STUDENTS OF PSORIASIS have struggled for centuries to distinguish the disease from its

‘mimics.’ With a wide range of clinical presentations,psoriasis may resemble many other dermatoses,inflammatory, infectious, and neoplastic. Character-istics that hint at the presence of psoriasis includefamily history, aspects of symmetry, distribution,silvery scaling, and nail changes1. Some diseases,however, emulate the appearance of psoriasis so

closely that a therapeutic trial of topical therapy maybe necessary. If uncertainty persists, biopsy, culture,and selected laboratory tests may aid in confirmingthe presence or absence of psoriasis. Fortunately, withtime, the vast majority of cases of psoriasis declarethemselves, evolving into the classic form (Table 7).

DIFFERENTIAL DIAGNOSIS357

Mimics Features distinct from psoriasis

INFLAMMATORY

Atopic dermatitis Flexural distribution, degree of erythema, ‘weeping’ lesions, lack of scale and lesser naildisease, significant pruritis, personal and/or family history of atopy

Dyshidrotic eczema Vesicles with ‘tapioca’-like fluid, involvement of sides of fingers, toes and webs, significantpruritus

Nummular eczema Lesions do not expand, less silvery scale and erythema, uniform size, distal leg a common site

Pityriasis rubra pilaris Orange hue, follicular orientation, patches of normal skin among diseased skin (‘islands ofsparing’), less broad array of nail disease (no pitting, onycholysis, or ‘oil drop’), hyperkeratoticpalms and soles (yellowish)

Pityriasis rosea Presence of ‘herald patch,’ ‘Christmas tree’ distribution, collarette of scale, salmon color, self-limiting 2–3 months’ course

INFECTIOUS

Tinea capitis Alopecia, broken hair shafts, possible adenopathy

Tinea corporis/tinea cruris Active scaly border, central clearing, asymmetry

Tinea pedis Involvement of lateral web space, unilaterality, vesicular, ‘moccasin’-type diffuse scaling

Tinea unguium Asymmetry, predominantly toenails, lack of pitting

Candida Peripheral pustules (‘satellite’ pustules), moist, whitish appearance, involvement of cruralareas and finger webs

Candida of genitalia (‘balanitis’) Pustules, diffuse erythema, erosions and fissures

Secondary syphilis Early erythematous exanthem, copper-colored lesions (‘pennies’) on palms and soles,mucosal lesions, condyloma lata, history of chancre

NEOPLASTIC

Squamous cell carcinoma in-situ Sun-exposed distribution, lesions few in number, gradual increase in size, resistant to (Bowen’s disease) treatment, potential progression to erosions

Cutaneous T-cell lymphoma Often initially diagnosed as psoriasis; asymmetry, more irregular and fewer lesions, (CTCL) wrinkled appearance, ‘bathing-trunk’ distribution common, unresponsive to traditional

topical therapies, potential progression to plaques, nodules and tumors

Table 7 Psoriasis mimickers with differentiating features.

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I N F L A M M A T O R Y S K I N D I S E A S E

EczemaEczema appears at the top of the list of dermatosescausing confusion with psoriasis. Although many formsexist, three types – atopic, dyshidrotic, and nummular –particularly resemble subtypes of psoriasis.

Atopic dermatitisA multifactorial condition beginning in childhood,atopic dermatitis (AD) manifests in a variety of waysdepending on age and severity. In children under 2years, characteristic plaques with vibrant erythema andminor scale appear on the face and extensor surfaces ofthe limbs. In older patients, distribution becomes flexural and plaques thickened with exaggerated skinmarkings (lichenification), the result of chronic excoria-tion. Patients report a long personal and/or family

history of asthma and allergic rhinitis, known as theatopic diathesis. Paramount among the subjectiveaspects of the disease, pruritus may be triggered bychanges in temperature or humidity. Contact with irri-tants, such as water, or allergens may also exacerbatesymptoms. Indeed, pruritus with resultant excoriationoften incites characteristic lesions, leading to the laydescription of atopic dermatitis as ‘the itch that rashes.’Beyond flexural surfaces, other sites of involvementinclude periorbital and perioral areas, as well as thehands. Nails may be affected, although typically to amild degree. Despite similarities with psoriasis, ADremains distinct. Key differentiating features of ADinclude characteristic history, severe pruritus, distribu-tion of lesions, marked erythema, as well as paucity ofscale and nail changes2–4. Often lesions are ‘weepy’ orsecondarily infected (impetiginized). Topical steroids

187186

184

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I N F L A M M A T O R Y S K I N D I S E A S E and emollients are mainstays of treatment with topicalimmunomodulating agents and systemic antipruriticsimportant additions. In severe cases, systemic cortico-steroids, cyclosporin or, on occasion, even azathioprineand mycophenolate mofetil are utilized (184–191)5.

