In 1978, Breckenridge et al. described a patient with a deficiency of apolipoprotein C-II, the activator of the enzyme lipoprotein lipase.1 It was predicted that the newly discovered disorder would provide additional understanding of the relation between the metabolism of the triglyceride-rich lipoproteins — the chylomicrons and very-low-density lipoproteins (VLDL) — and the low-density and high-density lipoproteins (LDL and HDL). It was anticipated that studies of first-degree relatives would yield important information about the inheritance of the disorder and contribute to an understanding of the pathophysiology induced by a deficiency of apolipoprotein C-II or lipoprotein lipase. It was also hoped.
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