Rashes

Can You Identify These Rashes?

Volume 44 - Issue 8 - August 2004

Case 1: A 78-year-old man presents with an asymptomatic acute eruption on both legs that extends from the ankles to just above the knees. Individual macules range from 4 to 10 mm in diameter and from light brown to red. Almost all of the lesions have multiple, tiny, discrete red puncta.
                                   
To what would you attribute this rash?

Case 1: This eruption is classic for Schamberg disease, a form of capillaritis. In this disorder, the smallest and most superficial blood vessels become inflamed and leak red blood cells. The underlying brownish color represents hemosiderin deposition from erythrocyte degeneration within the skin. The eruption is typically symptom-free, although mild pruritus may occur. Capillaritis may be idiopathic; however, it may be precipitated by ingestion of thiazide diuretics and aspirin (and less commonly other NSAIDs). Topical corticosteroids may ameliorate the condition. If an offending drug is identified, it needs to be discontinued.

This patient had started taking hydrochlorothiazide a month before the onset of the rash. After the antihypertensive agent was discontinued and 2.5% hydrocortisone lotion was applied twice daily for 4 weeks, the rash resolved.

(Case and photograph courtesy of Ted Rosen, MD.)



Case 2: Erythematous folliculocentric papules are noted on the flexor aspects above and below the elbows of a 25-year-old man. The asymptomatic lesions—seen here on the patient's right arm—are symmetric on both upper extremities and have been present for 2 and a half weeks. The patient states that his arms were recently exposed to rope fibers before the onset of this dermatitis. He takes no medications. A bacterial culture of a lesion is negative.
                                        
Do you recognize this rash?
 
             
Case 2: This rash is acneiform folliculitis. Acneiform (pustular) eruptions mimic acne but contain no comedones. The eruption may be caused by a host of drugs, including bromides; hormones, including adrenocorticotropic hormone and androgens; corticosteroids; oral contraceptives; iodides; isoniazid; lithium; phenobarbital; and phenytoin. Abuse of anabolic steroids also has been reported as a cause.1 In this patient, exposure to rope fibers in conjunction with heat occlusion most likely precipitated the rash. Because a bacterial infection was initially suspected before the culture results were available, oral cephalexin was prescribed. After 1 week, the patient’s condition had not improved and the antibiotic was discontinued. The standard treatment for acneiform folliculitis is an exfoliative agent and a topical antibiotic. In this patient, twice-daily applications of benzoyl peroxide and antibiotic ointment for about 7 to 10 days promptly resolved the lesions.

REFERENCE:

1. Habif TP. Clinical Dermatology: A Color Guide to Diagnosis and Therapy. 4th ed. Philadelphia: Mosby; 2004:486, 490.
(Case and photograph courtesy of Robert P. Blereau, MD.)


Case 3: For 10 years, a 45-year-old man has had a recurrent nonpruritic rash on his upper outer arms and lateral trunk. The shallow crusted ulcerations, some with scarring, arise as a small papule. The top of the lesion then ulcerates and heals, leaving brown hyperpigmentation. In the previous 6 months, similar lesions have occurred on his scalp. His mother has had a nearly identical rash for about 8 years.
What do you suspect, and how would you proceed to arrive at a diagnosis?
                          


     
                       
 Case 3: Multiple biopsies of the lesions were performed. The specimens were reviewed by a pathologist as well as a dermatologist who, after examining the patient, diagnosed dermatitis herpetiformis. Histopathologic findings pointed to a nonspecific neutrophilic vasculitis. Results of immunofluorescent studies showed no linear deposits of IgA or other immunoglobulins or complement in the basement membrane zone but revealed weak to moderate granular deposits of IgA in normal skin; these findings are suggestive of dermatitis herpetiformis. No perivascular deposits or immunoreactants were detected. Epidermal nuclear fluorescence and intercellular staining within the epidermis showed no immunoglobulins or complement. Results of serum studies with indirect immunofluorescence for epidermal antibodies and IgG and a test for endomysial IgA antibody (tissue transglutaminase) were negative. The glucose-6-phosphate dehydrogenase level and complete blood cell (CBC) count were normal. The differential diagnosis includes linear IgA dermatitis, which is usually associated with little if any pruritus, and drug-associated IgA dermatitis. Dermatitis herpetiformis is usually associated with pruritus, which this patient denied, and a subclinical gluten-sensitive enteropathy.1 The patient was treated with dapsone, 100 mg/d, and his CBC count was monitored weekly for 1 month. This regimen was repeated 2 years later. After both courses of therapy, the lesions partially resolved following the first 2 weeks of treatment, and the rash has recurred less frequently.

REFERENCE:
1. Habif TP. Clinical Dermatology: A Color Guide to Diagnosis and Therapy. 4th ed. Philadelphia: Mosby; 2004:554.
(Case and photographs courtesy of Robert P. Blereau, MD.)

Case 4: A 58-year-old man has had a generalized maculopapular dermatitis on his trunk and proximal upper extremities for 3 or 4 days. The rash is mildly pruritic.
                       
What is your clinical impression?
                                    

Case 4: Based on the clinical appearance of the rash, pityriasis roseawas diagnosed. Unlike many patients with this form of dermatitis, this patient did not have a herald patch—a round to oval maculopapular lesion that precedes the remainder of the eruption by several days. During the eruptive phase, the lesions develop mainly on the trunk and proximal extremities in a dermatomal distribution. A fine tissue paper–like scale forms within the confines of each lesion. The rash is typically self-limited.

 

Most patients have only mild pruritus. Reassurance is usually the only treatment necessary. Topical corticosteroids and oral antihistamines may be used to treat pruritus. Pityriasis rosea–like eruptions may be secondary to use of drugs, such as arsenicals, barbiturates, bismuth compounds, captopril, clonidine, gold compounds, methoxypromazine, metronidazole, and pyribenzamine.

This patient’s rash resolved spontaneously after about 6 weeks. He used diphenhydramine for the mild pruritus.

(Case and photographs courtesy of Robert P. Blereau, MD.)