PATIENT HISTORY
A 36-year-old White woman with a history of hypertension presents to clinic with numerous severely pruritic, confluent, erythematous, edematous papules and plaques affecting her chest and bilateral dorsal arms for the past month with the exception of her left wrist where she wore a wrist watch (Figure 1). She had no known exposures or contact with potentially sensitizing products, and she reports no past history of similar breakouts. She started a new medication 1-2 months before developing the rash.
MULTIPLE-CHOICE QUESTION
Often, medication can be the cause of pruritic dermatitis such as the patient who presented in our clinic. Which of the following medications is most likely to have caused a sensitivity reaction in our patient?
A. Escitalopram
B. Cetirizine
C. Hydroxyzine
D. Hydrochlorothiazide
Answer:
D. Hydrochlorothiazide
DISCUSSION
Thiazide diuretics are a common cause of photosensitivity reactions, with an estimated frequency between 1 and 100 per 100,000 patients (Gomez-Bernal et al., 2014). This patient started taking hydrochlorothiazide 1-2 months before developing a photodistributed lichenoid drug eruption (LDE). Thiazide-induced light eruptions can exhibit a variety of clinical manifestations including sunburn-like reactions, eczematous changes, photo-onycholysis, pseudoporphyria, and lichenoid reactions, such as in this clinical example (Gomez-Bernal et al., 2014). Other drugs associated with LDEs include certain nonsteroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, penicillamine, antimalarial drugs, beta-blockers, and sulfonylurea agents (Ellgehausen, Elsner, & Burg, 1998).
LDE is similar histologically and clinically to idiopathic lichen planus (O'Connor, Flynn, Crowther, Tobin, & Connolly, 2017). Compared with lichen planus, lichenoid photosensitivity reactions are symmetrical and sharply demarcated, typically on sun-exposed areas such as the extensor surfaces (vs. the flexor, volar surfaces classically seen in lichen planus) with zones of clearance in areas of skin shielded by clothing and jewelry, as seen in this patient who has an area of sparing on her left wrist that was covered by her watch (Figure 1). In addition, Wickham striae are normally absent in LDEs, and mucous membranes are generally spared (Brauer, Botava, Meehan, & Soter, 2009).
The exact pathogenesis of LDE is unknown, but there is evidence that it is a T-cell-mediated phenomenon (Lage, Juliano, Metze, de Souza, & Cintra, 2012). The diagnosis ideally should be confirmed via phototesting or with a challenge-rechallenge test, but that is often not practical. Therefore, the diagnosis is commonly made clinically after reviewing the patient's drug intake history (Collazo, Sanchez, & Figueroa, 2009). The time between starting the offending medication and developing the cutaneous eruption ranges from a couple of weeks to several years, but most patients become symptomatic within a few months (Ellgehausen et al., 1998).
The mainstay of treatment for patients with suspected LDE is stopping the offending medication. If withdrawing the drug is not possible, patients must practice diligent sun protection (Dawe & Ibbotson, 2014). Of note, the rash may persist for several weeks or months after discontinuing the medication, and many patients experience residual postinflammatory hyperpigmentation (Brauer et al., 2009; Collazo et al., 2009). Other treatments include oral antihistamines and topical corticosteroids to help alleviate symptoms such as pruritus. Alternative therapies for refractory lesions include oral corticosteroids and retinoids (Ellgehausen et al., 1998).
REFERENCES