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      Respuesta inflamatoria, metabolismo del colesterol y arteriosclerosis Translated title: Inflammatory response, cholesterol metabolism and atherosclerosis

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          Esta revisión tiene por objeto remarcar la relación existente entre las reacciones de fase aguda o respuesta inflamatoria con el metabolismo lipídico y su potencial implicación en el proceso de aterosclerosis. El amiloide A sérico es una proteína reactante de fase aguda que se caracteriza por incorporarse a las lipoproteínas de alta densidad durante los procesos inflamatorios, como se ejemplariza en la sarcoidosis, una enfermedad sistémica granulomatosa. Esta apolipoproteína actúa bien desplazando a las otras apolipoproteínas, principalmente a la apo A-I, bien interfiriendo en el proceso de esterificación del colesterol mediado por la actividad de la enzima lecitín-colesterol aciltransferasa. Ambos mecanismos de acción producen una aceleración del catabolismo del colesterol unido a las lipoproteínas de alta densidad ocasionando una disminución de sus concentraciones séricas. Esta alteración del metabolismo lipoproteico, sumado a un posible efecto directo del amiloide A sérico sobre el endotelio vascular y la placa de ateroma, implica a la actividad inflamatoria, expresada a través de las concentraciones séricas de amiloide A, en el desarrollo de la arteriosclerosis.

          Translated abstract

          The goal of the present review consists on the relationship between inflammatory disorders, such as that represented by systemic granulomatous diseases like sarcoidosis, and the cholesterol metabolism and its implication in the atherosclerosis process. Serum amyloid A is an acute phase reactant that transiently binds to the high density lipoproteins during an inflammatory response. Serum amyloid A may act either displacing apo A-I, which in turn result in increased catabolism of high density lipoproteins, or inhibiting lecithin-cholesterol acyltransferase activity which leads to low levels of esterified serum cholesterol. This lipoprotein alteration together with a direct effect of the serum amyloid A on the endothelium of the atheromatous plaque suggest a potential pathophysiological link between the inflammatory responses expressed by the serum concentrations of amyloid A and the development of the atherosclerotic process.

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          Most cited references 91

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          Inflammation, pravastatin, and the risk of coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events (CARE) Investigators.

          We studied whether inflammation after myocardial infarction (MI) is a risk factor for recurrent coronary events and whether randomized treatment with pravastatin reduces that risk. A nested case-control design was used to compare C-reactive protein (CRP) and serum amyloid A (SAA) levels in prerandomization blood samples from 391 participants in the Cholesterol and Recurrent Events (CARE) trial who subsequently developed recurrent nonfatal MI or a fatal coronary event (cases) and from an equal number of age- and sex-matched participants who remained free of these events during follow-up (control subjects). Overall, CRP and SAA were higher among cases than control subjects (for CRP P=0.05; for SAA P=0.006) such that those with levels in the highest quintile had a relative risk (RR) of recurrent events 75% higher than those with levels in the lowest quintile (for CRP RR= 1.77, P=0.02; for SAA RR= 1.74, P=0.02). The study group with the highest risk was that with consistent evidence of inflammation (elevation of both CRP and SAA) who were randomly assigned to placebo (RR=2.81, P=0.007); this risk estimate was greater than the product of the individual risks associated with inflammation or placebo assignment alone. In stratified analyses, the association between inflammation and risk was significant among those randomized to placebo (RR=2.11, P=0.048) but was attenuated and nonsignificant among those randomized to pravastatin (RR=1.29, P=0.5). Evidence of inflammation after MI is associated with increased risk of recurrent coronary events. Therapy with pravastatin may decrease this risk, an observation consistent with a nonlipid effect of this agent.
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            Serum amyloid A-containing human high density lipoprotein 3. Density, size, and apolipoprotein composition.

            Serum amyloid A protein (apo-SAA), an acute phase reactant, is an apolipoprotein of high density lipoproteins (HDL), in particular the denser subpopulation HDL3. The structure of HDL3 isolated from humans affected by a variety of severe disease states was investigated with respect to density, size, and apolipoprotein composition, using density gradient ultracentrifugation, gradient gel electrophoresis, gel filtration, and solid phase immunoadsorption. Apo-SAA was present in HDL particles in increasing amounts as particle density increased. Apo-SAA-containing HDL3 had bigger radii than normal HDL3 of comparable density. Purified apo-SAA associated readily with normal HDL3 in vitro, giving rise to particles containing up to 80% of their apoproteins as apo-SAA. The addition of apo-SAA resulted in a displacement of apo-A-I and an increase in particle size. Acute phase HDL3 represented a mixture of particles, polydisperse with respect to apolipoprotein content; for example, some particles were isolated that contained apo-A-I, apo-A-II, and apo-SAA, whereas others contained apo-A-I and apo-SAA but no apo-A-II. We conclude that apo-SAA probably associates in the circulation of acute phase patients with existing HDL particles, causing the remodeling of the HDL shell to yield particles of bigger size and higher density that are relatively depleted of apo-A-I.
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              Human serum amyloid A (SAA) protein: a prominent acute-phase reactant for clinical practice

               F De Beer,  E. Malle (1996)

                Author and article information

                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Anales de Medicina Interna
                An. Med. Interna (Madrid)
                Arán Ediciones, S. L. (Madrid )
                February 2001
                : 18
                : 2
                : 56-60
                [1 ] Ciutat Sanitària i Universitària de Bellvitge Spain
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