Age and sex

Distribution of lesions

Configuration of lesions

Individual lesions

Course

Psoriasis in dark-skinned peoples misdiagnosed clinically as lichen planus:

• Denominators in common: Purplish scaly papules and plaques

• Factors differentiating: Psoriasis differs clinically from lichen planus by the presence of micaceous scale and Auspitz's sign, and by the absence of polygonal outline of papules and of Wickham's striae

1. Palmar-plantar, inverse, erythrodermic, and pustular (localized and widespread) variations exist.

2. Arthritis may be an accompaniment, as may dystrophy of nails.

3. Geographic tongue is a manifestation of psoriasis in the oral cavity.

1. Dermatophytic pustules differ from those of pustular psoriasis by tendency to asymmetrical distribution and to development usually of few lesions.

2. Guttate dermatosis (guttate parapsoriasis, small-plaque parapsoriasis, mycosis fungoides) differs from guttate psoriasis by being less papular and less scaly.

3. Pityriasis rosea differs from guttate psoriasis by the presence of a "herald patch," distribution of lesions in a so-called Christmas tree fashion, and the presence of collarettes of scale.

4. Pityriasis rubra pilaris often has accentuation infundibular and zones within an erythroderma that appear to be spared.

5. Chronic nummular and dyshidrotic dermatitis consists of lesions that are not as sharply circumscribed as plaques of psoriasis.

6. Lichen simplex chronicus differs from a plaque of psoriasis by accentuation of skin markings and greater thickening of the lesion.

7. Rupial syphilis differs from guttate psoriasis by being crusted as well as scaly.

Early

Fully developed

Late

Papules of psoriasis are smooth when mounds of parakeratosis are covered by the original cornified layer prior to its being expelled. When that protective cornified layer is lost, mounds of parakeratosis are then revealed to the naked eye, and the lesion then is seen as scaly. The remainder of a papule is constituted of an acanthotic epidermis, an edematous papillary dermis, and an infiltrate of lymphocytes of variable density. A plaque is covered by scales made up of confluent parakeratosis and, while the plaque is still evolving, of neutrophils laced throughout the region of parakeratosis. The substance of a plaque is composed of psoriasiform acanthosis, edema of the papillary dermis, and an infiltrate of lymphocytes. An erythroderma exhibits all the signs of a plaque of psoriasis, but less parakeratosis because of shedding constant of scales; the amount of parakeratosis still adherent to the surface of the lesion may be scant. A pustule of psoriasis consists of clusters of neutrophils in the spinous zone (a microabscess of Munro), in sponge-like array in the upper part of the epidermis (spongiform pustule of Kogoj), beneath the normal stratum corneum (subcorneal pustule), or within parakeratosis (intracorneal pustule).

1. Mounds of parakeratosis with neutrophils at their summit is a clue to guttate (eruptive) psoriasis and dermatophytosis.

2. Neutrophils scattered among compressed keratocytes at the periphery of a tense intraepidermal vesicle on a palm or sole is a clue to pustular psoriasis or dermatophytosis.

3. Thin, elongated epidermal rete ridges of nearly equal length above a superficial infiltrate of inflammatory cells is a clue to psoriasis.

4. Findings typical of psoriasis in the near absence of a cornified layer are a clue to psoriatic erythroderma.

5. Striking pallor of cells in the upper part of the spinous layer and in the granular layer is a clue to evolving lesions of psoriasis, deficiency diseases such as pellagra, acrodermatitis enteropathica, and necrolytic migratory erythema, Mucha-Habermann disease, and secondary syphilis.

6. Dilated tortuous capillaries in thin dermal papillae, those vessels spiraling to near the undersurface of the epidermis are a clue to psoriasis and dermatophytosis.

Periodic acid-Schiff stain, when negative, eliminates the possibility of dermatophytes when that diagnosis is suspected either by changes in sections stained by hematoxylin and eosin or by virtue of the clinical history.

Neither is known, but a variety of factors are known to be important, among them genetic, immunologic, and infectious ones.

