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Guttate psoriasis_0212 Derm Dx
A 6-year-old Hispanic girl was brought by her mother to the dermatology clinic with a two-week history of a scaly rash. According to the mother, the child had a throat infection two weeks prior to developing the rash. The rash was mildly pruritic, but the girl was otherwise asymptomatic. Physical examination revealed the presence of numerous 1- to 2-cm erythematous patches with scale located on her face, scalp, chest, back, arms and legs. What’s your diagnosis?
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The girl had guttate psoriasis, which often follows an acute streptococcal infection. Among patients with acute guttate psoriasis, two thirds have a preceding upper respiratory infection and one half have positive antistreptolysin titers.
The guttate variety is a common manifestation of psoriasis in children, who experience spontaneous remission with treatment of the underlying infection. This is unlike the chronic course of other forms of psoriasis, including guttate psoriasis in adults.
Psoriasis is a chronic disease that affects 2% of the world’s population with great worldwide variation in incidence. Men and women are affected equally. Onset can be at any age but occurs most often in the third decade of life. The disease is less common in children; earlier onset predicts more severe disease.1
All psoriasis skin lesions share the characteristics of erythema, thickening and scale. The majority of lesions are sharply demarcated erythematous scaly plaques. The most common type of psoriasis is chronic plaque psoriasis. Other types include guttate, erythrodermic, pustular, and palmoplantar psoriasis and acrodermatitis continua of Hallopeau. Psoriatic lesions can also present in unique anatomic locations, such as the scalp, oral mucosa, and nails.
The differential diagnosis of psoriasis is limited when the clinical manifestation is typical, but atypical presentations can mimic eczema, seborrheic dermatitis, and lichen simplex chronicus. Erythrodermic psoriasis can resemble other causes of erythroderma, including mycosis fungoides, drug reactions and pityriasis rubra pilaris.
The differential diagnosis of guttate psoriasis includes secondary syphilis, pityriasis rosea, pityriasis lichenoides and small plaque parapsoriasis. Pustular psoriasis can imitate acute generalized exanthematous pustulosis, Sneddon-Wilkinson disease, immunoglobulin A pemphigus and other causes of subcorneal pustulosis.
The pathogenesis of psoriasis is not fully understood, but studies reveal a T-lymphocyte-mediated autoimmune disease. The genetic nature of psoriasis has been seen in the predisposition to disease development with certain HLA types.1
External factors may trigger psoriasis in genetically susceptible patients. Trauma and injury can lead to psoriatic lesions (Koebner phenomenon). Other triggering factors include infection, as seen with streptococcal infection in guttate psoriasis; HIV; stress; and drugs, such as beta-blockers and lithium.
If the superficial scaly portion of a psoriatic lesion is removed, characteristic pinpoint bleeding can be seen (Auspitz sign), a reflection of the dilated capillaries that are the earliest histologic change seen in psoriasis. At times, a ring of pallor (Woronoff ring) surrounds the lesions.
Histologically, a fully developed psoriasis lesion demonstrates regular acanthosis with an absent granular layer. Parakeratosis is present, and collections of neutrophils are seen in the stratum corneum (microabscess of Munro) and within the epidermis (spongiform pustule of Kogoj).
Psoriatic arthritis occurs in 5% to 30% of psoriasis patients, who are also said to be at increased risk of cardiovascular diseases and diabetes. Studies have shown that psoriasis can affect both physical and mental functioning. Patients complain mainly of low self-esteem and frustration with their appearance.
Treatment depends on the extent of the disease. Mild disease can be treated with topical corticosteroids and vitamin D3 analogs. Other topical treatments include ret-inoids and anthralin. Among the systemic options are methotrexate, oral retinoids and cyclosporine. Phototherapy utilizes oral psoralen followed by UVA or UVB treatment.
The recent development of biologic agents has greatly improved success rates in psoriasis treatment. These agents include tumor necrosis factor-a inhibitors like infliximab, adalimumab and etanercept as well as other biologics, such as efalizumab and alefacept. Oral corticosteroids should be avoided because although the skin lesions will clear during treatment, a severe flare commonly follows discontinuation.
Our patient’s streptococcal infection had already been treated. Topical corticosteroids resulted in resolution of the skin lesions with post-inflammatory hypopigmentation.
Deborah Yang, MD, practices dermatology at the Michael E. DeBakey VA Medical Center in Houston, Texas.
Reference
1. Kapp A, Piskorski A, Schöpf E. “Elevated levels of interleukin 2 receptor in sera of patients with atopic dermatitis and psoriasis.” Br J Dermatol. 1988;119:707-710
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