Growing skin plaques with scale
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A man aged 41 years was referred for evaluation of lesions on his legs, trunk and forearm. The lesions were first seen several months ago after the man lost his job, was threatened with divorce, began to drink heavily and gained 30 lbs. All of the lesions had grown in size and developed more scale. Pruritus was minimal but persisted despite OTC clotrimazole recommended by his pharmacist. Examination of the lesions showed several 1- to 8-cm annular, salmon-pink plaques covered with a thick, adherent white scale.
A 50-year-old man noticed a small area of scaling on his forearm. Self-treatment with OTC hydrocortisone 1% cream reduced the itching, but the rash continued to grow over the next year. A pharmacist suggested tolnaftate cream, which only reduced the redness and itching slightly and seemed to worsen the problem. The primary-care clinician prescribed triamcinolone 0.1% cream t.i.d. After two months, the rash had grown to cover almost his entire dorsal forearm and itched even more. The man was then referred to dermatology.
What is the diagnosis?
For CASE #1, click "NEXT." For CASE #2, click "3."
CASE #1: Plaque psoriasis
Plaque psoriasis, also known as psoriasis vulgaris, is quite common. The condition affects approximately 1% to 2% of whites, usually presenting in the third to fourth decade of life. Men with mycosis fungoides outnumber women by 2:1. Psoriatic lesions typically first appear on extensor surfaces and truncal skin. Psoriasis is a noncontagious, chronic, multisystem inflammatory disorder. Anywhere from 10% to 30% of those with the disease will also have a related form of arthritis called psoriatic arthropathy (PsA).
Psoriasis is a complex multifactorial condition that appears to be influenced primarily by genetic and immune-mediated factors. Environmental factors—especially stress, infection, and medications—seem to influence the course of the disease as well. In many patients, no trigger is ever identified, but once triggered, the disease appears to involve significant leukocyte recruitment to the dermis and epidermis, resulting in the formation of typical psoriatic lesions.1
The activated T-cells infiltrating the skin appear to be capable of inducing keratinocyte proliferation. Ultimately, this ramped-up, deregulated inflammatory process also promotes the production of such cytokines as tumor necrosis factor alpha and interleukin-12, which effectively mediate many of the features of plaque psoriasis.
In an individual with psoriasis, the turnover time for affected keratinocytes is reduced from 23 days to three to five days. This process greatly interferes with keratinocyte maturation and affects such functions as the adhesion of corneocytes that build up on the surface, accounting for the silvery lamellar scales seen with this disease.
Normally, these keratinocytes have time to gradually lose their nuclei as they migrate upward, a phenomenon known as orthokeratosis. In someone with psoriasis, however, the transit time is too short, and the cells retain their nuclei until they are shed. This microscopic finding is described as parakeratosis. Superficial vascular engorgement adds to the peculiar redness of the lesions.2 These theories are supported by voluminous research as well as by the positive response to immune-mediating biologic medications that are specifically designed for these functions.3
Histologically, all psoriasis is pustular,4 including spongioform intraepidermal pustules as well as Munro microabscesses within the stratum corneum. Neutrophilic microabscesses are generally seen above multiple small areas of parakeratosis. Cases of well-developed psoriasis feature regular epidermal acanthosis with long, bulbous rete ridges that thin over the dermal papillae but only scant spongiosis, except in the areas immediately surrounding collections of neutrophils.
For the most part, the diagnosis of psoriasis is clinical. In this case, the lesions and patient history were a near-perfect fit. The onset or flaring of psoriasis is related to stress, alcohol consumption, and obesity. Psoriasis takes a heavy toll on the patient in terms of stress and depression.5 At times, the diagnosis of psoriasis can be rendered difficult by clinical presentations in which the disease is relegated to inverse areas, nails, scalp, palms, soles or even the eyes.
