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• W2024509007 abstract "It was with great interest that I read the letter by G. Miltiadous and colleagues in the October 2001 issue of Atherosclerosis, vol. 157 pages 255–256 [1]. An elevated Lipoprotein(a), (Lp(a)) level above 25 mg/dl is an independent risk factor for coronary artery disease (CAD) [2]. Around 36.7% of the United States population judged to be at high risk for coronary artery disease, as defined by the new NECP guidelines, have elevated Lp(a) levels [2]. Around 14% of the population, considered to be low risk according to the new NECP guidelines, have elevated Lp(a) levels [2]. Although all the underlying mechanisms for variance in Lipoprotein(a) levels are not known, it appears that in Familial Hypercholesterolemic (FH) homozygotes the levels of Lp(a) are about two-fold higher than FH heterozygotes, and that FH heterozygotes have significantly higher Lp(a) than non FH individuals [1]. As noted by Miltiadous, this can not be entirely explained by differences in apo(a) allele frequencies and although the underlying mechanisms are not clear, it is thought that a delayed Lp(a) catabolism through the low-density lipoprotein receptor (LDLR) or possibly the metabolism of fatty acids can affect lipopoprotein synthesis or direct synthesis of LDL and Lp(a) [1] The underlying genetic defect of a class V mutation or a class II mutation in the LDLR may affect the classic lipid profile of patients with homozygous FH and also the Lp(a) levels. Gene-environment interactions are also important in assessing the impact of gene variants (polymorphisms) [3,4]. There are several methods for reduction of Lp(a) and these methods may have an impact on gene variants that warrants further study. Niacin in high doses can lower Lp(a), but the disadvantage of Niacin is that in high doses it can be toxic to the liver and can cause flushing and headaches and its use requires the close monitoring of liver function tests [5,6]. Ascorbic acid at a dose of 3 g per day with l-lysine monohydrochloride at a dose of 3 g per day can reduce Lp(a) at a lower dose than Vitamin C alone with no toxic side effects [6,7]. l-Carnitine at a dose of 2 g per day has also been shown to reduce Lp(a) without major side effects [8]. Both tamoxifen and estrogen lower Lp(a) in postmenopausal women [9,10]. Estrogen and progestin lowers Lp(a) levels significantly especially in postmenopausal women with high initial levels [11]. Although Lp(a) levels are generally thought to be refractory to diet and exercise, in obese women with initial high Lp(a) levels, a low-calorie diet with weight loss showed a significant reduction in Lp(a) levels which was independent of hormonal changes in weight reductions [12]. If Lp(a) testing is added to the general lipid screening panel especially in high risk individuals, low cost methods with low toxicity are available to reduce Lp(a) [2,6–12]." @default.
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• W2024509007 date "2002-08-01" @default.
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• W2024509007 title "Multiple Methods for Reduction of Lipoprotein(a)" @default.
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• W2024509007 doi "https://doi.org/10.1016/s0021-9150(02)00031-x" @default.
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