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Acta bioquímica clínica latinoamericana
Print version ISSN 0325-2957On-line version ISSN 1851-6114
Abstract
ESPONDABURU, Omar Raúl; FARA HUNT, Verónica Alicia and OCAMPO, Liliana Inés. The aterogenic process and its development in autoimmune diseases. Acta bioquím. clín. latinoam. [online]. 2004, vol.38, n.2, pp.181-192. ISSN 0325-2957.
Atherosclerosis is the most prevalent vascular pathology. The triggering event of the atherogenic process is the oxidation of LDL in the sub-endothelium. These oxidized LDL activate the vascular endothelium originating the expression of cell adhesion molecules, cytokines and growth factors that initiate the recruiting of pro-inflammatory cells and interrelate the different cellular types which take part in the plaque formation. Then, lipids are accumulated in the macrophages, giving origin to the formation of foam cells and, finally, the smooth muscle cells proliferate and emigrate to the arterial intima. In the autoimmune diseases like rheumatoid arthritis, systemic lupus erythematosus, antiphospholipid syndrome, etc. acute coronary events take place without the presence of previous traditional risk factors. The analysis of the mechanisms which lead to a premature and accelerated atherosclerosis in these pathologies let us establish similarities between aterogenesis and chronic inflammation processes which characterise these illnesses. They show increment in the expression of adhesion molecules, cytokines and growth factors, increase in the cellular recruiting, hydrolytic enzymes freeing, etc. Thus, atherosclerosis could be considered as a chronic inflammatory disease at vessel level, characterised by the accumulation of lipids which begins with the endothelium activation caused by oxidized LDL or by a chronic inflammation process. The presence of an autoimmune disease is a very important aterogenic risk factor because the probability of a greater thrombotic event rises to a higher degree and in less time than in the traditional risk factors.
Keywords : Atherogenic process; Rheumatoid arthritis; Systemic lupus erythematosus; Antiphospholipid syndrome.