Especially in early psoriasis, a biopsy can be less than helpful. This is particularly true in cases of chronic psoriasiform spongiotic dermatitis (a major item in the differential). Ideally, biopsy of psoriasis should show a lack of edema; the relative lack of spongiosis; tortuosity of capillary loops; and the presence of neutrophils above foci of parakeratosis, alternating in a rhythmic fashion with orthokeratosis.
The differential for psoriasis is extensive and includes such diagnoses as Bowen disease, nummular eczema, tinea corporis and mycosis fungoides (a form of cutaneous T-cell lymphoma). Early on, mycosis fungoides can manifest as what is termed large plaque parapsoriasis, with psoriasiform lesions ranging in size from 1 cm to 5 cm. These annular lesions feature faint scale, mild surface atrophy, mottled dyspigmentation and telangiectasia, and appear predominately on the lower abdomen, buttocks and breasts. Over a considerable amount of time, these lesions can evolve into infiltrative plaques, which, if left undiagnosed, can develop into a case of full-blown lymphoma. Biopsy and expert examination of the specimen are essential in making the diagnosis.4
Psoriasis can be difficult to treat. Options include topical calcipotriene (Dovonex), intralesional steroid injection, phototherapy and methotrexate (Rheumatrex, Trexall). Use of such injectible biologics as etanercept (Enbrel) and infliximab (Remicade) has revolutionized the treatment of this condition. The biologics have the potential to treat cutaneous psoriasis as well as PsA but are expensive and possess several potentially dangerous side effects.6
Other types of psoriasis that have been described include guttate, inverse, pustular and sebopsoriasis (an overlap between psoriasis and seborrheic dermatitis). Psoriatic arthritis is perhaps the most significant type of psoriasis. Left undiagnosed and untreated, PsA can lead to crippling destruction of the joint and must therefore be detected and treated early on. Unfortunately, there is no correlation between the severity or onset of psoriasis and the appearance of PsA. The sheer multiplicity of types of PsA makes diagnosis problematic, so this task is probably best left to a rheumatologist.4
Treatment of this patient's psoriasis was relatively simple, employing the use of topical clobetasol spray and counseling for to reduce the patient's weight and alcohol intake.
CASE #2: Dermatophytosis
Dermatophytosis, or tinea, is a fungal infection involving superficial portions of the skin, hair and nails. The infection is usually caused by one of three genera: Epidermophyton, Microsporum or Trichophyton. This relatively minor condition can be acquired from animals, humans, or soil. Variations include tinea corporis (body), tinea capitis (head), tinea pedis (feet), tinea unguium (nails), tinea cruris (groin), tinea manus (hands), tinea faciei (face) and tinea barbae (beard).7
The public — and even some medical texts — still use the term "ringworm" to describe this family of infections, but this is misleading provokes unreasonable fear among many patients. Part of this legacy of fear stems from the fact that these infections were quite common many years ago, and effective treatment simply did not exist.
Far from having anything to do with worms, dermatophytes are a group of molds that invade and feed only on keratinous tissue, skin, hair and nails. Increased warmth and moisture encourage dermatophytic infections, which are limited to the upper epidermis by host defense mechanisms and therefore distinct from the so-called deep mycoses. This group of potentially serious diseases affects the deep layers of skin, lungs and internal organs and includes such conditions as histoplasmosis, blastomycosis, coccidioidomycosis and sporotrichosis.8
As this case illustrates, topical and systemic steroids can promote tinea infection because they effectively diminish host defenses. What was missing from this patient's workup was a definitive diagnosis, which could have been obtained with a biopsy, culture or KOH preparation to identify fungal elements. The source of this patient's dermatophyte was not clear, but T. rubrum causes the great majority of this type of tinea corporis (also known as tinea circinata).
The active border of dermatophytic infections expands centrifugally, triggering a cell-mediated response. Among other effects, this response causes an increase in epidermal cell proliferation and resultant shedding, leaving new, uninfected cells central to the advancing border. Ultimate elimination is accomplished by the development of cell-mediated immunity, but the cell wall of the organisms slows this process, making their treatment difficult.
