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
- 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.
- 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.
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.
- 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.
- 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.
- Finally, faced with erythematosquamous pruritic lesions, the existence of Norwegian scabies should be borne in mind.
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.
- 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]
- 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:
- 2019/05/21 Focus on...SPIN2019 is now available on your screen!
- 2019/04/18 Focus on...SPIN Congress 2019 in Paris coming soon
- 2019/04/17 Focus on...Do not miss Spin Congress 2019 highlights
- 2018/07/16 Focus on...SPIN Sister Society Meeting at the EADV - 12 September 2018
- 2018/07/09 Focus on...SPIN 2019 Congress Website is Open !
News from the web office
- 2017/06/05PIN becomes SPIN - Skin Inflammation & Psoriasis International Network
- 2016/10/29PSO 2016 Congress - Webcasts Available!
- 2016/05/26PIN Survey on Phototherapy
- 2016/02/20PIN Study on Therapeutic Patient Education
- 2016/02/19World Directory of Psoriasis Medical Resources - February 2016 Update
- 2019/04/18 Focus on...SPIN Congress 2019 in Paris coming soon
- 2018/07/16SPIN Symposium at the Spring continental meeting - Tehran, 25-27 April 2018
- 2018/02/222nd National Meeting of the Egyptian Society for Psoriasis
- 2018/02/211st Psoriasis Symposium - Sarajevo 2017
- 2017/06/2815th São Paulo Meeting of Psoriasis and Vitiligo
News from medical groups
- 2018/04/183rd Turkish National Psoriasis Symposium
- 2017/06/21Brazilian Center for Psoriasis Studies joins SPIN!
- 2017/06/21Costa Rica Psoriasis Group - Meet them!
- 2017/02/02Works of the 1st Senegalese Psoriasis Day published!
- 2016/07/29Swiss S1 Guidelines for Systemic treatment of psoriasis vulgaris
News from patients associations
- 2017/02/08France Psoriasis - 2016 World Psoriasis Day
- 2016/05/26Senegal Patients Association joins PIN!
- 2015/08/04Epidermia Greece: a new partner association of PIN
- 2015/08/01Canadian Association of Psoriasis Patients joins PIN!
- 2015/04/09AEPSO Argentina launches digital map to find people with psoriasis in the country
Recent publications on Psoriasis and Atopic Dermatitis
IL-33 contributes to disease severity in Psoriasis-like models of mouse.
Cytokine. 2019 Jul , 119:159-167.
Immune cells infiltrating the psoriatic skin secrete high amounts of pro-inflammatory cytokines IL-17, TNF-α, IL-21 and IL-36 resulting in chronic inflammation. However, the exact cellular and molecular mechanisms have not been fully understood. We report here elevation of IL-33 expression in psoriatic lesions. Studies in imiquimod (IMQ)-induced mice with psoriatic inflammation confirmed a critical role for IL-33 in driving the disease. IL-33 reduces the CD4 and CD8 cells, inhibits autophagy (...)see on pubmed
Association of plasma and urine metals levels with kidney function: A population-based cross-sectional study in China.
Chemosphere. 2019 Jul , 226:321-328.
Although environmental exposure to multiple metals is common, epidemiological studies on the associations of exposure to 23 metals with kidney function have not been analyzed. We aimed to investigate the associations of 23 metals levels with renal function.see on pubmed
Models of human psoriasis: Zebrafish the newly appointed player.
Dev. Comp. Immunol.. 2019 Aug , 97:76-87.
Psoriasis is a human chronic, immune disease with severe cutaneous and systemic manifestations. Its prevalence, among the world population, highly varies with ethnicity and geography, but not sex from remarkable low levels in Asia to 2.3% in Spain, or an impressive 11.5% in Norway. The pathogenesis of psoriasis derives from complex genetic and environmental interactions, which creates aberrant crosstalk between keratinocytes and variated immune cell, resulting in open amplified inflammatory (...)see on pubmed
What's new in atopic eczema? An analysis of systematic reviews published in 2016. Part 3: nomenclature and outcome assessment.
Clin. Exp. Dermatol.. 2019 Jun , 44, (4):376-380.
This review forms part of a series of annual updates that summarize the evidence base for atopic eczema (AE). It presents the key findings from 11 systematic reviews published in 2016 that focus on AE outcome assessment, disease impact and nomenclature. Systematic reviews on the treatment and prevention of AE are summarized in Part 1 of this update, and systematic reviews on the epidemiology of and risk factors for AE are summarized in Part 2. Six reviews summarized what outcome measurement (...)see on pubmed
Discovery of a class of highly potent Janus Kinase 1/2 (JAK1/2) inhibitors demonstrating effective cell-based blockade of IL-13 signaling.
Bioorg. Med. Chem. Lett.. 2019 Jun 15, 29, (12):1522-1531.
Disruption of interleukin-13 (IL-13) signaling with large molecule antibody therapies has shown promise in diseases of allergic inflammation. Given that IL-13 recruits several members of the Janus Kinase family (JAK1, JAK2, and TYK2) to its receptor complex, JAK inhibition may offer an alternate small molecule approach to disrupting IL-13 signaling. Herein we demonstrate that JAK1 is likely the isoform most important to IL-13 signaling. Structure-based design was then used to improve the (...)see on pubmed
Effect of cinnamamides on atopic dermatitis through regulation of IL-4 in CD4 cells.
J Enzyme Inhib Med Chem. 2019 Dec , 34, (1):613-619.
This study aimed to evaluate the effects of cinnamamides on atopic dermatitis (AD) and the mechanisms underlying these effects. To this end, the actions of two cinnamamides, (E)-3-(4-hydroxyphenyl)-N-phenylethyl acrylamide (NCT) and N-trans-coumaroyltyramine (NCPA), were determined on AD by orally administering them to mice. Oral administration of the cinnamamides ameliorated the increase in epidermal and dermal thickness as well as mast cell infiltration. Cinnamamides suppressed serum (...)see on pubmed