NEW YORK (Reuters Health) – The presence of certain inflammatory and atherogenic lipoprotein markers, in combination with chronic inflammation, may explain why the risk of CVD and CVD-related mortality is increased in patients with rheumatoid arthritis.
A group led by Dr. Eva Hurt-Camejo, of Gצteborg University and AstraZeneca in Sweden, has found that the amount and size distribution of LDL differs between patients with rheumatoid arthritis and matched controls. Plasma levels of small LDL particles (LDL-1) were greater in 31 patients than in 28 controls, and levels of large LDL particles (LDL-3) were lower (p < 0.05).
"Clinical studies indicate that such small, dense LDL particles, which are poor in phospholipids, contribute to the risk for CVD, even when total plasma levels of LDL are not elevated," the investigators note in their report in the December issue of Arthritis and Rheumatism.
In rheumatoid arthritis patients LDL showed increased affinity for chondroitin 6-sulfate glycosaminoglycan (GAG), compared with controls. According to the research team, previous laboratory and clinical studies suggest that this binding is a key step in atherogenesis and is associated with a higher risk of CVD.
Dr. Hurt-Camejo's group also determined that plasma levels of secretory group IIA phospholipase A2 (sPLA2-IIA) were higher in patients than in controls, and that in patients sPLA2-IIA levels correlated with plasma levels of LDL-1 (p < 0.05).
"Previous experiments from our laboratory have shown that treatment of LDL with sPLA2 decreases the phospholipid content in the LDL particles and, as a consequence, diminishes the particle size, increases its density, and increases its affinity for arterial smooth muscle cell proteoglycans and GAG," the authors comment.
Furthermore, they report, levels of sPLA2-IIA correlated with plasma levels of C-reactive protein and intercellular adhesion molecule, two other markers of systemic inflammation that have been linked to an increased risk of CVD.
"Taken together," the investigators conclude, "these data imply that increased sPLA2-IIA levels in plasma may reflect an inflammatory activity related to the development of atherosclerosis and its clinical symptoms."
Arthritis Rheum 2001;44:2761-2767.
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