Differentiation of hydrochlorothiazide-induced dermatitis from stasis dermatitis

Background

Thiazide diuretics, ACE inhibitors, angiotensin II receptor blockers, and calcium channel blockers are the three major classes of drugs used to treat primary hypertension.1 Hydrochlorothiazide-induced dermatitis is a rare side effect of thiazide diuretics that has a significant impact on patient morbidity and mortality. Soliciting a detailed history is essential to differentiating drug-induced dermatitis from stasis dermatitis or other causes of dermatitis.

Case presentation

A woman in her 60s with a history of hypertension and stasis dermatitis presented to her primary care clinic with a bilateral, erythematous rash involving the legs (figure 1) after a road trip consistent with stasis dermatitis. The patient denied respiratory distress, extensive sun exposure, sulfa drug allergy, or a family history of rash.

The patient was then seen by primary care and was found to have elevated blood pressure. The patient was started on 12.5 mg of hydrochlorothiazide per day and her triamcinolone was renewed. Around 1 week after initiation of hydrochlorothiazide, the patient returned to the clinic with concerns about nausea, fatigue, headache and paraesthesias in the feet. The patient’s quality of life was significantly impacted by these symptoms and included depressed mood, sleep problems, and inability to complete activities of daily living due to the painful and pruritic nature of the rash. On further investigation, the rash was seen to now extend beyond the legs to also involve the chest (figure 2) and abdomen (figure 3).

When seen in the primary care clinic, the extensive nature of the rash and accompanying fatigue raised suspicion of hydrochlorothiazide-induced dermatitis.

Differential diagnosis

Photosensitive rash and dermatitis may be caused by many conditions.

Stasis dermatitis: asking the patient about the presence of other rashes on the body elucidated the extensive nature of the rash, which had been overlooked in previous visits. Although the patient had varicosities and lichenification of the legs, it could not explain the rash on the stomach and chest or the accompanying fatigue.

Sulfa or other allergies: reviewing the patient record and asking the patient about any medication or allergies yielded no new information. The patient denied any other over-the-counter medications, natural remedies or supplements other than those listed in the patient’s chart.

Drug-induced (hydrochlorothiazide) dermatitis: evaluating the patient’s medication list and history may elucidate a pharmacological trigger for rash development. Special attention should be given to evaluate if the development of the rash coincides or falls soon after drug initiation. The initiation of hydrochlorothiazide seemed to coincide with the exacerbation of the rash. On confirmation of diagnosis, new drug sensitivities should be noted in the patient’s chart. Because the lesions do not have well-defined borders, a phototest, where the minimal dose of ultraviolet light which induced the erythema is determined, can be used to confirm the diagnosis and assess photosensitivity.

Contact dermatitis and patch test: inquiring about laundry detergents, fabric softeners, fragrances, perfumes and other products that the patient uses may highlight an environmental trigger for the rash. No new products or fragrances had been started.

Systemic lupus erythematosus: if a new drug or environmental trigger remains unlikely, a biopsy or panelantinuclear anitbody may be needed to confirm the diagnosis.

Drug-induced lupus: hydrochlorothiazide can cause drug-induced lupus. When considering the patient’s systemic symptoms, antinuclear anitbody, anti-smith, anti-histone, double stranded DNA, SSA and SSB antibodies should be considered if further work-up is needed.

Id eruption/autoeczematisation: autoeczematisation is an acute disseminated eczematous reaction associated with stasis dermatitis that erupts after a stimulus; our patient with primary contact stasis dermatitis would increase suspicion of the diagnosis. Eczematous dermatitis spreads to previously uninvolved sites. Diagnosis is mostly based on history and clinical manifestation, but concurrent contact dermatitis patch testing and rarely biopsy that demonstrates acute eczematous skin manifestations, can confirm the diagnosis.

Delayed drug hypersensitivity: some patients may develop drug sensitivities to medications that they have been taking for years. In this situation, the clinician may try switching to another class of drugs and assess if the rash resolves. New drug sensitivities should be noted in the patient’s chart.

Treatment

The patient was told to stop the hydrochlorothiazide, begin 20 mg of Lasix (furosemide), and wait 10 days. The patient was given enough triamcinolone steroid cream for relief during this trial period.

Outcome and follow-up

Three weeks later, the patient confirmed the complete resolution of the rash, fatigue, pain and pruritus.