Erythematous truncal plaques
A 17-year-old male was referred to the dermatology service for a pruritic scaly rash over his trunk and extremities. The eruption, which had first appeared eight months earlier, was not responding to superpotent topical steroids. Numerous erythematous scaly plaques were visible on his chest, abdomen, back, axillae, and extremities. No one in the patient's family had a similar skin condition. He reported that he had two cats. A KOH skin scraping of the abdominal plaque revealed numerous branching hyphae.
The patient, a 42-year-old man, complained of a mildly pruritic rash that had been present for 15 years on his abdomen, chest, lower back, elbows, and knees. Physical examination revealed numerous well-demarcated erythematous scaly plaques with overlying silvery scale. No family history of skin problems was reported. Mid-potency topical steroids alternating with topical calcipotriene had yielded mild improvement over the past few years, but the patient was looking for better control of his condition.
What is the diagnosis?
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CASE #1: Tinea incognito
The atypical lesions referred to as tinea incognito are the result of morphologic changes induced by topical corticosteroid treatment of tinea corporis. The changes may include loss of the raised, scaly, advancing border that is characteristic of tinea corporis lesions and a more widespread eruption.
A superficial dermatophyte infection, tinea corporis can involve the skin of the trunk and extremities, while excluding the scalp, beard area, face, hands, feet, and groin. Commonly seen in tropical regions, tinea corporis can be found worldwide. Its most common global cause is Trichophyton rubrum, followed by Trichophyton mentagrophytes; however, tinea corporis can be caused by any of the dermatophytes. The organisms are transmitted from human to human, animal to human, or soil to human. Domestic animals are common carriers of the zoophilic dermatophyte species.1
Tinea corporis is most commonly characterized by one or more circular, slightly scaly, erythematous plaques with central clearing and a prominent advancing edge, creating an annular outline and leading to the lay term “ringworm.” These lesions are generally associated with pruritus or burning. Widespread lesions of tinea corporis can occur in immunodeficient states and may be the presenting sign of AIDS.2
Tinea corporis can mimic many dermatoses, including nummular eczema, contact dermatitis, psoriasis, granuloma annulare, parapsoriasis, and pityriasis rosea. The atypical appearance of tinea incognito is more likely than classic tinea corporis to be confused with other entities, and not uncommonly, biopsy of a chronic refractory dermatosis will reveal tinea incognito.2
Classic lesions of tinea corporis can be easily recognized clinically; however, the diagnosis can be easily confirmed by visualizing fungal elements microscopically in skin scrapings.2 Microscopic examination is performed by scraping scale from the lesion onto a glass slide with either a scalpel blade or the side of another glass slide. A 10% KOH solution is added to the scrapings to dissolve cellular components while leaving fungal hyphae intact. This process can be accelerated by gently heating the slide with a flame. The slide is covered with a cover slip and viewed under the microscope. The presence of fungal hyphae is considered a positive result. Additionally, tinea corporis and tinea incognito may be diagnosed with fungal culture or skin biopsy using appropriate fungal stains.
Localized lesions of tinea corporis can be treated with topical antifungals once or twice daily for at least four weeks and for at least one week after symptoms resolve. Topical antifungal therapies include terbinafine, ketoconazole, miconazole, clotrimazole, tolnaftate, ciclopirox, naftifine, econazole, oxiconazole, butenafine, or sulconazole.3 Oral terbinafine, fluconazole, or itraconazole may be required for recalcitrant or extensive lesions.1
In our patient with recalcitrant lesions, oral terbinafine 250 mg daily for four weeks resulted in complete resolution of symptoms. No scaly lesions were noted at the follow-up examination, and the patient did not complain of persistent pruritus.
CASE #2: Psoriasis
A very common skin condition, psoriasis affects approximately 2% of the world's population. The disease can occur at any age, but 75% of cases occur before age 40 years. Frequently, there is a genetic predisposition to psoriasis, with many individuals reporting a positive family history.4
External factors are important in the pathogenesis of psoriasis. The isomorphic or Koebner phenomenon describes the appearance of lesions two to six weeks after an insult to the skin, such as trauma, sunburn, morbilliform drug eruption, or viral exanthem.4 This phenomenon may also explain the affinity of psoriatic lesions for chronically traumatized areas of the body, such as the elbows, knees, and presacrum.
Systemic factors are also important in triggering and affecting certain types of psoriasis. Streptococcal infections may cause a flare of guttate psoriasis. More severe disease may be seen in HIV-infected patients. Pregnancy may exacerbate or relieve disease. Multiple medications can exacerbate psoriasis, including lithium, interferon, beta blockers, and antimalarials, as can rapid corticosteroid tapers.4 Given the potential for post-treatment disease flare, systemic corticosteroids are generally avoided in patients with psoriasis.
