Reduction of Serum Lipoprotein(a) Using Estrogen in a Man With Familial Hypercholesterolemia

1992 
To the Editor. —The significance of lipoprotein(a) [Lp(a)] as a genetic risk factor for atherosclerotic vascular disease has been well documented. 1-3 However, many aspects of its metabolism remain unclear. 1,2 There have been reports that Lp(a) is removed from the circulation by low-density lipoprotein (LDL) receptors, 4 but the role of this receptor in the catabolism of Lp(a) is still controversial. We recently observed interesting changes in serum lipids, including Lp(a), in a patient with familial hypercholesterolemia following estrogen therapy for prostatic cancer, which may help our understanding of Lp(a) catabolism. A 67-year-old man with familial hypercholesterolemia (which consists of a marked elevation of LDL-cholesterol to more than 6.45 mmol/L and thickening of the Achilles tendon to 18 mm) and non-insulin-dependent diabetes mellitus was admitted to the hospital for the treatment of prostatic cancer. He had been treated for a long time with cholestyramine (8 g/d) and probucol (1
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