Understanding drug-induced lupus erymatosus
Around 10% of systemic lupus erymatosus (SLE) cases are related to drug-induced lupus, where symptoms begin after exposure to a certain medication (Chang and Gerschwin, 2011).
The identification of the drug that causes SLE can be difficult due to delayed disease onset occurring months to years after initial drug exposure, but it is clinically very useful because symptoms will resolve after one stops taking the medication (Chang and Gerschwin, 2011).
Drug-induced lupus erymatosus (LE) can be subdivided into drug-induced SLE, drug-induced subacute cutaneous lupus erythematosus (SCLE), and drug-induced chronic cutaneous lupus erythematosus (CCLE). Drug-induced LE is linked with >80 medicines, and this number is increasing with the advent of new immunological therapies (Dalle Vedove et al., 2012a). The incubation period for start of disease varies widely and is dependent on the drug that was used.
The most common subtype of drug-induced LE is drug-induced SCLE, which commonly appears with lesions similar to idiopathic SCLE (erythematous plaques with or without scale in a photosensitive distribution).
However, the lesions tend to be limited in number and affect more often the legs (Lowe et al., 2010). The histologic findings are also similar between idiopathic and drug-induced SCLE.
Drug-induced SCLE is linked with a wide number of drugs but is most commonly seen with antifungals, antihypertensive drugs, diuretics, statins, and proton pump inhibitors (Dalle Vedove et al., 2012a; Lowe et al., 2010).
Patients with drug-induced SLE do not develop typical cutaneous LE (CLE) skin manifestations or interface dermatitis and could have nonspecific LE cutaneous manifestations instead.
More often, the affected patients usually have concurrent systemic symptoms, like fever, arthralgia, and myalgia (Chang and Gerschwin, 2011).
Drug-induced SLE is strongly linkef with a antihistone antibodies, but the characteristic serological findings of SLE, such as hypocomplementemia and positive anti-dsDNA antibodies, are less prevalent.
Chemotherapy and biologic agents, antiarrhythmics, antihypertensive medications, antipsychotics, and antibiotics are the most common precipitating medications (Dalle Vedove et al., 2012).
Drug-induced CCLE can be further divided into discoid lupus erythematosus (DLE) and lupus erythematosus tumidus (LET) subtypes, which are rare. These subtypes are associated with nonsteroidal antiinflammatory drugs, chemotherapy agents, and antitumor necrosis factor (TNF) alpha agents (Dalle Vedove et al., 2012). Drug-induced LE induced by anti-TNF alpha agents is distinct from classic drug-induced LE and occurs in an older, predominantly female population. These patients frequently have systemic symptoms, such as fever, myalgia, arthralgia, and serositis, and more commonly experience cutaneous manifestations (Chang and Gerschwin, 2011). Anti-dsDNA antibodies are often present in this group (Chang and Gerschwin, 2011; Dalle Vedove et al., 2012).