Mediators of inflammation
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The pathogenesis of pruritus in psoriasis remains unclear. Many possible mediators were implicated to transmit or modulate this sensation in psoriasis, but none has been clearly proven to be a causative agent of itching. The most often discussed theory mentioned the importance of impaired innervations and neuropeptides imbalance in psoriatic skin. ⋯ Whether these mechanisms are also involved in pruritus accompanying psoriasis requires further investigation. Limited knowledge of pruritus origin in psoriasis is responsible for the lack of the effective antipruritic treatments for psoriatics. Here, we summarize the current knowledge about the pathogenesis of pruritus in psoriasis and point out possible directions of future studies aiming the pathogenesis of this symptom in psoriasis.
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Mediators of inflammation · Jan 2007
Accumulation of oxidized low-density lipoprotein in psoriatic skin and changes of plasma lipid levels in psoriatic patients.
Psoriasis is a chronic inflammatory skin disease characterized by an accelerated turnover of epidermal cells and an incomplete differentiation in epidermis with lesion. However, the exact etiology of psoriasis is unknown. Abnormalities in essential fatty acid metabolism, free radical generation, lipid peroxidation, and release of lymphokines have been proposed. ⋯ Lipid peroxidation mediated by free radicals is believed to be one of the important causes of cell membrane destruction and cell damage. This study shows for the first time the accumulation of oxidized low-density lipoprotein in psoriatic skin lesion. We believe that accumulation of ox-LDL in psoriatic skin may have an important role in the immune-inflammatory events that result in progressive skin damage.