Dyshidrotic eczemaDyshidrotic eczema, also known as pompholyx, causessymmetric, bilateral vesiculation of the hands and feet.One of the few lesions resembling palmoplantar pustu-lar psoriasis, dyshidrotic vesicles evolve into punctate,scaly papules and even pustules5. The ‘tapioca-like’vesicular fluid, intense pruritus, and involvement of thefinger webs and dorsal hands differentiate dyshidrosisfrom its psoriatic counterpart. Morbidity is great andtreatment difficult (192–196).

Nummular eczemaA puzzling relative of atopic dermatitis, nummulareczema presents with disk-shaped, scaly plaques fre-quently on the extremities. Unlike psoriatic plaques,lesions of nummular eczema typically do not expand1.Scale is also less exuberant and erythema less uniform.Like AD, nummular eczema may cause extreme pruri-tus, especially in the elderly (197–200).

190

189188

191

DIFFERENTIAL DIAGNOSIS 59

Eczema versus psoriasis184–187 Atopic dermatitis. Compared with psoriasis,lesions tend to be less vivid, well-defined, and scaly.188–191 Psoriasis.

Pityriasis roseaA self-limited, inflammatory disease possibly related toinfection with human herpes virus 6 and 7, pityriasisrosea (PR) begins with a 2–10-cm, salmon-red plaqueusually on the trunk, known as the ‘herald patch.’ Theplaque precedes the eruption of smaller (1–2-cm)patches, papules, and thin plaques on the trunk andproximal extremities, developing 1–2 weeks later. Clas-sically, lesions develop along skin cleavage lines anddisplay a thin rim of scale. This ‘Christmas-tree’ distri-bution and ‘collarette’ of scale help to distinguish PRfrom guttate psoriasis. The eruption is usually self-limited, lasting 2–3 months (201, 202).

194

196

192

195

193

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Eczema versus psoriasis192, 193 Dyshidrotic eczema. Note the characteristicclear vesicles.194–196 Palmoplantar pustular psoriasis with yellowishpustules.

Eczema versus psoriasis197 Nummular eczema. Lesions are thin, moist, and lacksilvery scale.198–200 Small-plaque psoriasis.

201 202

199

197

200

198

DIFFERENTIAL DIAGNOSIS 61

Pityriasis rosea versus psoriasis201 Pityriasis rosea. The peripheral rim of scale is a distinguishing feature.202 Guttate psoriasis. Gentle scraping of the surface willelicit silvery scale.

207

Pityriasis rubra pilarisThe scaly plaques of pityriasis rubra pilaris (PRP) strong-ly evoke psoriasis. Indeed, PRP was originally describedas a psoriasis subtype6. Decades later, dermatologistsbegan to appreciate the distinct orange hue and follicu-lar distribution of PRP. Waxy plaques affect the palms,soles, trunk, limbs, and scalp. Despite often extensivedisease, patches of normal skin intermingle, known as‘islands of sparing.’ Nails may demonstrate subungualdebris, as with psoriasis, but lack pitting, oil drops, andonycholysis7. In sum, distinguishing features of PRPinclude the follicular orientation and color of lesions,‘islands of sparing,’ more acral distribution, and narrowrange of nail changes. Additionally, PRP may be evenmore refractory to therapy than psoriasis (203–213).

204203

205 206

62

Pityriasis rubra pilaris versus psoriasis203–209 Pityriasis rubra pilaris. Note the more yellow-orange hue and follicular appearance.210–213 Psoriasis.

213212

208

211210

209

DIFFERENTIAL DIAGNOSIS 63

I N F E C T I O U S D I S O R D E R S

Dermatophye infectionA diverse group of fungi, the dermatophytes, alsotermed ‘tinea,’ infect keratinized tissues of the skin, hair,and nails. While the clinical manifestations of dermato-phytic infection range widely, many features mimic psoriasis. Infection of the skin and hair can lead to ery-thematous, scaly plaques with an active border, typicalof psoriasis. Nail involvement may present with sub-ungual hyperkeratosis identical to psoriatic nail disease.The astute clinician, however, will note asymmetry ofdermatophytic lesions, as well as subtle differences inthe quality of the active border and central clearing.

Tinea capitisA disease mainly of young children, tinea capitis evolvesfrom infection of the scalp hair shaft by a dermatophyte,most commonly Trichophyton tonsurans8. Of the variousmanifestations of tinea capitis, the noninflammatorysubtypes are most often confused with psoriasis.Lesions appear circular with abundant scale and rela-tively sharp demarcation. Alopecia with broken hairshafts also hints at tinea. Regional lymphadenopathymay be present with more inflammatory forms. Wood’slamp examination and microscopy of affected hairs isusually sufficient to clinch the diagnosis, with fungalcultures occasionally required. Oral, not topical, anti-fungals are the standard treatment (214–217).

