Drug-Induced Lupus

Drug-induced lupus shares several clinical and serologic features with SLE but is due to ongoing exposure to a drug and resolves when the offending drug is discontinued. In contrast to SLE, the sex ratio is nearly equal.

Diagnostic Essentials

• Symptomatic during exposure to offending drug; symptoms resolve when drug is stopped.
• Unlike in SLE, kidney involvement is unlikely.
• Elevated ANA but unlikely to have anti-DNA antibodies unless secondary to TNF inhibitors.

Clinical Findings

As a general rule, drug-induced lupus presents with fever, arthralgia, myalgia, and serositis but not kidney involvement, neurologic symptoms, or other features of SLE.

Serologic testing reveals elevated titers of antinuclear antibodies in all patients, but antibodies to DNA, Sm, RNP, SS-A, and SS-B are rare.

Antibodies to histones occur in up to 95% of patients but also are seen in SLE and thus do not distinguish drug-induced lupus from SLE; the absence of anti-histone antibodies, however, make either diagnosis unlikely.

Complement levels are usually normal.

The list of drugs implicated as possible causes of drug-induced lupus in observational studies and case reports is extensive. There are definite associations between the development of drug-induced lupus and the use of hydralazine, isoniazid, and minocycline as well as several less commonly prescribed drugs (procainamide, methyldopa, chlorpromazine).

The incidence of drug-induced lupus in patients taking hydralazine for a year or longer is as high as 5–8%; for most other medications, the risk is considerably lower (less than 1%).

TNF inhibitors can induce antibodies to DNA but usually not anti-histone antibodies; the incidence of lupus-like syndromes resulting from these medications is low (0.5–1%).

Management

Drug-induced lupus generally resolves within weeks to months after discontinuing the offending agent.