Psoriasis is a disease systemic of nature genetic whose lesions in the skin are those of a distinctive pattern morphologic, i.e., clinical and histopathologic, that can be brought into being by a variety of factors that range from trauma local to infection systemic. That psoriasis is more than just a disease of skin and nails may be determined from its involvement of mucous membranes, such as in the guise of geographic tongue, and of joints in the form of psoriatic arthritis. Moreover, different expressions morphologic of psoriasis reflect various influences, such as site anatomic, pace of the process itself, and extent of distribution. For one example, psoriasis that develops in skin compromised severely by stasis fails to achieve the appearance of stereotypical lesions of the condition developed fully on other sites, i.e., it never exhibits thin rete ridges, thin suprapapillary plates, and dilated capillaries that spiral in thin dermal papillae to repose just beneath the epidermis, the reason being that the superficial blood vessels distorted by the effects of marked stasis are unable to spiral as they do in psoriasis elsewhere and, that being the case, the changes epidermal expected do not come into being. For another example, psoriasis positioned on palms and soles often manifests itself histopathologically as a spongiotic dermatitis that seems to be a caricature of changes early in the process psoriatic, spongiosis mediated by lymphocytes is present then in the lower part of the epidermis. Lymphocytes precede neutrophils into the epidermis of an evolving lesion of psoriasis. In short, psoriasis on volar skin looks different from psoriasis on other anatomic sites (probably because of the restrictive character of the thick, compactly arranged cornified layer that is normal for that particular site). Spongiosis in psoriasis on volar skin may be so prominent that it comes to resemble classic "spongiotic" dermatitides, i.e., allergic contact dermatitis, nummular dermatitis, dyshidrotic dermatitis, and "id" reactions. Vesicles may be seen in sections of tissue, and, not surprisingly, they even may be discernible clinically. The clue most helpful to differentiation of psoriasis from well-established spongiotic dermatitides on volar skin is scale-crusts that are staggered throughout the cornified layer, a finding that reflects the periodic, pulsatile nature of psoriasis. Neutrophils that reside in those scales-crusts are yet another evidence of psoriasis.

The speed of the process psoriatic also influences the appearance morphologic of lesions. For example, acceleration mightily of the process results in formation of guttate lesions characterized by drop-sized macules that soon become smooth papules and, rapidly thereafter, scaly papules. If the process of psoriasis is sped up still further, pustules of psoriasis spring forth; if, however, the pace of the process is slow, scaly plaques develop. Pustules of psoriasis are to guttate papules of psoriasis what bullous lesions of lupus erythematosus are to a "butterfly blush" and vesicles of lichen planus are to papules of lichen planus. In each set, the first represents acceleration dramatic of the process pathologic.

If the process psoriatic no longer is expressed as discrete papules or plaques, but as involvement of the skin universally, the result is erythroderma. In the case of psoriasis, the erythroderma is exfoliative because the disease is accompanied by countless scales. Biopsy of psoriatic erythroderma reveals changes indistinguishable from those of fully developed plaques of psoriasis, except, at times, for near absence of parakeratosis. The equivalent biologic of exfoliation associated with psoriatic erythroderma is shedding of parakeratotic cells at a rate phenomenal. That loss of corneocytes becomes a clue to diagnosis; a typical fully developed plaque of psoriasis is replete with parakeratosis, whereas psoriatic erythroderma may be nearly devoid of it.

The findings histopathologic most revealing of psoriasis during the evolution of lesions are neutrophils in the epidermis, particularly in zones of parakeratosis, and especially at the summit of mounds, mitotic figures well above the basal layer, spiraled capillaries that wind through dermal papillae to rest just beneath the epidermis, and edema of the papillary dermis. The findings essential for diagnosis of lesions of psoriasis developed fully are confluent parakeratosis in which neutrophils may be scattered, thin suprapapillary plates, elongated epidermal rete ridges, some of them thin and of approximately equal length, mitotic figures in keratocytes situated well above the basal layer, edema of dermal papillae, and a spiraled capillary in each dermal papillae. During devolution of lesions of psoriasis, the crucial signs for diagnosis are acanthosis that is less dramatically psoriasiform but with rete ridges of about equal length, some thin rete ridges, and dilated tortuous capillaries seated just beneath the epidermis. As is apparent, the character of capillaries in dermal papillae is an attribute important of psoriasis throughout the course chronological of a lesion.

Pustular psoriasis assumes many forms clinically. The pustules may be confined to palms and soles, at which sites the condition is known eponymically for Barber. Sometimes, pustules develop within established plaques of psoriasis. Yet another expression, accompanied usually by signs of acute illness, e.g., fever and chills, is universal pustulosis, a condition named eponymically for von Zumbusch. Other manifestations of pustular psoriasis have been given a variety of names that do not convey the reality of their being those of psoriasis because the persons who bestowed the names thought they were dealing with a disease other than psoriasis, e.g., acrodermatitis continua (Hallopeau), dermatitis repens (Crocker), subcorneal pustular dermatosis (Sneddon and Wilkinson), pustular bacterid (Andrews), impetigo herpetiformis, keratoderma blennorrhagicum and, presumably, acropustulosis of infancy. All those terms, in our estimation, are evasions from diagnosis with specificity of particular presentations of pustular psoriasis, e.g., acrodermatitis continua for pustular psoriasis secondary to trauma on a digit, especially a thumb (a Köbner phenomenon), and dermatitis repens being a synonym for acrodermatitis continua; pustular bacterid for pustular psoriasis on palms or soles; subcorneal pustular dermatosis for pustular psoriasis characterized by arcuate, annular, and polycyclic shapes of lesions; impetigo herpetiformis for pustular psoriasis in pregnancy; and keratoderma blennorrhagicum for pustular psoriasis as an expression of Reiter's disease (which itself is psoriasis*).

