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Drug eruptions can mimic a wide range of dermatoses. The morphologies are myriad and include morbilliform (most common, see image below), urticarial, papulosquamous, pustular, and bullous. Medications can also cause pruritus and dysesthesia without an obvious eruption.
Morbilliform drug eruption.
A drug-induced reaction should be considered in any patient who is taking medications and who suddenly develops a symmetric cutaneous eruption. Medications that are known for causing cutaneous reactions include antimicrobial agents, nonsteroidal anti-inflammatory drugs (NSAIDs), cytokines, chemotherapeutic agents, anticonvulsants, and psychotropic agents.
Prompt identification and withdrawal of the offending agent may help limit the toxic effects associated with the drug. The decision to discontinue a potentially vital drug often presents a dilemma.
Next Section: Pathophysiology
The first step is to review the patient's complete medication list, including over-the-counter supplements. Document any history of previous adverse reactions to drugs or foods. Consider alternative etiologies, especially viral exanthems and bacterial infections. Exanthematous eruptions in children are more likely to be due to a viral infection than another infection; however, most such reactions in adults are due to medications.
Note any concurrent infections, metabolic disorders, or immunocompromise (eg, due to HIV infection, cancer, chemotherapy) because these increase the risk of drug eruptions. Immunocompromised persons have a 10-fold higher risk of developing a drug eruption than the general population. Although HIV infection causes profound anergy to other immune stimuli, the frequency of drug hypersensitivity reactions, including severe reactions (eg, TEN), is markedly increased in HIV-positive individuals. Patients with advanced HIV infection (CD4 count < 200 cells/µL) have a 10- to 50-fold increased risk of developing an exanthematous eruption to sulfamethoxazole.
Note and detail the following:
All prescription and over-the-counter drugs, including topical agents, vitamins, and herbal and homeopathic remedies
The interval between the introduction of a drug and onset of the eruption
Route, dose, duration, and frequency of drug administration
Use of parenterally administered drugs, which are more likely than oral agents to cause anaphylaxis
Use of topically applied drugs, which are more likely than other drugs to induce delayed-type hypersensitivity reactions
Use of multiple courses of therapy and prolonged administration of a drug, which can cause allergic sensitization
Any improvement after drug withdrawal and any reaction with readministration
History and physical examination are often sufficient for diagnosing mild asymptomatic eruptions. Severe or persistent eruptions may require further diagnostic testing, as follows:
Biopsy can be helpful in confirming the diagnosis of a drug eruption (eg, by showing eosinophils in morbilliform eruptions or numerous neutrophils without vasculitis in persons with Sweet syndrome).
CBC count with differential may show leukopenia, thrombocytopenia, and eosinophilia in patients with serious drug eruptions.
Serum chemistry studies may be useful. Liver involvement leading to death can occur in persons with hypersensitivity syndromes. Special attention should be paid to the electrolyte balance and renal and/or hepatic function indices in patients with severe reactions such as SJS, TEN, or vasculitis.
Antibody and/or immunoserology tests may be ordered. Antihistone antibodies are noted in persons with drug-induced SLE, whereas anti-Ro/SS-A antibodies are most common in persons with drug-induced SCLE.
Direct cultures may be needed to investigate a primary infectious etiology or secondary infection.
Urinalysis, stool guaiac tests, and chest radiography are important for patients with vasculitis.
The ultimate goal is always to discontinue the offending medication if possible. Individuals with drug eruptions are often the most ill patients taking the most 