Which autoantibodies are most commonly seen in Drug induced Lupus Erythematosus? How do these compare with the autoantibodies seen in idiopathic SLE?
• ANA: as in SLE, almost all patients with DILE will have a positive ANA; however, the spectrum of ANAs in DILE is much more limited than that seen in SLE. Notably, offending drugs are more likely to cause a positive ANA than symptomatic DILE. For example, procainamide causes a positive ANA in 90% of patients on the drug for over 2 years, but only 20% develop DILE.
• Antihistone antibodies: these are the most common autoantibodies in DILE but frequency and specificity vary between drugs. Most patients (95%) with symptomatic drug-induced disease due to procainamide, hydralazine, chlorpromazine, and quinidine demonstrate elevated levels of IgG antihistone antibodies. Alternatively, patients who develop DILE due to minocycline, PTU, TNFα antagonists, and statins have antihistone antibodies in fewer than 20% (minocycline) to 60% (TNFα antagonists) of patients. Note that antibodies to histones are not specific to DILE and are present in 50% to 80% patients with idiopathic SLE.
• Other autoantibodies against nuclear antigens: antibodies to dsDNA are highly specific for idiopathic SLE and rarely found in DILE, with the exception of DILE due to anti-TNFα agents or IFNα. Antibodies to Sm, RNP, Ro/SS-A, and La/SS-B are common in idiopathic SLE but are unusual or do not persist in DILE.
• Antiphospholipid antibodies: can be seen in both systemic DILE and idiopathic SLE. In systemic DILE, they occur most commonly with three drugs (chlorpromazine, procainamide, and quinidine), tend to be IgM, and are rarely associated with thrombosis.
