Journal of Drugs in Dermatology - Lisinopril-induced erythroderma in an 85-year-old male
Abstract
An 85-year-old male presented with a case of erythroderma secondary to lisinopril ingestion without a previous history of skin disease. While ACE inhibitors have been shown to elicit psoriatic erythroderma in previous cases, to our knowledge this is the first case report of iatrogenic erythroderma secondary to lisinopril in a patient without dermatologic comorbidities.
Introduction
Erythroderma, or exfoliative dermatitis, is characterized by generalized or nearly generalized erythema of the skin accompanied by a variable degree of scaling. (1) Several skin disorders may ultimately present as erythroderma, but an increasing number of drugs have been incriminated as secondary causes of this extreme state of skin irritation and inflammation. (2) The adverse-effect profile of lisinopril has been extensively reviewed in the MEDLINE database, and no reports of lisinopril as a cause of erythroderma were found.
Related Results
Iron Eases Cough From ACE Inhibitors, But Poses Risk
Drug patent expiration list. (Rx/Generic Drugs).(Brief Article)
Medicure Presents New Matched Results at the American Diabetes Association’s …
Active pharmaceuticals ingredient watch. (Market: Life Sciences).(Brief Article)
Ask the Doctor - Can exercise help my failing heart pump better?
Case Report
An 85-year-old Caucasian male was referred to the dermatology clinic in July 2006 with a 4-month history of erythroderma complicated by severe pruritus (Figures 1 and 2). The patient denied any prior dermatologic conditions to include atopic dermatitis, ichthyosis, or psoriasis. Active medications at presentation included levothyroxine, aspirin, allopurinol, atenolol, lisinopril, doxepin, folic acid, and cyanocobalamin. The physical exam was remarkable for diffuse, erythematous to bronze discoloration of the skin with profuse flaking with the exceptions of the patient’s genitals and scalp. The patient had bilateral palmoplantar keratoderma with painful fissuring. Notably, he had no lymphadenopathy or islands of sparing. A review of symptoms was noncontributory and a malignancy work-up was negative to include a normal prostate-specific antigen (PSA) test, a normal chest x-ray and chest CT, a negative stool guaiac test, and a negative colonoscopy 3 years previously. A CBC count showed a white blood cell count of 8.4 (normal=4-10.5) with a mild eosinophilia of 8.2% (normal=0-6%). A manual differential was without Sezary cells. Results from a thyroid stimulating hormone (TSH) blood test was within normal limits. Two punch biopsies were done several months apart and both revealed a spongiotic dermatitis with a superficial lymphohistiocytic perivascular infiltrate with scattered eosinophils (Figure 3).
On the initial visit, the patient denied starting any new medications prior to developing his rash, but on subsequent visits he was not as certain. The only medication he claimed he had been on longer than a year was atenolol. After conferring with his primary care physician, we asked him to discontinue his lisinopril and allopurinol. However, on follow-up 6 weeks later, the patient reported that he had restarted these 2 medications after only 3 weeks because his rash had not resolved, although he admitted it did mildly improve. The patient was again instructed to discontinue the allopurinol preferably for 4 to 6 months. After an extensive literature search, it was decided not to discontinue the lisinopril because no previous reports of lisinopril causing erythroderma were found in contrast to several references citing allopurinol as a definitive etiology of erythroderma.
Over the next 5 months the patient failed to improve. In addition to discontinuation of allopurinol, treatments included topical and intralesional steroids, emollients, antihistamines, and narrow band ultraviolet B (UVB) treatment for 3 months followed by ultraviolet A1 (UVA1) (20 J/[cm.sup.2]) for 2 months. Aside from temporary improvement following an intramuscular injection of 60 mg of Kenalog[R], the patient never demonstrated significant improvement.
After determining allopurinol was not the causative factor in this case, the lisinopril was discontinued. Within 2 to 3 weeks, the patient noticed improvement. At follow up 2 months later, the patient had almost complete resolution with only mild erythema present on the trunk and proximal extremities and without pruritus or exfoliation (Figure 1c). The patient declined a rechallenge of the medication for confirmation.
Discussion
Erythroderma represents an extreme state of skin irritation involving the whole or most of the skin surface which could be life-threatening, especially in the elderly. (3) The mean age of onset ranges from 55 to 65 years and 60% to 92% of patients are males. Apart from scaling and erythema, pruritus is the most common clinical finding followed by fever and lymphadenopathy. (1,3) Involvement of the palms and soles is common, (1) and patients may experience hair loss, onycholysis, and nail shedding. (4) Shivering and chills due to excessive vasodilation and loss of body heat often occur. (4) Systemic complications include infection, fluid and electrolyte imbalances, thermoregulatory disturbance, high output cardiac failure, acute respiratory distress syndrome, and gynecomastia. (5)
[FIGURE 1 OMITTED]
[FIGURE 1 OMITTED]
Determining the etiology of erythroderma can be a challenge, but is an important undertaking because it can effect treatment and prognosis. Erythroderma can result from the exacerbation of a preexisting dermatosis, an adverse drug reaction, a cutaneous or systemic malignancy, and it can also be idiopathic, sometimes referred to as “red man syndrome.” (2) In more than half of patients, the etiology is attributable to an exacerbation of a preexisting dermatosis5 including psoriasis, atopic dermatitis, pityriasis rubra pilaris, chronic actinic dermatitis, and congenital ichthyosiform erythroderma. (6) Topical and systemic medications are notorious for precipitating erythroderma and an apparent increase in the incidence of the disease may be directly proportional to the introduction of new drugs. (2) Drug induced erythroderma is sudden and rapid in onset and its resolution is typically faster than cases of erythroderma due to other causes. (5)
