Presse Med
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A MULTIFACTORIAL ORIGIN: Psoriasis is an inflammatory dermatosis resulting from abnormal epidermal homeostatis and characterized by hyperproliferation and abnormal keratinocyte differentiation as well as activation of the skinis immune system. This dermatosis is a prototype of multifactorial conditions implicating hereditary and environmental pathogenic mechanisms. TWO TYPES OF PSORISASIS: Familial psoriasis is observed early in life and is strongly associated with the major histocompatibility complex, particularly CW6, DR7, B1, and B57 molecules. The sporadic non-familial form develops later in life.
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THE CONTEXT: Psoriasic arthritis lies somewhere between rhumatoid polyarthritis and spondyloathropathy. Its prevalence is about 0.1% with a 1/1 sex ratio. Mean age at onset of symptoms is 40 years. ⋯ DISEASE SEVERITY: In general psoriasic arthritis is a benign condition. Severe forms have however been described with erosion and osteolysis involving the distal interphalangeal joints. Typical radiological may be observed.
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PREDOMINANT FEATURES: Psoriasis is a frequent inflammatory dermatosis. All age groups are involved. The typical lesion is a well-limited erythemato-squamaous non-pruriginous lesion. All skin areas may be involved but each individual has preferential zones.
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PERIPHERAL NERVE INVOLVEMENT: Peripheral nerve involvement is better known than central nervous system involvement. The dominant features are sensoromotor polyneuropathies or pure sensorial polyneuropathies. ⋯ OTHER LOCALIZATIONS: Diffuse encephalic involvement is less common: acute aseptic meningitis, intellectual deterioration. Psychiatric manifestations are also frequently observed.
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A NEW CLASS OF NSAID: All non-steroidal antiinflammatory drugs (NSAID) inhibit cyclooxygenase (COX) and prostaglandin synthesis implicated in inflammatory processes and also participate in protecting the gastric mucosa. The discovery of two isoforms of COX, called COX-1 and COX-2 has led to further research into dissociating NSAID efficacy and intolerance. COX-1 AND COX-2: It appears that the antiinflammatory and antalgesic effects of NSAID is related to COX-2 inhibition while the undesirable effects on the gastric mucosa would be related to COX-1 inhibition. A COX-2 specific inhibitor would thus provide the same efficacy as classic NSAID but without the digestive disadvantages.