Definition and Epidemiology

Dermatitis medicamentosa (drug eruption) is an eruption of the skin or mucous membranes that can occur within 1 hour and up to 2 weeks after drug administration. These eruptions imitate almost all of the morphologic variations in dermatology, including exanthems, urticaria, photosensitivity, fixed drug reactions, palpable purpura, bullae, alopecia, onycholysis, acral erythema, lichenoid and acneiform lesions, lupus erythematosus–like lesions, toxic epidermal necrolysis, and erythema multiforme syndrome. Maculopapular exanthema is the skin eruption that is most commonly induced by a wide range of drugs.¹

Drug eruptions may occur at any age, are more common in women, and are the most common form of drug sensitivity reactions.² Three percent of hospitalized patients experience a drug reacton,³ with elders at increased risk because of the high number of medications typically taken by individuals in this age group.⁴ There is a concern about underdiagnosis because of under-reporting, and also over-reporting because of the overuse of the term allergy. Specific skin testing, often not available or necessary, is the only way to distinguish a true allergy from a drug reaction, so the most recent terminology refers to both as drug hypersensitivity reactions (DHRs).

Immediate emergency department referral or physician consultation is indicated for anaphylaxis, severe erythema multiforme, or Stevens-Johnson syndrome.

Pathophysiology

Drug eruptions are hypersensitivity manifestations of immunologic (immunoglobulin E–dependent) or nonimmunologic (T-cell–mediated) mechanisms stimulated by oral, topical, or parenteral drug administration.⁵ Immunologic responses (true allergies) occur when specific antibodies or specifically sensitized lymphocytes to a drug develop during the sensitization period, which may be 4 or 5 days after initial exposure. Subsequent exposure to the drug results in a reaction that may occur within minutes, hours, or days.

Nonimmunologic responses, the most commonly occurring condition, may be caused by cumulative accumulation of a drug, pharmacologic action of a drug, individual genetic predisposition, drug sensitization of the skin producing reaction with exposure to ultraviolet light, increased sensitivity to irritating topical solutions, and other factors, such as individual immune status.⁵ Hypersensitivity reactions to antibacterial agents (mostly penicillin), aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs), and protease inhibitors are examples of the last, involving maculopapular rashes and urticaria.⁵

Protease inhibitors, antibiotics, and chloroquine may cause acute generalized exanthematous pustulosis (AGEP). A very rare reaction, AGEP manifests with onset of acute clinical symptoms, including temperature higher than 38° C (100.4° F) and widespread exfoliative dermatitis after a pustular, morbilliform eruption that heals within 15 days of discontinuation of the medication.⁶

Clinical Presentation

Patients may come in for an office visit with a variety of skin reactions (itching, burning, pain), with or without rash (Table 51-1). The most common is a confluent, maculopapular rash that may be pruritic (Fig. 51-1). Knowledge about onset, progression of symptoms, fever, recent medication change, and family history is essential. Onset can occur 7 to 10 days after the drug is started but may not occur until the course of medication is finished. The rash can last 1 to 2 weeks and then fade. The rash may also be urticarial (always highly suggestive of drug reaction) or a fixed drug reaction that occurs in the same area each time the drug is taken.⁷

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