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Lintje Ho, MD, MPH; Jacqueline C. M. Witteman, PhD; Baerbel Rohrer, PhD; Albert Hofman, MD, PhD; Paulus T. V. M. de Jong, MD, PhD, FRCOphth; Johannes R. Vingerling, MD, PhD

Arch Ophthalmol. 2009;127(3):340-341.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Lipoprotein-associated phospholipase A₂ (Lp-PLA₂) has been suggested to be a predictor of coronary heart disease and stroke. It is a calcium-independent serine lipase produced predominantly by macrophages, and it co-travels with circulating low-density lipoprotein. Its biological role is controversial. Initial reports suggested anti-inflammatory properties because of its ability to hydrolyze platelet-activating factor and to remove polar phospholipids in modified low-density lipoprotein.¹ Conversely, recent studies indicated a proinflammatory role of Lp-PLA₂ mediated by its reaction products (lysophosphatidylcholine and oxidized free fatty acids). Lipoprotein-associated phospholipase A₂ is an inflammatory marker and can directly promote atherogenesis.² The potential clinical benefit associated with Lp-PLA₂ inhibition or its use as an inflammatory marker provides a rationale for this study. Because inflammation, atherosclerosis, and other . . . [Full Text of this Article]

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