Not all erythematosquamous eruptions are psoriasis.

When confronted with an acute erythematosquamous outbreak, a mere diagnosis of guttate psoriasis will not suffice.

  • Some thought must be given to secondary syphilis and primary HIV infection and to making a serological assessment

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  • Pityriasis rosea may pose a problem, with its oval erythematosquamous maculae and peripheral collarette scaling, often arranged on the back in the form of a “Christmas tree”. One must look for the largest-sized initial patch predating the generalized outbreak by several days. Spontaneous clearing within a few weeks will provide final reassurance.

Photo 52.

  • Eruptive forms of guttate parapsoriasis - with their “sealing wax” scales detaching from a block with a curette, and the juxtaposition of differently aged papular, squamous then pigmented, cicatricial components - may raise questions, especially since they tend to develop towards chronicity. Diagnostic can be confirmed by means of anatomico-pathological examination.
  • Lichen planus, with its violaceous papules covered in fine whitish latticework, its cutaneous and mucous attack and the extent of the pruritus, will rarely pose problems except in the palmoplantar and/or ungual sites, where a biopsy will be sometimes necessary.

Photo 53. Faced with a chronic erythematosquamous outbreak, diagnosis may be more difficult:

  • Nummular eczema is sometimes difficult to tell apart from inflammatory and pruritic psoriasis. Biopsy will not always be of much help, and it is mainly the questioning with the help of the allergological testing that will enable a diagnosis to be made. One should not forget that contact eczema might be at the root of Köebner’s phenomenon, and thereby associated with psoriasis.

Photo 54.

  • Porokeratosis will not pose a diagnostic problem as long as lesions are carefully examined, allowing to detect the highly characteristic “surrounding wall” edging. Only palmoplantar sites may pose problems.
  • The distinction between psoriasis and pityriasis rubra pilaris is much more difficult. The follicular hyperkeratosis, the yellow colour of the palmoplantar keratoderma and the hyperkeratosis of the hand lines, the chalky appearance of the face and the spaces left for healthy skin, so characteristic of pityriasis rubra pilaris, are not always present. The histological signs are essentially negative, since there is no visible migration of neutrophilic polynuclears in pityriasis rubra pilaris, but they are not always observed in psoriasis. Finally, some psoriasis, particularly in children, start in the form of what we French call “spinulosism” with peripilar hyperkeratosis, especially on the tibial crests. There will be cases in which the diagnosis can only be rectified in step with the evolution.

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  • Parapsoriasis en plaque, early forms of mycosis fungoides, may look very much like psoriasis. Moreover, certain psoriasis have proved capable of evolving towards a cutaneous T cell lymphoma. That is why T cell lymphoma should always be suspected when faced with pruritic psoriasis, and it could be necessary to perform and repeat biopsies.

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  • Finally, faced with erythematosquamous pruritic lesions, the existence of Norwegian scabies should be borne in mind.

Photo 59. Some clinical forms of psoriasis pose special problems as regards differential diagnosis.

  • Erythrodermae cannot be distinguished one from another with any certainty by clinical examination alone. Therefore, when considering any erythroderma, not only will any past history of psoriasis need to be sought but also anything that may be reminiscent of drug-induced toxidermia, generalized contact or atopic eczema, pityriasis rubra pilaris or cutaneous T cell lymphoma of the Sézary syndrome type. Erythroderma is always a medical emergency.
  • Conversely, some highly localized erythematosquamous lesions must not be judged to be psoriasis too hastily. Thought must be given to the possibility of Bowen or Paget disease and to performing a biopsy. The difficulty in diagnosing is particularly important when psoriasis is combined with actinic keratosis or pagetoid basal cells carcinoma. This is not a rare situation, given that numerous antipsoriatic treatments are prone to favouring the occurrence of skin carcinomas. In this situation, the only way of not confusing clinically the two types of lesion is to eliminate the psoriatic lesions by a powerful treatment such as methotrexate, during the period necessary to treat the precancerous or cancerous lesions.

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  • Exanthametous pustulosis is generally easy to distinguish from pustular psoriasis, particularly by its onset around the skin folds and, of course, by its triggering by a drug; however, it is interesting to note that this toxidermia seems to present itself more often in psoriatics.

Some psoriasis sites pose specific differential diagnosis problems.

  • Psoriasis in the folds is made of erythematous plaques, due to maceration and given to being pruritic. Particularly if isolated, these lesions are far too often considered, without mycological sampling, to be mycotic intertrigo. By contrast, the existence of intertrigo during classic psoriasis may have mycotic origins. Therefore, mycological sampling must not be forgotten.
  • The same wrong diagnoses are often made in onychopathy. A distortion of the nail, particularly a toenail, may certainly be psoriatic but may be equally as well connected with a trichophyton’s infection or repeated traumas. Such traumas may trigger Köebner’s phenomenon in the nail. Here again, mycological sampling is of great help. [|I have very little to add to a well-written chapter. One area that has always given me personally a great deal of difficulty is distinguishing between psoriatic nails and onychomycosis, particularly in affected toenails. Thus, I do believe psoriatic nails are more prone to fungal infections. Could the opposite also be appropriate? Thus, in a psoriatic patient with positive mycology, does the treatment of the nail fungus potentially improve the underlying nail psoriasis? Better methodologies, outside of biopsying and mycological evaluations would be helpful to reduce the clinical problems inherent in psoriatic toenails.|auteur215]

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  • A diagnosis of palmoplantar keratoderma of psoriatic origin must always be discussed at length, especially if this palmoplantar keratoderma is isolated.
    • Trichophytosis must always be searched for, especially since there is a secondary infection to a trichophyton in about 20% of psoriatic palmoplantar keratodermae and this secondary infection may produce Köebner’s phenomenon.
    • Contact eczema or orthoergic dermatitis may look like psoriasis or be the trigger for palmoplantar psoriasis.
    • Some T cell lymphomas may start with palmoplantar keratoderma.
    • Climacteric palmoplantar keratoderma, occurring in postmenopausal women, often obese, is never associated by definition with psoriasis in other areas of the body. Most likely, it is a special ailment different from psoriasis
    • .Palmoplantar keratodermae of genetic origin generally pose few diagnostic problems.

Many other skin diseases may be confused with psoriasis:

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