*Reiter was a notorious Nazi physician who oversaw heinous experiments on innocents at extermination camps. There is no need to refer to "Reiter's disease," anymore than there is to impetigo herpetiformis; both are psoriasis and should be designated that.

Because pustular psoriasis is so protean, it has been known by many designations that becloud the truly psoriatic nature of the process. Another illustration of that phenomenon concerns mucous membranes of the oral cavity, namely, geographic tongue, which has a figurate appearance very much like that of subcorneal pustular dermatosis of Sneddon and Wilkinson, and, like that latter "dermatosis," is manifested histopathologically by spongiform pustules, it being psoriasis. The configuration of the lesions as they appear clinically on the tongue and in the skin of Sneddon-Wilkinson disease are the same, to wit, arcuate, annular, and polycyclic, they migrating in centrifugal fashion. In brief, geographic tongue and subcorneal pustular dermatosis are psoriasis. In the context of the remarks preceding, it is apparent that distinctions should not be made among variations morphologic of pustular psoriasis. The diagnosis should be pustular psoriasis.

Certain drugs, various antibiotics and codeine phosphate among them, induce changes clinical and histopathologic like those of pustular psoriasis. That condition, known generically as "acute generalized exanthematous pustulosis," could be a pustular drug eruption that simulates pustular psoriasis or could represent induction by a drug of true pustular psoriasis, i.e., Köbnerization in a person predisposed genetically to psoriasis.

The first inflammatory cells to enter the epidermis of psoriasis are lymphocytes and they are accompanied there by slight spongiosis. Soon thereafter, neutrophils follow, and they traverse the entire extent of the epidermis, including the cornified layer. When numerous neutrophils move briskly through the epidermis, they may be captured, in collections, in the spinous zone where traditionally they have been termed microabscesses of Munro, lodged immediately beneath the stratum corneum, where they have been dubbed "subcorneal pustules," and not arrayed in discrete collections but in a "sponge-like" arrangement in the upper part of the spinous zone, the granular zone, or the cornified layer, where they have been named eponymically for Kogoj, who first called attention to the finding. In short, the names "microabscess of Munro" and "spongiform pustule of Kogoj" simply describe the appearance of neutrophils in the epidermis at different stages in the course of the process psoriatic. Findings identical to those of psoriasis are induced by dermatophytes, the presence of hyphae in sections of tissue being the key to differentiation between them. It cannot be stressed too strongly that, except for the presence of hyphae, dermatophytosis is an exact simulator of psoriasis in all expressions of it. It is incumbent on histopathologists, therefore, to scour lesions of what seems to be psoriasis for stigmata of superficial fungal infection. If the description of the lesions clinical is not consonant with psoriasis, a specialized stain for fungi should be employed. Not uncommonly, what was thought to be psoriasis histopathologically turns out to be dermatophytosis. Nowhere is that more true than in the nail unit.

Whether pustules are seen clinically depends on the size of the collections of neutrophils in surface epidermis. If collections of neutrophils are large sufficiently, discrete pustules of psoriasis will be apparent clinically. In time, those pustules tend to become confluent to form "lakes of pus." When pustules rupture, the surface of the skin is dotted by collarettes of scale-crusts that represent residua of sloughed pustules that were admixed with parakeratotic cells. All the changes histopathologic just recorded for pustular psoriasis may be seen in papules of guttate psoriasis.

As can be imagined, psoriasiform acanthosis is not a component of what clinically is pustular psoriasis because that process charges forward too rapidly to permit the epidermis time to become thickened. For the same reason, mitotic figures are fewer in the lower portion of the epidermis of pustular psoriasis than they are in papules of eruptive psoriasis.

Last, a few words should be devoted to the subject of the Köebner phenomenon (isomorphic effect) in psoriasis. Köebnerization usually refers to the induction of lesions of a disease, especially psoriasis, lichen planus, and lichen sclerosus et atrophicans, by the effects of trauma physical. Sometimes, however, an inflammatory disease, such as graft-versus-host reaction, or a neoplastic disease, such as mycosis fungoides, may induce in a person genetically psoriatic findings of psoriasis in addition to those of the "primary" disease, e.g., mycosis fungoides. In that circumstance, attributes of two different processes pathologic will be apparent concurrently in a single section of tissue.