Isoniazid‐Related Secondary Drug‐Induced Autoimmune Hepatitis in a Patient Diagnosed With Ankylosing Spondylitis and Tuberculous Lymphadenitis: A Case Report

Autoimmune hepatitis is a type of chronic hepatitis that is usually progressive, has unknown etiology, and can occur at any age. In the present case, drug‐associated autoimmune hepatitis (DIAIH) was discussed, and DIAIH secondary to isoniazid (INH) was found in two case reports in the literature. We believe that our patient differs from the other two INH‐related secondary DIAIH cases in the literature in terms of presentation, follow‐up, side effects of various treatment agents, and management of complications. A 52‐year‐old White/Caucasian woman with known axial spondyloarthropathy (diagnosed in 2018 with radiographic ankylosing spondylitis, human leukocyte antigen B27, positive; history of bilateral sacroiliitis on sacroiliac magnetic resonance imaging) and active tuberculous lymphadenitis. Quantiferon analysis was positive in the biological agent treatment evaluation at follow‐up, approximately 1 year after adalimumab initiation. In her laboratory investigations, 5 × upper limit of normal hypertransaminasemia, 1.8 g gammaglobulinemia, anti‐nuclear antibody (ANA): ++++ > 1/80 titer, and perinuclear anti‐neutrophil cytoplasmic antibody: positive. A biopsy revealed mild fibrosis of the liver tissue and lymphocytic cell infiltration in the portal areas. Periportal interface hepatitis has also been observed. After the pathological findings were consistent with autoimmune hepatitis, the revised original autoimmune hepatitis scoring system was reapplied, and a score of 22 was obtained. A “definitive” diagnosis of autoimmune hepatitis was made, and the etiology of the hypertransaminasemia was established. INH‐associated DIAIH is rare. While INH‐associated systemic lupus erythematosus is more frequently encountered, INH‐associated DIAIH was found in two case reports in the literature. Notably, algorithms are not always valid, and typical clinical findings may not always be observed, especially in the autoimmune disease spectrum. Key Clinical Message ( KCM )Isoniazid can trigger drug‐induced autoimmune hepatitis (DIAIH) in genetically susceptible individuals, particularly those with pre‐existing autoimmune conditions or prior biological agent exposure. DIAIH may persist after drug withdrawal and requires immunosuppressive therapy. A high index of suspicion for autoimmune mechanisms is essential when hypertransaminasemia does not resolve after anti‐tuberculosis drug discontinuation.