Drug-Induced Systemic Lupus Erythematosus: A Rare Presentation of Hydralazine-Induced Lupus

Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder characterized by the production of autoantibodies directed against nuclear and cytoplasmic antigens. SLE can be induced by various medications, such as hydralazine, procainamide, isoniazid, methyldopa, chlorpromazine, quinidine, and minocycline. Hydralazine-induced lupus syndrome was first reported in 1953, and only occurs in 5-10% of patients taking hydralazine. We present a case of a 76-year-old female with a past medical history of chronic kidney disease (CKD) stage II, hyperlipidemia, primary hypertension, and type II diabetes mellitus who was initially admitted for complaints of pre-syncope. Initial chest X-ray demonstrated right lower lobe lung opacity with small pleural effusion, and computed tomography (CT) chest with intravenous (IV) contrast was negative for pulmonary emboli but showed small bilateral effusions and a small pericardial effusion. A transthoracic echo (TTE) was performed and demonstrated an ejection fraction of 65% and no signs of pericardial effusion. CBC was remarkable for pancytopenia with a notable drop in all cell lines compared to her baseline from prior admissions. Antinuclear antibody (ANA) titer elevated at 1:1280, and anti-histone titers were positive. Medication reconciliation was performed, and hydralazine was discontinued with marked improvement in her clinical course. The patient had a bone marrow biopsy performed, and the results were negative for any myeloproliferative or myelodysplastic changes. The patient was then discharged with outpatient follow-up with hematology/oncology and rheumatology.