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Hypertriglyceridemia clinical presentation

Because of the similarity, it is difficult to conclude whether the lipid changes induced by SERMs offer any advantage over the profile determined by HT. Triglyceride levels have been proposed as an independent risk factor for CVD in postmenopausal women (Miller 1998). Further, there are some indications that increases in triglycerides may favor the reduction in the size of LDL particles. Smaller LDL particles are more susceptible to oxidation and have been associated with a higher risk potential (Austin et al. 1988), but whether this observation confers any clinical prejudice to hypertriglyceridemia has not been proven at present. [Pg.225]

CETP exchanges cholesteryl esters of HDL with triglycerides of VLDL, IDL, and LDL. The HDL-derived cholesteryl esters are subsequently removed from the circulation via the LDL receptor pathway [28, 91]. Absence of functional CETP results in pronounced elevations of plasma concentrations of HDL cholesterol (2.5-8 mmol/1) and apoA-I. In parallel, plasma concentrations of LDL cholesterol and apoB are relatively low. Heterozygous CETP deficiency is associated with a milder elevation of HDL cholesterol. Most patients with CETP deficiency do not present with specific clinical symptoms. Some were reported to exhibit corneal opacities. CETP deficiency has been claimed to reduce the risk of atherosclerotic vascular disease and to prolong life expectancy. However, in some situations (e.g., in hypertriglyceridemia or in the absence of high HDL cholesterol), CETP deficiency may also increase cardiovascular risk [15, 28,91]. [Pg.540]


See other pages where Hypertriglyceridemia clinical presentation is mentioned: [Pg.506]    [Pg.320]    [Pg.324]    [Pg.118]    [Pg.302]   
See also in sourсe #XX -- [ Pg.99 ]

See also in sourсe #XX -- [ Pg.99 ]




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