Recent reports indicate that psoriatic patients have increased risk of a number of comorbidities. Individuals with more widespread psoriasis have a higher incidence of cardiovascular disease, hypertension, obesity, and psoriatic arthritis. Moreover, these patients are at a higher risk of mortality and are more likely than the general population to smoke and drink alcohol to excess.5 Both dermatologists and primary-care clinicians must be prepared to screen for and address these issues in the psoriatic population.
A spectrum of clinical features is seen in psoriasis, and psoriatic lesions may have different morphologies depending on where the lesions are located. Plaque-type psoriasis usually presents as sharply defined erythematous plaques with overlying silvery scales most commonly on the elbows, knees, presacrum, and scalp. Lesions are also frequently found on the hands, feet, and genitals; lesions may also be seen, albeit less often, anywhere on the body.4 Plaques may be asymptomatic or associated with pruritus or a burning sensation.6 Removal of the scale on a psoriatic plaque may lead to pinpoint bleeding; this phenomenon is called Auspitz sign.4
The differential diagnosis of psoriasis includes eczema, lupus erythematosus, dermatomyositis, seborrheic dermatitis, pityriasis rosea, lichen planus, psoriasiform syphilis,6 squamous cell carcinoma in situ, cutaneous T-cell lymphoma,4 and tinea corporis. Psoriasis can often be diagnosed clinically; confirmation can be made readily by histologic examination of skin biopsy specimens revealing confluent parakeratosis and regular acanthosis of the epidermis with suprapapillary thinning of the epidermis, dilated capillaries in the dermal papillae, and neutrophils in the stratum corneum and spinous layer of the epidermis.4
The available treatments for psoriasis are extensive and, therefore, will not be covered in detail here. Therapy for the psoriatic patient is based on both extent of disease and response to previous therapies. Patient comorbidities and convenience of obtaining and administering various therapies should also be considered.
Limited plaque-type psoriasis can generally be managed with topical therapy. The most commonly utilized topical therapies are corticosteroids and vitamin D analogs, such as calcipotriene. Long-term use of topical steroids can lead to local adverse effects, so these agents must be prescribed judiciously.6 Phototherapy remains a cost-effective treatment with relatively limited side effects for extensive disease, but patients must return for treatment multiple times each week. Numerous systemic agents, such as methotrexate and cyclosporine, have been available for some time for treatment of more severe or recalcitrant disease and are still widely used today.6 These treatments carry potentially serious risks and require close monitoring.
Also available for the treatment of psoriasis are newer biologic immunomodulators, including tumor necrosis factor (TNF)-alpha antagonists and agents that inhibit T-cell activation.7 These agents have demonstrated dramatic results in many psoriatic patients; however, they are expensive and have potentially serious side effects, including an increased risk of infection or reactivation of latent infections, such as TB.7 One biologic medication, efalizumab, was pulled from the market because of increased risk of progressive multifocal leukoencephalopathy. The long-term risks associated with use of biologic medications are not entirely clear.
Our patient was given adalimumab, a monoclonal antibody to TNF-alpha, because he was not responding to topical therapies and lived too far away for phototherapy to be feasible. Three months after initiating therapy, he had almost complete resolution of the psoriasis, with only a small residual plaque on his left elbow.
Dr. Doherty is a resident in the Department of Dermatology at Baylor College of Medicine in Houston, Texas. He has no relationships to disclose relating to the content of this article.
1. Sobera JO, Elewski BE. Fungal diseases. In: Bolognia JL, Jorizzo JL, Rapini RP, eds. Dermatology. 2nd ed. Spain: Mosby-Elsevier; 2008:1135-1163.
2. James WD, Berger TG, Elston DM. Diseases resulting from fungi and yeasts. In: Andrews' Diseases of the Skin: Clinical Dermatology. 10th ed. Canada: Saunders-Elsevier; 2006:297-332.
3. Lesniak R. Tinea incognito. Dermatol Nurs. 2008;20:403-404.
4. van de Kerkhof PCM, Schalkwijk J. Psoriasis. In: Bolognia JL, Jorizzo JL, Rapini RP, eds. Dermatology. 2nd ed. Spain: Mosby-Elsevier; 2008:115-135.
5. Kimball AB, Gladman D, Gelfand JM, et al; National Psoriasis Foundation. National Psoriasis Foundation clinical consensus on psoriasis comorbidities and recommendations for screening. J Am Acad Dermatol. 2008;58:1031-1042.
6. James WD, Berger TG, Elston DM. Seborrheic dermatitis, psoriasis, recalcitrant palmoplantar eruptions, pustular dermatitis and erythroderma. In: Andrews' Diseases of the Skin: Clinical Dermatology. 10th ed. Canada: Saunders-Elsevier; 2006:191-205.
7. Doherty SD, Van Voorhees A, Lebwohl MG, et al; National Psoriasis Foundation. National Psoriasis Foundation consensus statement on screening for latent tuberculosis infection in patients with psoriasis treated with systemic and biologic agents. J Am Acad Dermatol. 2008;59:209-217.