[|This is a wonderful grouping of 39 clinical photographs, mirroring my earlier comments about the tremendous variation in phenotypic expression of this disease we call psoriasis. My great friend, the late Jim Gilliam from Dallas, in the 1970’s with his discovery of subacute cutaneous lupus erythematosus, showed dermatologists and rheumatologists the full spectrum of lupus from mild skin involvement to devastating multi-organ involvement. I do believe psoriasis also has a similar spectrum with an even more protean clinical manifestation than lupus, from a few minor patches or even purely skin involvement to devastating joint disease with or without other systemic immune-mediated diseases such as Crohn’s, diabetes, multiple sclerosis, etc plus aspects of the Metabolic Syndrome. A most important aspect coming out of this wonderful array of clinical photographs is, I believe, the need for all dermatologists to do a total body evaluation of the patient at each visit, as too often a cursory examination is done, or patients because of their natural shyness to expose the surface of their skin to the public frequently will not disclose to the dermatologist areas of concern, such as flexural psoriasis, genital and perianal involvement, etc. In addition, are the various different manifestations of nail psoriasis important as a marker for psoriatic arthritis as discussed in Chapter 6?|auteur215]
The clinical manifestations of psoriasis are varied. The elementary lesions are the result of all possible combinations of: epidermal proliferation and parakeratosis leading to the exaggerated formation of squamae, epidermal and dermal inflammation responsible for infiltration of the lesions but also for erythema and the formation of micropustules, and sometimes even clinically visible pustules. Consequently, the psoriasis plaques can take highly varied appearances, from simple erythema covered with light desquamation, to the characteristic erythematosquamous plaque, or even to the emergence of a carpet of pustules. Erythema and desquamation are thus the only anomalies to be constantly observed (photos 2 and 3).
The typical elementary lesion of psoriasis combines all these components and presents a papular, erythematosquamous rounded lesion that is well circumscribed and covered with micaceous, silvery-white scales (photo 4). Scratching these scales with a curette causes one last glossy squama to appear. If tugged at, a characteristic bloody dew connected to the abrasion of the turgescent dermal papillae starts to well up. Sometimes, one can observe a lighter halo, as described by Woronoff, surrounding the plaque. It is not known whether this is a sign of the plaque’s progression or, conversely, of an anti-inflammatory response by restricting the spread (vasoconstriction?).
[|Regarding the Woronoff ring, I
have only seen this sign in healing psoriatic plaques, close to their final
disappearance. I regard it as being caused by different propensity to be
stained to topical antipsoriatic drugs such as anthralin.|auteur195]
The body areas most often affected and often most resistant to treatment are the elbows (photo 5), the knees (photos 6 and 7), the scalp (photo 9) and the lumbar region (photos 8, 10 and 11).
But all body areas may be affected, even the mucosa. Each of the
possible sites may be associated with other sites, making its diagnosis
easier, or may be isolated, often making diagnosis more difficult
(photos 12 and 13).
Hence the descriptions: psoriasis of the scalp, psoriasis of the face (photo 14), psoriasis of the eyelids (photo 15), psoriasis of the external auditory canals (photo 16), psoriasis of the skin folds (photos 17 and 18)—also called inverse or flexural psoriasis, wherein the squamae are not observed due to maceration, psoriasis of the mucous membranes: lingual mucosae, with geographic tongue (photo 19), genital mucosae (photos 20 and 21), psoriasis of the nails (photos 26, 27, 28, 29 and 30) and palmoplantar psoriasis. Each site poses different differential diagnosis problems, has specific repercussions on the quality of life and raises particular therapeutic problems, which will be detailed.
[Depending on the surface of the plaques|In my view this
distinction is made on the size of the lesion rather than on its surface.|auteur195], we distinguish guttate psoriasis (photo 31) (guttate psoriasis), nummular psoriasis, generalized psoriasis – so-called universalis (photo 34) – in which a few sites of healthy skin persist, and finally erythrodermic psoriasis, affecting the entire skin area (photo 32). The shape of the plaques can also vary, some being annular with central clearing, with the rings potentially joining up to form circinate psoriasis (photos 33 and 35).
The extent of neutrophils migration in epidermis may lead to the formation of clinically visible pustules characteristic of pustular psoriasis (photo 36). The latter may be generalized, with pustules appearing on the plaques of classic psoriasis, as sometimes observed after stopping general corticotherapy, or generalized pustulosis, as described by von Zumbusch (photo 37). Pustular psoriasis may be localized: palmoplantar pustulosis (photo 38) and acrodermatitis continua of Hallopeau.
Depending on people’s age, psoriasis poses particular therapeutic problems. There can be psoriasis in the child (photo 39), psoriasis in the fertile woman and the pregnant woman (with this exceptional generalized pustular form, called impetigo herpetiformis) and psoriasis in the elderly. Comorbidities play, of course, an important role in the choice of therapeutic strategy. Their impact will be discussed when we come to look at different ways of organizing therapeutic strategies.
[ Pruritus is associated in 70% of cases. |Is that really true?? 30%?|auteur193] Two quite disparate situations need to be distinguished:
- generalized pruritus leading to look for an associated atopic diathesis, contact eczema, scabies… , responsible for psoriasis eruption (Köebner’s phenomenon), or an epidermotropic psoriasiform lymphoma;
- localized pruritus, often producing a habit of repetitive scratching and ending not only in a permanent Köebner’s phenomenon but also in an associated neurodermatitis that will need to be treated in its own.
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News from medical groups
- 2018/04/183rd Turkish National Psoriasis Symposium
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- 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
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- 2015/08/04Epidermia Greece: a new partner association of PIN
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- 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