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Abstract Psoriasis is a hereditary, chronic immune-mediated inflammatory skin disorder of unknown etiology. The disease is estimated to affect 2-3% of the general population worldwide. Indeed, psoriasis has a complex genetic predisposition, but its development and/or exacerbation appear to involve an interaction between multiple genetic and environmental risk factors. Cardiovascular disease is an important cause of morbidity and mortality in patients with psoriasis. The risk factors for cardiovascular disease (eg. Obesity, hypertension, diabetes mellitus, smoking, hyperlipidemia, oxidative stress,…. ) occur with higher incidence in patients with psoriasis and appear to be highest for those with more severe disease. Moreover, psoriasis was suggested as an independent risk factor for cardiovascular disease. With the introduction of recent developments in understanding the role of inflammation in the pathogenesis of psoriasis, it is widely believed that psoriasis is not just a skin disease but a systemic inflammatory process. This inflammatory process plays a major role in the formation of atherosclerosis which is a hallmark of cardiovascular disease. Psoriasis is associated with changes in plasma lipid and lipoproteins, which may play a role in the development of occlusive vascular disease. Ox-LDL plays an important role in the development of atherosclerosis. Studies suggest that LDL cholesterol, under certain circumstances, will undergo an oxidative pathway which changes LDL cholesterol into ox-LDL cholesterol. It is more atherogenic than. Ox-LDL enhances endothelial production of leucocyte adhesion molecules, i.e., cytokines and growth factors that regulate smooth muscle cell proliferation, collagen degradation, and thrombosis. |