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[|I agree to the historical overview, but miss the
history of psoriatic arthritis, where the association between psoriasis and
arthritis was first noted by Alibert in 1818, and the term psoriatic arthritis
(psoriasis arthritiques) first used by the French physician Pierre Bazin
in 1860. In the late19th and
early 20th century however, there was no consensus that psoriatic
arthritis was an entity of its own. But
following the clarification of a circulating rheumatoid factor associated with
rheumatoid arthritis in 1948 and a later
finding that the majority of patients with arthritis and psoriasis were
seronegative a distinction became
easier. In spite of this, opposing
concepts of psoriatic arthritis still went on in the early nineteen sixties. Eugene Farber supported a smaller group of
rheumatologists who kept holding on so-called psoriatic arthritis as a
coincidental association between rheumatoid arthritis and psoriasis, while the
majority of rheumatologists lead by Wright & Moll presented their evidence
for the distinction between the two entities. An assumption which to-day is well established.|auteur196]

[|Psoriasis has always “lagged behind” other autoimmune (immune-mediated) diseases such as rheumatoid arthritis, Crohn’s disease, and even lupus erythematosus. The “fathers of psoriasis” mentioned in this chapter, including Willan, Köbner, Auspitz, and Munro, paved the way for the modern generation to understand not only the clinical manifestations but the genetics and immunopathology of this unique disease called “psoriasis”. I enjoyed the discussion relating to serendipitous discoveries of important treatments, some of which are still in use today. I do believe dermatologists need to be given a great deal of credit for the initial use of methotrexate well before our rheumatology colleagues discovered it for rheumatoid arthritis. Thus, a number of California dermatologists in the 1950’s established aminopterin, the forerunner of methotrexate, as a viable treatment option for psoriasis. Thereafter, with dogged determination, they continued to conduct clinical studies with methotrexate until finally the Food and Drug Administration of the United States “gave way” in 1971 and approved methotrexate usage for what they considered a “benign skin disorder”. Another serendipitous discovery in the history of psoriasis, which I do believe changed the total research focus on psoriasis from that of a hyperproliferative epidermal disease to a T-cell driven disease was that of ciclosporin’s value in the treatment of psoriasis in 1979. This brings us to the 21st century and the biological revolution, a direct result of our understanding of how ciclosporin affects T-cells.|auteur215]

The history of psoriasis falls under four headings: a social history, an identification process, the search for aetiology and the development of therapy. Each of these approaches shed light on the present-day situation in its own particular way.

In social terms, psoriasis clearly is and always has been a part of those disorders that bring with it social exclusion. Having been long confused with leprosy, it led since biblical times to a verdict of social exclusion on the grounds of impurity. This form of branding persists down to this day, and the look of others is often to blame for the psychological suffering caused by psoriasis and hence for its severity.

The development of semiology applied to the skin, based on the analysis of the elementary lesions, enabled psoriasis to be identified at the heart of the large group of squamous or scaling dermatoses by Robert Willan in 1805. Interestingly, psoriasis is described by this author in two chapters: the one entitled psoriasis and the one entitled leprosy. In it, psoriasis is called Lepra vulgaris, a good illustration of the old confusion between the two diseases. Today the question is one of knowing whether psoriasis is an illness with various clinical manifestations or rather a syndrome grouping together diseases with different physiopathologies, whose only common trait is clinical manifestations linking proliferation, abnormal differentiation of epidermis and skin inflammation.

The succession of theories about the cause of psoriasis is also very interesting, with confusion still prevailing in the minds of patients between the causes and the triggers.

The interactions between microbial agents and psoriasis are still under study. Bacteria can play the role of super antigen, and some believe that fragments of the HPV genome in the lesions can trigger the inflammatory reaction.

The isomorphic response described by Köebner in 1872 still arouses excitement. It remains the only model that allows studying the kinetics of the emergence of a psoriatic lesion. Recall that this reaction requires an attack on the epidermis and the dermis.

Psychological factors have only been taken into account much more recently. This approach is associated in particular with the works of P. de Graciansky in the 1960s.

The development of histology during the second half of the 19th century, enabled in particular Auspitz and Munro to identify acanthosis, parakeratosis and neutrophilic polynuclear microabscesses. Thirty years ago, I. Braverman drew attention to the importance and persistence of anomalies in the microcirculation of the superficial dermis in psoriasis plaques. Only very recently, thanks to the development of immunopathology enabling intratissual identification of the lymphocytic subpopulations, has the attention been directed towards the importance of T lymphocyte infiltrates, CD 4 predominating in the dermis and CD8 predominating in the epidermis. Progress in cellular biology has allowed research on psoriasis to be focused firstly on epidermal proliferation, then on the role of the epidermal inflammation mediators, then on the role of the neutrophils on the maintenance of psoriatic plaques, then on the anomalies of the non-lesional psoriatic skin, then on the role of the fibroblasts in epidermal proliferation, then on the role of proteases expressed in the subcorneal region and finally on the role of lymphocytes T activation. As a result of advances in molecular genetics, analysing families affected by psoriasis has made it possible to try to identify the gene modifications implicated in this illness. Progress in immunology is currently allowing the study of lymphocytic activation mechanisms in psoriasis and ways of controlling this activation pharmacologically. Finally, there are around ten models of genetically modified mice expressing skin anomalies reminiscent of psoriasis: inflammation and epidermal proliferation. The multiplicity of these animal models is a powerful argument for thinking that numerous genetic anomalies may result in a common phenotype with the clinical and histological features of psoriasis.

As to the treatments for psoriasis, most have been discovered by chance. The reason for this is that the majority of the new therapeutic families discovered throughout time have been empirically tried on psoriasis: sulphur, tar, arsenic, salicylic acid, chrysophanic acid, X-rays in the 19th century, anthralin, UV rays, psoralens, topical and systemic corticosteroids, then methotrexate, retinoids, cyclosporine, and calcipotriol in the 20th century. The reasons for these drugs’ antipsoriatic activity are not known with certainty, and the molecular targets responsible for their activity are poorly understood. Only very recently, synthesized biological molecules to inhibit a particular cellular interaction or a specific cytokine have been made available to patients. In the course of this therapeutic development, we have progressed from a situation in which efficacy was the main preoccupation to a period when the efficacy/toxicity ratio was the main assessment criterion, to finally arrive to a point where, in addition to the preceding criteria, account is taken of the treatment’s impact on the patients’ quality of life.

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