S2C3d-Psoriasiform Dermatitis

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Psoriasiform Dermatitis (parent chapter for 9 pictorial pages)

Of lesions in the psoriasiform category, psoriasis might be characterized as prototypic. Edema of the basal unit generally is not a significant feature of a lesion of psoriasis. Lesions of psoriasis have a life history; the histologic features vary with the stage of the life-history at the time a particular lesion is selected for biopsy. In addition, the anatomic site may impact on the histologic patterns in lesions of psoriasis. Lesions on the lower extremities are commonly associated with changes of angiodermatitis; they may be complicated by areas of edema and fibrosis; in addition, the inflammatory infiltrates may be prominent.

Classic lesions of psoriasis are histologically characteristic (S2C9P3-2-6). The features include: a rather uniform zone of parakeratosis with clusters of degenerating neutrophils in the parakeratotic cap; a thin, pale superficial unit with a poorly developed granular layer; an hyperplastic basal unit with regular elongation of the rete ridges; minimal inter-cellular edema; thinning of the suprapapillary epidermal plates; edematous, club-shaped, and elongated, dermal papillae; a tortuous, dilated capillary in each dermal papilla; and mild perivascular infiltrates of lymphocytes and histiocytes. In addition to all these features, dendritic histiocytes are widely spaced in the expanded basal unit of the epidermis; they are not associated with significant intra-epidermal infiltrates of lymphocytes. This deficiency is in contrast to the close association between lymphocytes and histiocytes in the epidermis in lesions of both eczema and contact dermatitis. The migration of neutrophils into the epidermis in lesions of psoriasis is variable but, in some examples, rich infiltrates are to be found in the superficial unit of the epidermis as well as among keratinized lamellae. In such lesions, the neutrophils of the superficial unit may collect in cytolytic defects among surviving keratinocytes. Keratinized cell walls (remnants of keratinocytes that have undergone cytolysis) form the walls of the defects; such lesions show a distinctive pustular alteration in the epidermis. The pattern qualifies as spongioform pustulosis (S2C9P3-7, & S2C13aP7a-1-7). The mucosal lesions of psoriasis generally are spongioform pustules (S2C10P4-1-3); lesions of this type on mucous membranes have also been classified as annulus migrans and as geographic tongue. The lesions of impetigo herpetiformis are spongioform pustules. This disorder apparently represents pustular psoriasis in association with the effects of pregnancy; the process is additionally characterized by hypocalcemia. The pustules of pustulosis palmaris et plantaris are intra-epidermal, but often show a spongioform pustular quality in the epithelium forming the wall of the defects.

Psoriasiform and spongioform pustular patterns may be seen in the setting of superficial fungus infection.

A variation of the pattern seen in the spongioform pustule is characterized by a subcorneal defect containing loose infiltrates and scattered clusters of neutrophils. Generally, the keratin layer forming the roof of the defect is minimally altered. Neutrophils migrate into the epidermis beneath the defect but, for the most part, the patterns do not qualify as a well-developed spongioform pustule. Subcorneal pustular dermatitis shows lesions of this type. Similar lesions may be seen in bullous impetigo and even in some examples of pemphigus foliaceus.

Psoriasiform processes commonly have a hypertrophic quality; such lesions show both a prominent degree of epidermal hyperplasia and a widened papillary dermis. In these hypertrophic variants, the papillary dermis shows a distinctive pattern of lamellar fibrosis; the lamellae outline the dermal papillae and the number of lamellae, as well as the width of the lamellae, provide a rough measure of duration of the process. This type of lamellar fibrosis is a response to external trauma, such as scratching. One example of a psoriasiform process showing this pattern of lamellar fibrosis qualifies as lichen simplex chronicus. Lesions of “lichen simplex chronicus” may be associated with nodular, pruritic lesions. Such lesions may be somewhat polypoid with central fibrous stalks; these nodular variants qualify as prurigo nodularis. The pattern of fibrosis in prurigo nodularis is non-specific; the nodular lesions may efface the rete ridges. In the areas of fibrosis, some of the small nerves in both the mid-portion and the upper portion of the dermis may be enlarged (increased diameter). They often show hyperplasia of Schwann cells. This type of change in peripheral nerves has been cited as a requisite for the diagnosis of prurigo nodularis, but is not a regular feature.

Some examples of superficial fungus disease are represented in remarkable psoriasiform patterns (S2C13P7-1). For some examples, the patterns qualify as those of a spongioform, pustular disorder (S2C13P7-2 & S2C13bP7b-1-6).

The cutaneous manifestations of Reiter’s disease are an extreme expression of the spongioform pustule; in older lesions of Reiter’s disease, the thick scale at the surface of the lesion is parakeratotic and contains neutrophils in the pattern of an inspissated pustule. The pattern in a lesion of Reiter’s disease is exuberantly psoriasiform. The lesions are characterized by remarkable scales of keratinized debris (S2C13P7-3); degenerating neutrophils collect among the keratinized lamellae. This out-pouring of neutrophils is a psoriasiform characteristic.

Pityriasis rubra pilaris is easier to define clinically than histologically. For some examples, the epidermis shows compact hyperkeratosis (with a tendency for zones of parakeratosis to be confined to the lips of plugged hair follicles), acanthosis, and effacement of the rete ridges. In addition, focal, mild liquefaction degeneration is a feature (S2C13P7-4). More commonly, the patterns have a psoriasiform quality with elongation of the rete ridges. In these more common variants, the keratin layer shows compact, orthokeratotic hyperkeratosis and parakeratosis (S2C13P7-5), with the zones of parakeratosis “stratified horizontally and vertically.”

Some examples of psoriasiform dermatitis are linear in distribution; this clinical feature is often cited as evidence of the Koebner phenomenon (S2C13P7-6 & 7). Rare epithelial nevi are manifested in the patterns of a psoriasiform process.

 

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