Introduction: Autoimmune hepatitis (AIH) is an immune-mediated inflammatory liver disease with a highly variable clinical presentation ranging from mildly abnormal liver tests to fulminant liver failure. Symptoms can vary and are not limited to nausea, vomiting, and anorexia. It is difficult to discern an inciting culprit for AIH, but it may be triggered by infections, environmental factors, and medications. The most common medications reported to induce AIH are nitrofurantoin and minocycline. Non-steroidal anti-inflammatory drug (NSAID)- induced AIH is less frequently reported. In this case report, we describe a rare presentation of drug-induced AIH from the NSAID meloxicam.
Case Description/Methods: A 33-year-old female with history of obesity and rheumatoid arthritis presented for symptoms of abdominal pain, fatigue, nausea, and non-bloody emesis for one month. She denied alcohol or drug abuse, liver disease, and recent herbal supplements. Medications included meloxicam for one year prior and tizanidine. Physical exam was unremarkable. Labs were remarkable for severe transaminitis (table 1), elevated immunoglobulin G (IgG), positive ANA. Liver biopsy revealed periportal and pericentral lymphoplasmacytic inflammatory infiltrate associated with interface hepatitis and marked hepatocyte dropout. Meloxicam was discontinued and the patient received IV N-acetylcysteine and prednisone taper. Follow up in clinic showed significant improvement of patient’s labs, symptoms, and resolution of her IgG autoantibody.
Discussion: Early diagnosis of DI-AIH, as well as distinguishing it from other forms of acute liver injury, is important because DI-AIH is responsive to immunosuppressive therapy, and early initiation of treatment can obviate the need for liver transplantation. Some distinguishing factors of DI-AIH include resolution of transaminitis after discontinuation of the offending agent, and lower duration of treatment required without relapse. To our knowledge, there are very few case reports describing meloxicam induced-AIH. However, a retrospective cohort did report that most DI-AIH cases were due to nitrofurantoin (67%), followed by NSAIDS (17%). NSAIDs are more frequently associated with this disease process than previously considered and should be on the differential when posed with acute liver injury. This would allow early identification and management of affected patients, and may prevent chronic liver injury progression and the need for liver transplantation.