A deeper follicular form of tinea caused by the use of topical and/or systemic steroids is called tinea incognito, because its appearance is atypical enough to render it unrecognizable. Occasionally, under the same but prolonged circumstances, the fungal infection goes even deeper, becomes indurated, and develops pinpoint areas of pustular drainage that resemble a carbuncle. This form of fungal folliculitis, also called Majocchi granuloma, is often KOH- and culture-negative and must be diagnosed with a biopsy.4
Some individuals appear susceptible to dermatophytic infections, either because of the types of lipids their skin produces or because they are able to carry T. rubrum asymptomatically (a tendency possibly inherited autosomally).9
The differential for tinea corporis is vast, so limit it to such annular and/or scaly lesions as seborrhea, eczema, psoriasis, granuloma annulare, lichen planus, erythema annulare centrifigum, nummular eczema and tinea versicolor.
Tinea versicolor is not caused by the dermatophytes and will not necessarily respond to the same antifungal medications used for true tinea. Allylamines like terbinafine (Lamisil, Terbinex) are relatively ineffective against Malassezia furfur, the commensal yeast that causes tinea versicolor.
As mentioned, a simple KOH preparation usually distinguishes fungal from nonfungal infection. Punch biopsies are routinely stained for fungal elements. Fungal cultures are simple to obtain and can be incubated at room temperature but take up to two weeks to provide definitive results.7
There are a multitude of effective treatments for tinea corporis. Mild infections can easily be treated with a topical imidazole cream, such as oxiconazole (Oxistat), econazole (Spectazole) or ketoconazole (Feoris, Nizoral), b.i.d. until clear. Other effective topical treatment includes the allylamines terbinafine or ciclopirox (Penlac). Once treated persistently with topical steroids, tinea corporis can be severe enough to require topical and oral antifungals, including terbinafine 250 mg/day for up to one month. In rare cases, terbinafine can cause hepatotoxicity, as can griseofulvin, the most commonly used alternative.10
The patient in this case was successfully treated with oral terbinafine 250 mg daily for two weeks and twice-daily application of oxiconazole lotion. Total resolution occurred one month after treatment was initiated.Joe Monroe, PA-C, is a physician assistant specializing in dermatology at Springer Clinic in Tulsa, Okla. The author has no relationships to disclose relating to the content of this article.
2. Dover JS. Cutaneous Medicine and Surgery: Self Assessment and Review. Philadelphia, Pa.: W.B. Saunders; 1996:104-105.
3. Menter A, Korman NJ, Elmets CA et al. "Guidelines of care for the management of psoriasis and psoriatic arthritis. Section 3. Guidelines of care for the management and treatment of psoriasis with topical therapies." J Am Acad Dermatol. 2009;60:643-659.
4. James WD, Berger TG, Elston DM. Viral diseases. In: Andrews' Diseases of the Skin: Clinical Dermatology. 10th ed. Philadelphia, Pa.: Saunders-Elsevier; 2006:191-201, 297.
5. Sampogna F, Tabolli S, Söderfeldt B et al. "Measuring quality of life of patients with different clinical types of psoriasis using the SF-36." Br J Dermatol. 2006;154:844-849.
6. Callen JP, Krueger GG, Lebwohl M et al. "AAD consensus statement on psoriasis therapies." J Am Acad Dermatol. 2003;49:897-899.
8. Aly R. Ecology and epidemiology of dermatophyte infections. J Am Acad Dermatol. 1994;31(3 Pt 2):S21-S25.
9. Jones HE. Immune response and host resistance of humans to dermatophyte infection. J Am Acad Dermatol. 1993;28(5 Pt 1):S12-S18.
10. Drake LA, Dinehart SM, Farmer ER et al. "Guidelines of care for superficial mycotic infections of the skin: tinea corporis, tinea cruris, tinea faciei, tinea manuum and tinea pedis. Guidelines/Outcomes Committee. American Academy of Dermatology." J Am Acad Dermatol. 1996; 34(2 Pt 1):282-286.
All electronic documents accessed March 8, 2012.