Photosensitive drug eruptions occur with the combination of a sensitizing drug and ultraviolet (UV) exposure.

Photosensitive drug eruptions may be less common in skin of color because of the relative photoprotection provided by the melanin especially in darker skin types. However, when photosensitive drug eruptions do occur, they present unique challenges for the practitioner educating parents and patients with skin of color. Many patients (especially those with darker skin types) may not have been accustomed during their lives to practicing photoprotection. In general studies not particularly related to drug photosensitivity, parental use of photoprotective measures was directly related to children’s sun protection practices [9]. The most common photosensitizing drugs are antibiotics (especially tetracycline family), isotretinoin, thiazide diuretics, amiodarone [10], NSAIDs, antidepressants, psoralens, and voriconazole [11]. Some photosensitivity can also be seen as a side effect of topical retinoid use.

Photosensitive drug eruptions have erythema and papules in a photodistributed pattern. In richly pigmented skin, the erythema can be more difficult to appreciate (Fig. 35.3).

Withdrawal of the offending drug is the initial step for treatment. Sun avoidance and/or use of sunscreen are recommended especially if the drug is felt to be essential and is continued. Topical or oral corticosteroids can provide additional relief.

Once the offending drug is withdrawn and UV exposure is avoided, the eruption typically improves.

Determination of factors which predispose individuals to photosensitive drug eruptions is essential for minimizing these reactions.

Avoidance of UV exposure is important for a child with a photosensitive drug eruption.

Erythema multiforme minor (EM) is an immune-mediated condition which can occur in response to infectious or pharmacologic inciting agents. The minor designation denotes no mucous membrane involvement.

The most common associated infectious agent in children is herpes simplex virus, although causation from Mycoplasma pneumonia infection has been reported [12]. The most common pharmacologic agents associated with EM minor include nonsteroidal anti-inflammatory drugs (NSAIDs), anticonvulsants, and antibiotics. The incidence of EM in skin of color is the same as the general population.

The “target” lesion is the most well-known lesion of EM. It consists of a “dusky” center (from epidermal necrosis) with an annular edematous surround (Fig. 35.4). EM lesions are most often located on the extensor extremities, but can occur on any area of the body. The “multiforme” designation of the term refers to changing appearances of the lesions (not to any movement of the lesions).

If the EM is due to Herpes Simplex virus, antivirals such as acyclovir are recommended [12]. Withdrawal of any offending pharmacologic agent is indicated as an initial measure. Topical corticosteroids have been reported as useful. The use of systemic corticosteroids remains controversial [12].

EM minor has a good prognosis; however, in skin of color, postinflammatory dyspigmentation may occur.

Continued vigilance for associations of erythema multiforme minor with new medications as they are released is warranted.

Erythema multiforme minor is a hypersensitivity reaction which can be triggered by infectious agents or drugs.

DRESS syndrome, aka drug reaction with eosinophilia and systemic symptoms, is a drug reaction with characteristic features. Other terms which have been applied are: (a) Drug-induced hypersensitivity syndrome and (b) Phenytoin hypersensitivity syndrome.

Phenytoin had been the medication most often associated with DRESS; however, other medications have since been identified as causative agents. Those medications include anticonvulsants, antidepressants, antihypertensives, antimicrobials, antivirals, biologics, and nonsteroidal anti-inflammatory agents (NSAIDs) [13].