaga, Spain, Professor Raul J. Andrade of the Malaga Biomedical Research Center at the University of Malaga delivered a fascinating lecture on drug-induced autoimmune hepatitis. Our journal had the privilege of conducting an exclusive interview with Professor Andrade, delving into the specific characteristics of the disease, diagnostic challenges, treatment strategies, and future research directions. We have organized the content into an article, hoping to enhance clinicians' understanding of the disease, optimize patient treatment outcomes, and improve quality of life.

“Hepatology Digest”: Drug-induced autoimmune hepatitis, as a new phenotype, what are its characteristics? How does it differ from traditional drug-induced liver injury?

Professor Andrade: Drug-induced autoimmune hepatitis has gradually been recognized as a phenotype in recent years. There is currently no consensus on its definition. Generally speaking, drug-induced autoimmune hepatitis manifests as DILI (drug-induced liver injury) with typical autoimmune features, such as elevated autoantibody titers or abnormal IgG levels, after exposure to certain drugs. It also exhibits histological features similar to classic autoimmune hepatitis on liver biopsy. However, not all cases will present all these features.

“Hepatology Digest“: What challenges does the diagnosis of drug-induced autoimmune hepatitis face in clinical practice? How do you think its diagnostic accuracy can be improved?

Professor Andrade: Currently, there is no widely accepted standard for the diagnosis of drug-induced autoimmune hepatitis. Diagnosis is mainly based on the patient’s history of drug exposure and the presence of some but not all typical features of autoimmune hepatitis. In addition, the patient’s response to glucocorticoid therapy, especially the absence of relapse after discontinuation, is also an important diagnostic criterion. Therefore, improving diagnostic accuracy requires a comprehensive consideration of clinical manifestations, biochemical characteristics, drug exposure history, and response to treatment.

“Hepatology Digest”: Which drugs are most likely to cause drug-induced autoimmune hepatitis? Are there specific patient populations or risk factors that are more susceptible to this effect?

Professor Andrade: Some drugs, such as antibiotics (nitrofurantoin, minocycline), antihypertensive drugs (methyldopa), and biologics (infliximab), are clearly associated with drug-induced autoimmune hepatitis. Statins are also considered relatively common causes. Long-term use of these drugs may be one of the risk factors. In addition, if a patient has experienced a DILI event with one drug and subsequently experiences a DILI event with a different drug, or if the patient has another autoimmune disease, these situations may increase the risk of drug-induced autoimmune hepatitis.

“Hepatology Digest”: What are the effective treatment strategies for drug-induced autoimmune hepatitis? In recent years, what significant advances or new treatment methods have emerged in treatment?

Professor Andrade: The treatment strategy for drug-induced autoimmune hepatitis is similar to that for classic autoimmune hepatitis, mainly relying on immunosuppressive therapy, especially the use of glucocorticoids. After symptoms are relieved, attempts are made to completely discontinue immunosuppressive therapy within 3-6 months and observe whether the patient fully recovers without relapse. There have been no new treatment methods emerging so far.

“Hepatology Digest”: In your opinion, what directions should research on drug-induced autoimmune hepatitis focus on in the future? How will these research findings be applied in clinical practice to improve patient treatment outcomes and quality of life?

Professor Andrade: This is a difficult question to answer. It is certain that strengthening international cooperation in this field is extremely important. We need to collect confirmed cases of drug-induced autoimmune hepatitis from different regions around the world, including Western countries, Asia, Latin America, etc., to observe how the etiology of drug-induced autoimmune hepatitis varies by region. Future efforts should focus more on prospective studies, defining patient phenotypes more accurately through international cooperation and collecting a sufficient number of cases. These efforts will help formulate more effective treatment strategies and may avoid unnecessary long-term use of immunosuppressive therapy, thus improving patient quality of life and treatment outcomes.