Psoriasis is a skin disease of unclear origin, in part genetic. This dermatological condition affects 1 to 3% of world population, both among women than among men. In its mild form, psoriasis confined to the scalp, nails, knees, elbows, feet, hands and sometimes the genitals. In severe cases, it expands and can win the whole body.
This chronic skin disease evolves very personal, with attacks, but also remissions during which the lesions disappear. We then say that psoriasis is “laundered”. The respite is very variable duration of remission and often incomplete.
To date, no cure for psoriasis heal completely is known, however, it is possible to control psoriasis, reduce the extent of damage and improve patients’ lives.
Historical Information:
One of the first accurate descriptions was made by Sir Robert Willan in his treatise on diseases of the skin dates back to 1808. American inventor Benjamin Franklin souffrait1. The writer John Updike has made the description of his own achievement in a new book, taken from Problems (1979).
Main Causes:
The precise causes are unknown although in nearly 30% of cases [ref. necessary], we can find a familial predisposition to develop it, especially if external factors come to add. The disease has genetic components, self-immune, microbiological and environmental or food (prohibiting the consumption of dairy products or certain other commodities are often used in the stories of people who managed to get rid of it without involving a treatment parallel).
The epidermis renews itself too quickly, in only four to six days, instead of the usual three weeks and this causes localized inflammation. The epidermal cells accumulate on the surface of the skin and form a white layer called dander. Perfectly harmless, yet they have the disadvantage of being unsightly. The presence of leukocytes in the dermis suggested the role of the immune system.
As mentioned above, there are a small third of people with a family component to psoriasis (yet to determine what other factors come into play) with almost 30% of patients have a family member also having the same maladie. A number of genes have been identified as potential markers of risk, including the PSOR. The most important seems to be the PSORS1 located on chromosome 6 that is responsible for nearly one third of psoriasis familiaux.
Outbreaks of psoriasis are often related to stress. They can also be caused by a factor of infection (streptococcal infection, for example). Their frequency is very variable and, in general, the trigger for the surge is not identifiable. Excessive consumption of alcohol is an aggravating factor in psoriasis.
Some medications may exacerbate psoriasis but their arrest must be considered on a case by case, it can cause other hazards, especially cardiovascular. These are mainly those of the class of beta-blockers. Other molecules have been reported as potentially aggravating, with a lower risk, however. These are the sartans and énalapril. Instead, sun exposure has a protective net.
During pregnancy, there is usually a decrease in relapses with an aggravation by cons following it. The mechanism cited is an immuno-modulation by high levels of progesterone and estrogen causes stimulation of immunity depending on B cells but decreased immune activity of Tlymphocytes Progesterone is known to have an immunomodulatory role during the key pregnancy.
Types of psoriasis:
Plaque Psoriasis:
Also known as psoriasis vulgaris, it is the most common form of psoriasis (over 90% of cas8) which gave its name to the disease: “large scales”. Skin lesions are red, irritated, scaly and infiltrated. The central region is normal. When the scales stand out, they leave the skin raw, sometimes bleeding.
The location of the plates is approximately symmetrical, mainly concerning the region of the elbows, knees, scalp, lower back or the peri-umbilical. It can also reach areas previously scarred or for exercising trauma (Koebner phenomenon).
Guttate psoriasis
The guttate psoriasis (or psoriasis guttata), as its name implies, is characterized by a scattering of small drops of psoriasis on the body. There is no evidence of plaques, but the drops, which have the advantage of their small size, “launder” faster and thus remain “irritant” to live as long. They are found on all areas of friction: lower abdomen, lower back (pants size) forearm, chest (bra), but also hair and flag of the external ear.
Pustular Psoriasis
It follows from the exaggeration of the phenomenon of exocytosis of neutrophils that characterizes psoriasis clinically: flat pustules yellowish-white (amicrobial) with a tendency to coalescence. Histologically: spongiform pustule of Kogoj. This type of psoriasis is usually palmar-plantar. It also speaks of Acropustulosis to serve it relates ends.
Inverse psoriasis or psoriasis folds
Red plate, although limited, shiny, smooth, and little or no flaky. Achievement of large folds (cross-buttock, groin extending into the genital area, under the breast, more rarely axillary and popliteal) and less often small folds (umbilicus).
Nail involvement
Achieving this is the nail in half of cases of psoriasis. It is most often a simple white stippling of the nail (pitting in thimbles), sometimes with a fragility of the latter with the possibility of separation into layers.
PSA
Inflammation produces the combined symptoms of arthritis in patients who developed or will develop psoriasis. Also known as psoriatic arthritis, affects about 5% (but the figure may reach 25% in some publications10) of psoriasis, and is generally associated with skin lesions (which rarely can start after rheumatism). It is a chronic inflammatory arthritis, deforming, which can be very disabling, which describes two main forms, which can be combined:
Axial arthritis: look very close to ankylosing spondylitis: SPA (neck, back, sacroiliac joints) and occurs more often in men carrying the HLA-B27.
Peripheral arthritis: look close to rheumatoid arthritis, but with a predilection for the distal inter phalangeal (finger skin, nails are often affected by psoriasis). No association with HLA-B27.
Some forms may develop after a joint injury.
Treatment
Local treatment involves applying a cream on the area of psoriasis.
Corticosteroids: they have a favorable effect on psoriasis, unfortunately plates often return upon discontinuation of treatment. This also causes a form of desensitization, which requires increasing doses over time. In addition, the effect is not only locally if we apply these ointments over large areas. This form of treatment should be limited to acute or very unattractive for a short period and on a limited area.
Calcipotriene: the Calcipotriol is a derivative of vitamin D. Normally, the latter is synthesized in the skin exposure to solar ultraviolet light. It is thus here a substitute for the exhibition (or PUVA). The maximum amount applies is limited because at high doses, calcipotriol becomes toxic.
Retinoids: tazarotene is a derivative of vitamin A available in ointment. His tolerance is however less than the calcipotriol.
Tars: they were once commonly used application on psoriasis but were particularly awkward because messy.
Anthralene: the dithranol is a derivative of tar. The dithranol has some efficacy, especially in combination with other treatments but it is sometimes irritating and inconvenient especially (very “marking”), which limits its use.
- Salicylic acid.
- Bains.
- Moisturizing the skin.
Phototherapy:
Sun exposure is most often a positive effect on psoriasis. However, in 10% of cases, this exhibition is actually harmful. The subject will then avoid the sun, or at least avoid being directly exposed to its rays.
Phototherapy with ultraviolet B (UVB): In all cases, the ultraviolet therapy (A or B) must be performed under medical supervision. It leads to a threshold of tolerance varies from one individual to another it is necessary not to exceed. Otherwise the patient is exposed to the photodamage and low-risk-of skin cancer (carcinoma, melanoma). Risks much lower a patient suffering from psoriasis skin controls much more than the “ordinary people”. which can detect the earliest any possible incipient neoplasia.



April 18th, 2010
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