214 215

216 217

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I N F E C T I O U S D I S O R D E R S Tinea corporisDermatophytoses of the skin subdivide according toanatomic location, with separate designations for thegroin, feet, hands, and all other surfaces. Tinea corporis,for instance, refers to dermatophyte infection of any epi-dermal location other than the scalp, groin, feet, orhands. Trichophyton rubrum is the most commonculprit8. Circular or annular asymmetric plaquesproduce marked erythema and scale. As with other dermatophytoses, the border appears relatively more

‘active’ than the remainder of the lesion. Microscopicevaluation with the application of potassium hydroxide(KOH) to a collection of scale collected from the activeborder followed by gentle heating will reveal septatehyphae. Biopsy specimen treated with periodic-acidSchiff (PAS) may be more sensitive for the detection offungi8. Unlike hair and nail dermatophytosis, treatmentwith topical antifungals is normally adequate (218,219).

218 219

DIFFERENTIAL DIAGNOSIS 65

Dermatophyte infection versus psoriasis214, 215 Tinea capitis. Alopecia and minor scaling areclues to diagnosis216, 217 Scalp psoriasis.218 Tinea corporis. Note the active, scaly border.219 Flexural psoriasis; minimal scale noted in this form.

Tinea crurisClosely related tinea cruris differs from the corporalsubtype in anatomic location (groin), relative paucity ofscale except at the border, and propensity for confluenceof plaques. As with tinea corporis, T. rubrum causes mostcases8. The diagnostic approach and treatment optionsare similar (220–222).

Tinea pedisExcessive moisture predisposes to dermatophyte infec-tion of the foot, known as tinea pedis or ‘athlete’s foot.’Several categories exist, however, the so-called ‘moc-casin-type’ most closely resembles nonpustular, plantarpsoriasis. Fine, whitish scale and leathery hyperkerato-sis encasing the foot characterize the clinical appearanceof this type of tinea pedis. Other manifestations of dermatophytosis may coexist, such as interdigital andbullous lesions, which distinguish the infection frompsoriasis (223–226).

Tinea unguiumTinea unguium refers to dermatophyte infection of thenail, also termed ‘onychomycosis.’ In its primary form,tinea unguium affects healthy nails causing discolora-tion and subungual hyperkeratosis similar to psoriaticnail disease. Alternatively, pre-existing nail damage,such as onycholysis in psoriatics, predisposes to sec-ondary onychomycosis, leading the two conditions tooften coexist. Patients with depressed immunity, such asthose with diabetes and HIV/AIDS, are prone to infec-tion, usually by T. rubrum or T. mentagrophytes8. Whileoften indistinguishable from nail psoriasis, tineaunguium may be differentiated by asymmetry, sparingof the fingernails, and lack of pitting. A KOH prepara-tion of clippings from the nail bed may secure the diag-nosis, but PAS staining of clippings and/or fungalculture of debris are often required (227–230).

222

221

220

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Dermatophyte infection versus psoriasis220 Tinea cruris in a psoriasis patient using topicalcorticosteroids.221 Tinea cruris. The relative paucity of scale differentiates this from psoriasis.222 Psoriasis of the groin.223, 224 Tinea pedis. Note the asymmetry and webinvolvement.225, 226 Psoriasis of the foot.227, 228 Tinea unguium. Pitting is not observed.229, 230 Nail psoriasis.

225

230229

223

226

228227

224

DIFFERENTIAL DIAGNOSIS 67

Candida infectionAnother infectious psoriasis mimic, the yeast speciesCandida albicans affects warm, moist areas of the body,including axillae, inguinal folds, gluteal cleft, perineum,finger webs, angles of the mouth, and breast folds. Ery-thematous papules coalesce to form eroded plaqueswith characteristic peripheral pustules. These so-called‘satellite’ pustules distinguish cutaneous candidiasisfrom psoriasis. A KOH preparation reveals buddingyeast with ‘pseudohyphae,’ confirming the diagnosis.Keeping affected areas dry and use of topical anti-candidal agents are first-line treatments (231–237).

Candida also affects the nonkeratinized epitheliumof the genitals, as does psoriasis. The term ‘balanitis’refers to candidiasis of the prepuce and glans penis. Discrete or coalescent pustules develop on erythema-tous, often eroded, skin. Diffuse erythema and pustulessuggest balanitis as opposed to psoriasis. Diagnosis isoften made clinically (238, 239).

Secondary syphilisWith its multitude of expressions involving the skin andother organ systems, syphilis is known as ‘the great imi-tator.’ Secondary syphilis, developing in untreatedpatients 2–6 months after initial infection with thespirochete, may very closely resemble guttate psoriasisand pityriasis rosea. Interestingly, patients with early sec-ondary syphilis develop a faint, erythematous exan-thema prior to the guttate-like papular eruption. In thelatter, copper-colored papules of various sizes up to 1 cmdevelop gradually over the trunk and limbs, ultimatelyinvolving the palms and soles. Lesions characteristicallylack signs of inflammation, but scaling may be present.Mucosal lesions, especially on the mouth and genitalia,are frequent. A typical eruption in the setting of a posi-tive screening, followed by treponemal antibody testconfirms the diagnosis. Though rarely performed, darkfield microscopy of samples from papular lesions willdemonstrate spirochetes (240, 241).

232

233

231

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Candida infection versus psoriasis231–233 Psoriasis.234–237 Candidiasis. Note the discrete pustules at the periphery.238 Balanitis. Note the moist, non-scaly quality of the lesion.239 Psoriasis of the genitals.

Secondary syphilis versus psoriasis240 Secondary syphilis. The characteristic copper color ofthe lesions distinguishes the eruption from psoriasis.Palms and soles are frequently involved.241 Guttate psoriasis.

236

238

240 241

234

237

239

235

DIFFERENTIAL DIAGNOSIS 69

N E O P L A S M S

Most ominous of the masquerade syndromes, neo-plasms affecting the skin may cause scaly, erythematousplaques identical to psoriasis. Lesions may be so similar,in fact, that only resistance to treatment guides the clinician away from a diagnosis of chronic psoriasis andtoward consideration of neoplasia. In such cases, histol-ogy aids in the diagnosis, although sequential biopsiesmay be required (see below).

Squamous cell carcinoma in situWell-circumscribed, isolated erythematous plaqueswith scale just as adequately describes the lesions ofsquamous cell carcinoma in situ (SCCIS), or Bowen’sdisease, as psoriasis. Lesions favor areas of sun damage,a risk factor for Bowen’s disease, including the ears,scalp, lower lip, upper chest, back, and hands. Malesappear more likely to develop SCCIS on the head andneck, whereas women the lower extremities9. Otherexposures increasing risk include human papillomavirus (HPV), arsenic, heating devices, and iatrogenicradiation. Treatment recalcitrance and/or progression toinvasive disease suggest Bowen’s disease rather thanpsoriasis. Paucity of scale, which is less than silvery, aswell as a dull background of erythema aid in distin-guishing SCCIS from psoriasis (242–244).

Cutaneous T-cell lymphomaA rare neoplasm of helper T cells, cutaneous T-cell lymphoma (CTCL) encompasses a variety of relatedconditions, including mycosis fungoides, lymphomacutis, and Sézary syndrome. Erythematous patches mayprogress to plaques, which may slowly evolve intonodules or tumors and, in some cases, erythroderma. Inthis final stage, extensive hematological and even viscer-al involvement may be seen. The early, ‘patch’ stage ofCTCL demonstrates erythematous plaques with mildscale similar to psoriasis or dermatophytoses, hence theterm ‘mycosis.’ Indeed, patients with ‘patch’ stageCTCL often carry the diagnosis of psoriasis for manyyears. Further confusing the picture, these lesions mayrespond well to both topical corticosteroids and photo-therapy initially, as with psoriasis. Biopsy specimensduring the patch stage may not consistently demon-strate the characteristic epidermotropism (homing of Tcells to the epidermis) and activated CD4+ lympho-cytes. Consequently, serial biopsies with special studies,

243

244

242

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Squamous cell carcinoma versus psoriasis242, 243 Bowen’s disease. Lesions are isolated, well-circumscribed, eroded, and resistant to anti-psoriatic therapies.244 Annular psoriasis.

N E O P L A S M S

such as T-cell receptor gene rearrangement and flowcytometry, are important for diagnosis.

Thus, the clinician must be wary of the isolated, psoriasiform plaque minimally responsive to topicaltherapy. If such a lesion raises suspicion for CTCL, initialwork-up should include at minimum a full lymph nodeexamination, biopsy of the lesion for routine histology

and special studies mentioned above, and completeblood count with peripheral smear. Early lesionsrespond well to phototherapy, particularly psoralen withultraviolet A (PUVA). Progression to Sézary syndrome,with generalized erythroderma, warrants consultationwith a hematologist/oncologist for appropriate systemictherapy (245–249).

247

245

248 249

246

DIFFERENTIAL DIAGNOSIS 71

Cutaneous T-cell lymphoma (CTCL) versus psoriasis245 CTCL; patch stage.246 CTCL; plaque stage.247 CTCL; erythroderma.248, 249 Psoriasis.