Drug-induced systemic lupus erythematosus: A comprehensive review

Hossam A. Elsisi *

Department of Pharmacology and Toxicology, College of Pharmacy, Qassim University, Buraydah 51452, Qassim Province, Kingdom of Saudi Arabia.
 
Review
International Journal of Science and Research Archive, 2024, 13(02), 2954-2959.
Article DOI: 10.30574/ijsra.2024.13.2.2474
Publication history: 
Received on 04 November 2024; revised on 12 December 2024; accepted on 14 December 2024
 
Abstract: 
Drug-induced systemic lupus erythematosus (DILE) is a rare autoimmune disorder that mimics idiopathic systemic lupus erythematosus (SLE), but with a clear temporal relationship to the use of certain medications. This comprehensive review explores the mechanisms, diagnosis, and management of DILE. The condition is primarily immunologically mediated, with drugs triggering immune responses through processes such as antibody formation, T-cell activation, and oxidative stress. Genetic predispositions, including variations in drug-metabolizing enzymes, play a role in susceptibility. Drugs such as hydralazine, procainamide, and minocycline are commonly implicated in DILE, each triggering the formation of autoantibodies, particularly anti-histone antibodies. Diagnosis relies on clinical history, serological testing, and the identification of specific autoantibodies. DILE shares many clinical features with idiopathic lupus but is distinguishable by its typically milder course and absence of renal or neurological involvement. Management primarily involves discontinuing the offending drug, with symptomatic treatment using NSAIDs or corticosteroids. The prognosis is generally favorable, with most symptoms resolving after drug cessation and minimal long-term organ damage. Early recognition and intervention are essential to ensuring a positive outcome and preventing unnecessary treatments.
 
Keywords: 
Drug-Induced Lupus Erythematosus; Autoimmune Disorders; Diagnosis of DILE; Anti-Histone Antibodies; Treatment of Drug-Induced Lupus
 
Full text article in PDF: