Well-demarcated pink plaques - Clinical Advisor

Well-demarcated pink plaques


  • Case #1

    May 2015 Dermatology Look-Alikes

    Case #1

  • Case #2

    May 2015 Dermatology Look-Alikes

    Case #2

Case #1

A 35-year-old man presented with a two-year history of persistent rash on his elbows, knees, and scalp. The rash initially appeared on the elbows and then slowly spread to other parts of the body. The rash was pruritic and responded to over-the-counter hydrocortisone cream. He admitted to intermittent joint pain. The patient was otherwise healthy and not taking any medications. His mother has had eczema for more than 15 years. His father and brother have psoriasis.

Case #2

The same patient had several small, well-defined pink papules on the right elbow for three months. He denied pruritus with these lesions. He admitted to scratching and sometimes picking these areas. Episodes of dry skin were frequent. Previously seen providers made a diagnosis of psoriasis and recommended topical steroid therapy. Initially, the topical steroids alleviated the erythema of the lesions but later, he would notice these lesions increasing in size and number.

This The Clinical Advisor CME activity consists of 3 articles. To obtain credit, read Multiple facial papules on a HIV-positive man and Blistering patch on 
infant’s forearm. Then take the post-test here.

This The Clinical Advisor CME activity consists of 3 articles. To obtain credit, read Multiple facial papules on a HIV-positive man and Blistering patch on 
infant's forearm. Then take the post-test here.Case #1Plaque psoriasis, also known as psoriasis vulgaris, is...

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This The Clinical Advisor CME activity consists of 3 articles. To obtain credit, read Multiple facial papules on a HIV-positive man and Blistering patch on 
infant’s forearm. Then take the post-test here.

Case #1

Plaque psoriasis, also known as psoriasis vulgaris, is a chronic, inflammatory skin disorder that initially manifests as small pink or red bumps. Over time, the lesions develop into thick, elevated, dry, red plaques with overlying silvery-white scales that can flake off. There is a wide spectrum of disease severity, ranging from a single plaque to involvement of nearly the entire body surface. 

In children, plaques are typically smaller and have finer scales than those in adults.1 Lesions are pruritic and reveal pinpoint-sized bleeding spots (Auspitz’s sign) when scratched or scraped. Plaque psoriasis tends to appear on the extensor surfaces of the elbows and knees, as well as the lower back and scalp with symmetric and bilateral distribution. A ring of hypopigmented skin (Woronoff’s ring) sometimes surrounds psoriatic plaques after phototherapy or treatment with topical agents.2 New skin lesions may appear on lines of trauma, which is a clinical feature of psoriasis known as the Koebner phenomenon.3

There are five types of psoriasis: plaque, guttate, inverse, pustular, and erythrodermic. The most common type is plaque psoriasis, which accounts for about 80% of psoriasis cases.4 About 2% to 4% of the world’s population is affected by psoriasis, including an estimated 6.7 million adult Americans.4 Higher prevalence rates among non-Hispanic whites and individuals with arthritis and cardiovascular disease have been reported.4 The age of onset of psoriasis has a bimodal distribution, with the first peak of onset between age 15 years and age 20 years and the second between age 55 years and age 60 years.5

The exact etiology of psoriasis is unknown, but current research indicates that psoriasis is a T-cell-mediated autoimmune disease that results from a combination of genetic susceptibility and environmental assaults. The heritability of psoriasis, determined through twin studies, is estimated to be 68%.6 Genome-wide linkage scans have identified several genes associated with psoriasis. The strongest association is with a gene locus residing in the major histocompatibility complex (MHC) on chromosome 6p21, which is documented as the psoriasis susceptibility region 1 (PSORS1).7,8 Environmental factors that may contribute to development and/or intensification of psoriasis include stressful life events, urban environments, cigarette smoking, body mass index, and alcohol consumption.9,10

The histopathologic features of plaque psoriasis include acanthosis, parakeratosis, spongiform pustules of Kogoj, and Munro’s microabscesses.1 The granular cell layer is absent, and there is regular elongation of rete ridges with bulbous thickening at the base in the epidermis.1 Dermal papillae are elongated and edematous, and they contain dilated and tortuous capillaries.1 There is a mononuclear inflammatory infiltrate present in the dermis.1

Psychological stress is both a consequence of and a causative factor for psoriasis. Mental distress, depression, anxiety, self-consciousness, and impaired social functioning are commonly reported in individuals with psoriasis.4 Patients with psoriasis tend to have higher BMIs, decreased work productivity or greater unemployment, and higher rates of smoking and alcohol consumption than individuals without psoriasis.4 Patients with psoriasis may also develop psoriatic arthritis, which is characterized by joint pain and inflammation. 

Plaque psoriasis can usually be distinguished by its clinical presentation: symmetrically distributed, elevated, red, scaly plaques that tend to appear on the extensor surfaces of the elbows, knees, lower back, and scalp. The presence of the Koebner phenomenon, Woronoff’s ring, and/or Auspitz’s sign and a family history including psoriasis also support the diagnosis of plaque psoriasis. Dermoscopic examination of the lesion may also be useful. The most common dermoscopic characteristics of plaque psoriasis are dotted vessels arranged in a regular distribution over a light red background and a diffuse distribution of white scales.11 If the diagnosis remains uncertain, a skin biopsy can provide confirmation.

Several diseases can mimic plaque psoriasis, including mycosis fungoides, pityriasis rubra pilaris, verruca plana, nummular dermatitis, hypertrophic lichen planus, pityriasis rosea, and tinea corporis.12 Although the rash of the mycosis fungoides variant of cutaneous T-cell lymphoma (CTCL) may resemble plaque psoriasis, psoriasis can be distinguished by its silver sheen and tendency to appear on extensor surfaces. Furthermore, CTCL often exhibits epidermal atrophy or poikiloderma, which allows for its differentiation from plaque psoriasis.12 Pityriasis rubra pilaris can be differentiated from plaque psoriasis by the presence of red-orange palmoplantar keratoderma, keratotic follicular papules, and sharply demarcated islands of unaffected skin on the trunk.12 Early plaque psoriasis may resemble verruca plana, as it manifests initially as small, circular-to-oval red or pink bumps. However, the lesions of verruca plana tend to be smooth, rather than scaly, and are rarely pruritic. Nummular dermatitis is more pruritic than psoriasis and is more likely in a patient with a history of atopy.12 Dermoscopy can also differentiate the two: nummular dermatitis shows diffuse yellow scales and some dotted vessels in patchy distribution, whereas plaque psoriasis shows regularly distributed dotted vessels over a light red background and overlying, diffuse white scales.11 Dermoscopy is also useful in distinguishing plaque psoriasis from hypertrophic lichen planus and pityriasis rosea.11 In pityriasis rosea, dotted vessels are associated with a yellowish background color and peripheral arrangement of scales, and in hypertrophic lichen planus, white crossing lines, a dull red background color, and peripheral arrangement of vessels are commonly apparent.11 Pityriasis rosea is also distinguished by its initial herald patch, followed by the appearance of oval plaques in Christmas-tree distribution. Tinea corporis can be distinguished from plaque psoriasis by its elevated border, slowly extending edge, and positive mycology.

While no cure for psoriasis exists, therapies that control and suppress the condition minimize the development of lesions and associated symptoms. Treatment options include topical treatments, phototherapy, systemic medications, or a combination of these. Topical treatments are usually the first line of defense against psoriasis and most prominently include vitamin-D analogues and topical corticosteroids, but tar-based preparations, dithranol, salicylic acid, and topical retinoids are also used.13 Emollients and moisturizers are often used in conjunction, as they are helpful in reducing inflammation and scale load by normalizing hyperproliferation, differentiation, and apoptosis.14 Narrowband ultraviolet-B (NB-UVB) therapy and oral 8-methoxypsoralen UVA (PUVA) are also well-established and effective treatments for plaque psoriasis. NB-UVB is usually the first line in phototherapy for plaque psoriasis due to the long-term safety concerns of PUVA, especially PUVA’s cutaneous carcinogenic risk. However, because UVA penetrates the skin more deeply than UVB, thick plaques are more effectively treated with PUVA.15 Systemic medications, including methotrexate, cyclosporine, and acitretin, are usually reserved for moderate-to-severe cases. Patients should be informed that the management of plaque psoriasis is challenging due to the unpredictable and relapsing nature of the disease. 

In our case, biopsy confirmed the diagnosis of psoriasis, and the patient was diagnosed with psoriasis and psoriatic arthritis. A regimen of topical steroids and weekly injections of the biologic etanercept at 50 mg was initiated. The patient reported improvement of his psoriasis and joint pain.

Key points on plaque psoriasis

Characteristic clinical presentation
  • Small pink or red bumps that evolve into thick, elevated, dry, red plaques with overlying silvery-white scales
  • Scratching off scales reveals pinpoint-sized bleeding spots
  • Distribution tends to be bilateral and symmetric
  • Koebner phenomenon frequently observed
Commonly involved sites Extensor surfaces of elbows and knees, lower back, and scalp
Typical age of presentation Can develop at any age, but there are two peaks of onset: 15 to 20 years and 55 to 60 years
Clinical course Chronic, unpredictable, and relapsing, even with treatment
Histology Acanthosis, parakeratosis, Kogoj’s micropustules, Munro’s microabscesses, loss of granular cell layer, elongated rete ridges with bulbous thickening at the lower ends, dilated and tortuous capillaries in dermal papillae, and inflammatory infiltrate in superficial dermis
  • First line of defense is topical treatments, including vitamin-D analogues, topical corticosteroids, tar-based preparations, dithranol, salicylic acid, and topical retinoids, which are often used in conjunction with emollients and moisturizers
  • For moderate-to-severe cases, narrow-band ultraviolet-B, psoralen plus ultraviolet A, and systemic medications, including methotrexate, cyclosporine, and acitretin, are used

Case #2

Verruca plana (VP) is a benign proliferation of epithelium commonly known as flat warts. 

VP can occur at any age, but lesions tend to appear in children and young adults. Patients on immunosuppressive therapy for transplants or those who are immunodeficient have a higher incidence of VP.16 Sun exposure appears to be a risk factor for the development of VP, and VP lesions are exacerbated by ultraviolet light.16 VP is most frequently caused by infection of the superficial skin with the human papilloma virus (HPV), most commonly HPV-3, -10, -28, and -41.17 Due to the contagious nature of the virus, linear configurations of VP are especially common on shaved areas of skin, as the trauma of shaving can induce autoinoculation.16 Furthermore, VP can be traumatically inoculated during tattoo placement.18

Clinically, VP manifests as skin-colored, light brown or slightly erythematous, homogenously pigmented, slightly elevated, flat-topped papules measuring 1 mm to 4 mm in diameter. The papules are sharply marginated, have a smooth surface, and are usually round or oval, but they may also have an irregular polygonal shape. VP presents preferentially on the face or dorsum of the hands, forearm, lower legs, and other areas prone to trauma such as shaved areas. The number of papules ranges from one to several hundred. When multiple are present, as in most patient presentations, they may be scattered irregularly, distributed in groups, or arranged linearly on lines of trauma (Koebner phenomenon).19

VP lesions themselves are not harmful, but multiple flat warts seen in otherwise healthy individuals may be evidence for a compromised immune system.19 Therefore, when there is extensive involvement in a patient with no obvious risk factors or lesions persist despite therapy, evaluation of the patient’s cellular immune function is recommended.19

Histopathologically, VP demonstrates basket-weave hyperkeratosis, acanthosis, a uniformly thickened granular layer, and a diffuse zone of vacuolization of cells in the granular and upper spinous layers around centrally located nuclei, which creates a “bird’s eye” appearance.20,21 Dermoscopic examination of VP lesions reveals even-colored light brown to yellow patches, which are often accompanied by dots and globular vessels.22

VP lesions are benign and tend to undergo spontaneous remission after a period of months to years. However, they are often a distressing cosmetic burden for patients and can spread by autoinoculation from scratching, shaving, or other skin trauma. For this reason, these warts are often removed by a variety of available therapies. While no true antiviral therapy is available, treatments that assault the virus and host tissue or induce a favorable immune response are typically effective.19 Therapeutic options include cryotherapy with liquid nitrogen, electrocautery, and application of topical agents, including tretinoin once or twice daily, salicylic acid products, tazarotene cream or gel, imiquimod 5% cream, 5-fluorouracil cream, and topical 5-aminolevulinic acid.17,23 For persistent lesions, intralesional immunotherapy with dinitrochlorobenzene, squaric acid, or dyphencyprone, laser therapy in low fluences, photodynamic therapy, and pulsed dye laser therapy should be considered before electrodesiccation due to the decreased risk of scarring.17,23 A combination of therapies may be employed due to the resilient nature of warts. Therapy should be as mild as possible to reduce the risk of scarring or discomfort, individualized to address the lesion location(s), extent, and desires of each patient, and modified when needed based upon the clinical response.

The differential diagnosis of VP includes seborrheic keratosis, tinea versicolor, plaque psoriasis, lichen planus, and verruca vulgaris. VP lesions can normally be identified upon clinical examination by their smooth, skin-colored-to-pink, nonscaly, papular appearance, but a biopsy may be indicated in diagnostically uncertain cases. The Koebner phenomenon is a useful clue for the clinical diagnosis of VP. Dermoscopic evaluation can distinguish VP from seborrheic keratosis: unlike lesions of seborrheic keratosis, which show multiple milia-like cysts, comedo-like openings, and a brain-like appearance, VP lesions have more even-colored light-brown-to-yellow patches and dots, and globular vessels.22 The small, tan patches of tinea versicolor may resemble VP, but they can be distinguished clinically by their scaly surface. Additionally, histologic examination of tinea versicolor shows multiple hyphae and spores in the stratum corneum, and that is not seen with VP. Early plaque psoriasis may resemble VP, as both manifest initially as small, circular-to-oval red or pink bumps that may be arranged linearly due to the Koebner phenomenon. However, early psoriatic lesions can be distinguished by their scaly surface, pruritic nature, and development into raised, thick plaques. Lichen planus can be distinguished from VP in that VP lesions are usually skin-colored, light brown or slightly erythematous (as opposed to violaceous), smooth (as opposed to scaly), and not pruritic. VP can normally be distinguished clinically from verruca vulgaris; VP lesions are smaller, smooth (as opposed to rough), tend to grow in larger numbers, and more commonly appear on the face and shaved areas of skin. Furthermore, upon histopathologic examination, VP shows minimal or no papillomatosis, unlike verruca vulgaris. 

In the patient in this case, biopsy was consistent with VP. The lesions were treated successfully with cryotherapy.

Key points on verruca plana

Characteristic clinical presentation
  • Skin-colored, light brown or slightly erythematous, homogenously pigmented, slightly elevated, sharply marginated, smooth, flat-topped, oval or round papules measuring 1 mm to 4 mm in diameter
  • Papules range from one to several hundred in number
  • Koebner phenomenon frequently observed
Commonly involved sites Face, dorsum of hands, forearms, lower legs, shaved surfaces
Typical age of presentation Tends to appear during childhood and adolescence
Clinical course Most lesions undergo spontaneous remission after months or years without treatment
  • Basket-weave appearance of stratum corneum
  • Granular layer thickening
  • Vacuolated cells in the granular and upper spinous layers with centrally located nuclei (“bird’s eye” appearance)
  • Not necessary, but cryotherapy with liquid nitrogen and application of salicylic acid are most common
  • Other treatment options include electrocautery, topical tretinoin, tazarotene cream or gel, imiquimod 5% cream, 5-fluorouracil cream, and topical 5-aminolevulinic acid
  • For persistent lesions, intralesional immunotherapy and laser treatments are used

Kate Travis, BA, is a medical student and Rana Mays, MD, is a dermatology resident at Baylor College of Medicine in Houston. 

This The Clinical Advisor CME activity consists of 3 articles. To obtain credit, read Multiple facial papules on a HIV-positive man and Blistering patch on 
infant’s forearm. Then take the post-test here.


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  3. Raychaudhuri SP, Jiang WY, Raychaudhuri SK. Revisiting the Koebner phenomenon: role of NGF and its receptor system in the pathogenesis of psoriasis. Am J Pathol. 2008;172(4):961-971. Available at ncbi.nlm.nih.gov/pmc/articles/PMC2276420 

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  6. Lønnberg AS, Skov L, Skytthe A, et al. Heritability of psoriasis in a large twin sample. Br J Dermatol. 2013;169(2):412-416. 

  7. Chandra A, Ray A, Senapati S, Chatterjee R. Genetic and epigenetic basis of psoriasis pathogenesis. Mol Immunol. 2015;64(2):313-323. 

  8. Nair RP, Stuart PE, Nistor I, et al. Sequence and haplotype analysis supports HLA-C as the psoriasis susceptibility 1 gene. Am J Hum Genet. 2006;78(5):827-851. Available at ncbi.nlm.nih.gov/pmc/articles/PMC1474031 

  9. Jankovic S, Raznatovic M, Marinkovic J, et al. Risk factors for psoriasis: A case-control study. J Dermatol. 2009;36(6):328-334. 

  10. Naldi L, Chatenoud L, Linder D, et al. Cigarette smoking, body mass index, and stressful life events as risk factors for psoriasis: Results from an Italian case-control study. J Invest Dermatol. 2005;125(1):61-67. Available at nature.com/jid/journal/v125/n1/full/5603236a.html 

  11. Lallas A, Kyrgidis A, Tzellos TG, et al. Accuracy of dermoscopic criteria for the diagnosis of psoriasis, dermatitis, lichen planus, and pityriasis rosea. Br J Dermatol. 2012;166(6):1198-1205. 

  12. Basko-Plluska JL, Petronic-Rosic V. Psoriasis: Epidemiology, natural history, and differential diagnosis. Psoriasis: Targets and Therapy. 2012;2:67-76. Available at dovepress.com/psoriasis-epidemiology-natural-history-and-differential-diagnosis-peer-reviewed-article-PTT 

  13. Mason A, Mason J, Cork M, et al. Topical treatments for chronic plaque psoriasis: An abridged Cochrane systematic review. J Am Acad Dermatol. 2013;69(5):799-807. 

  14. Fluhr JW, Cavallotti C, Berardesca E. Emollients, moisturizers, and keratolytic agents in psoriasis. Clin Dermatol. 2008;26(4):380-386. 

  15. Archier E, Devaux S, Castela E, et al. Efficacy of psoralen UV-A therapy vs. narrowband UV-B therapy in chronic plaque psoriasis: A systematic literature review. J Eur Acad Dermatol Venereol. 2012;26(Suppl 3):11-21. 

  16. Rosen T, Risner-Rumohr S. Flat Warts. In: Zeichner JA, ed. Acneiform Eruptions in Dermatology: A Differential Diagnosis. New York, N.Y.: Springer Verlag; 2013:71-77. 

  17. James WD, Berger TG, Elston DM. Andrews’ Diseases of the Skin: Clinical Dermatology. 10th ed. Philadelphia, Pa.: Saunders-Elsevier; 2006.

  18. Jung JY, Shin HS, Won CH, Cho S. Facial verruca plana that developed after semipermanent tattooing. Ann Dermatol. 2009;21(1):92-94. Available at ncbi.nlm.nih.gov/pmc/articles/PMC2883382 

  19. Frankel DH. Field Guide to Clinical Dermatology. 2nd ed. Philadelphia, Pa.: Lippincott Williams & Wilkins; 1999:144.20. Elder DE, Elenitsas R, Rubin AI, et al. Atlas and Synopsis of Lever’s Histopathology of the Skin. 3rd ed. Philadelphia, Pa.: Lippincott Williams & Wilkins; 2013.

  20. Kirnbauer R, Lenz P. Human papillomaviruses. In: Bolognia JL, Jorizzo JL, Schaffer JV, eds. Dermatology. 3rd ed. Philadelphia, Pa.: Elsevier Saunders; 2012: Chap. 79.

  21. Kim WJ, Lee WK, Song M, et al. Clinical clues for differential diagnosis between verruca plana and verruca plana-like seborrheic keratosis. J Dermatol. 2015;42(4):373-377. 

  22. Grillo E, Boixeda P, Ballester A, et al. Pulsed dye laser treatment for facial flat warts. Dermatol Ther. 2014;27(1):31-35. 

All electronic documents accessed on May 4, 2015.

This The Clinical Advisor CME activity consists of 3 articles. To obtain credit, read Multiple facial papules on a HIV-positive man and Blistering patch on 
infant’s forearm. Then take the post-test here.

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