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Mutation Raises HDL, Lowers Efflux From Macrophages

Efflux capacity may affect likelihood of coronary artery disease

WEDNESDAY, Jan. 12 (HealthDay News) -- A genetic mutation can cause increased high-density lipoprotein (HDL) cholesterol levels and reduced cholesterol efflux from macrophages in its carriers, and the capacity for HDL to accept cholesterol from macrophages may be predictive of the risk of coronary artery disease, according to two articles published in the Jan. 13 issue of the New England Journal of Medicine.

Menno Vergeer, M.D., of the University of Amsterdam in the Netherlands, and colleagues studied the effect of a P297S mutation in SR-BI on HDL binding, cellular cholesterol uptake and efflux, atherosclerosis, platelet function, and adrenal function. They found that P297S carriers had higher HDL cholesterol levels than noncarriers, a reduced capacity for efflux of cholesterol from macrophages, and increased unesterified cholesterol content and impaired function of platelets.

Amit V. Khera, M.D., of the University of Pennsylvania in Philadelphia, and colleagues tested cholesterol efflux capacity in 203 healthy subjects whose carotid artery intima-media thickness was measured and in 442 patients with and 351 patients without angiographically confirmed coronary artery disease to test the hypothesis that the capacity of HDL to accept cholesterol from macrophages could predict atherosclerotic burden. They found a strong inverse association between cholesterol efflux capacity from macrophages and both carotid-intima media thickness and the likelihood of angiographic coronary artery disease, independent of HDL cholesterol.

"In conclusion, cholesterol efflux capacity, a key metric of HDL function, is not explained simply by circulating levels of HDL cholesterol or apolipoprotein A-I and is independently related to both the presence and the extent of atherosclerosis. These findings reinforce the concept that assessment of HDL function may prove informative in refining our understanding of HDL-mediated atheroprotection," Khera and colleagues conclude.

One author of the second study disclosed a financial relationship with GlaxoSmithKline; another author of the second study disclosed ties to a patent regarding utilization of cell culture systems for determining cholesterol efflux potential of serum.

Full Text - Vergeer (subscription or payment may be required)
Full Text - Khera (subscription or payment may be required)

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