Effect of antiretroviral therapy on allele-associated Lp(a) level in women with HIV in the Women's Interagency HIV Study

Enkhmaa, Byambaa; Anuurad, Erdembileg; Zhang, Wei; Li, Chin Shang; Kaplan, Robert C.; Lazar, Jason; Merenstein, Dan; Karim, Roksana; Aouizerat, Brad; Cohen, Mardge H.; Butler, Kenneth R.; Pahwa, Savita; Ofotokun, Igho; Adimora, Adaora A.; Golub, Elizabeth T.; Berglund, Lars

doi:10.1194/jlr.p084517

Cited by 9 publications

(5 citation statements)

References 51 publications

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“…Several inflammatory conditions 45 Increase Tocilizumab (interleukin-6 inhibitor) 47,61 ∼30%-40% decrease Protease inhibitors or antiretroviral therapy 56,57 Increase…”

Section: Lp(a) and Aortic Valve Stenosismentioning

confidence: 99%

Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement

Kronenberg

Mora

Stroes

et al. 2022

European Heart Journal

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554

383

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This 2022 European Atherosclerosis Society lipoprotein(a) [Lp(a)] consensus statement updates evidence for the role of Lp(a) in atherosclerotic cardiovascular disease (ASCVD) and aortic valve stenosis, provides clinical guidance for testing and treating elevated Lp(a) levels, and considers its inclusion in global risk estimation. Epidemiologic and genetic studies involving hundreds of thousands of individuals strongly support a causal and continuous association between Lp(a) concentration and cardiovascular outcomes in different ethnicities; elevated Lp(a) is a risk factor even at very low levels of low-density lipoprotein cholesterol. High Lp(a) is associated with both microcalcification and macrocalcification of the aortic valve. Current findings do not support Lp(a) as a risk factor for venous thrombotic events and impaired fibrinolysis. Very low Lp(a) levels may associate with increased risk of diabetes mellitus meriting further study. Lp(a) has pro-inflammatory and pro-atherosclerotic properties, which may partly relate to the oxidized phospholipids carried by Lp(a). This panel recommends testing Lp(a) concentration at least once in adults; cascade testing has potential value in familial hypercholesterolaemia, or with family or personal history of (very) high Lp(a) or premature ASCVD. Without specific Lp(a)-lowering therapies, early intensive risk factor management is recommended, targeted according to global cardiovascular risk and Lp(a) level. Lipoprotein apheresis is an option for very high Lp(a) with progressive cardiovascular disease despite optimal management of risk factors. In conclusion, this statement reinforces evidence for Lp(a) as a causal risk factor for cardiovascular outcomes. Trials of specific Lp(a)-lowering treatments are critical to confirm clinical benefit for cardiovascular disease and aortic valve stenosis.

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“…Several inflammatory conditions 45 Increase Tocilizumab (interleukin-6 inhibitor) 47,61 ∼30%-40% decrease Protease inhibitors or antiretroviral therapy 56,57 Increase…”

Section: Lp(a) and Aortic Valve Stenosismentioning

confidence: 99%

Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement

Kronenberg

Mora

Stroes

et al. 2022

European Heart Journal

Self Cite

554

383

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“…Emphasizing the potential for gene-environment interactions, a population study of US Blacks and Nigerians with a common genetic background but two different environments showed significantly higher Lp(a) levels in US Blacks for the same sized apo(a) compared with Nigerians (18). We have recently shown that infection with human immunodeficiency virus suppresses Lp(a) levels and initiation of antiretroviral therapy normalizes these levels, underscoring the potential of an environmental impact (36).…”

Section: Discussionmentioning

confidence: 79%

Heritability of apolipoprotein (a) traits in two-generational African-American and Caucasian families

Enkhmaa

Anuurad

Zhang

et al. 2019

Journal of Lipid Research

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c 9 (2-35) 7 (2-37) ISL, larger (mg/dl) 9 (5-21) c 13 (5-25) c 3 (1-9) 3 (1-10) ISL, smaller (mg/dl) 20 (8-41) c 21 (6-39) c 5 (2-30) 5 (2-27) apo(a) isoform, larger (kringles) 30 (27-33) 30 (29-33) 32 (29-34) 31 (27-34) apo(a) isoform, smaller (kringles) 25 (21-28) 25 (23-28) 25 (22-30) 25 (23-30) Data are expressed as mean ± standard deviation or median (interquartile range) for non-normally distributed variables. ISL, larger, ISL associated with the larger allele in a given LPA allele-pair; ISL, smaller, ISL associated with the smaller allele in a given LPA allele-pair.

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“…On the contrary, protease inhibitors and antiretroviral therapy have been associated with increased Lp(a) levels when administered in human immunodeficiency patients with baseline Lp(a) levels > 20–30 mg/dL [ 100 ].…”

Section: Lp(a)-lowering Therapiesmentioning

confidence: 99%

“…Reduction up to 37.9% (not approved for clinical use) [91][92][93] Growth hormone Increase by 25% to 100% [94] Antibodies against interleukin-6 (e.g., tocilizumab) Reduction between 30% and 40% [98] Protease inhibitors or antiretroviral therapy Increase [100] Low-saturated fat diets Potential increase between 8% and 20% [102][103][104] Low-carbohydrate, high-saturated fat diets and diets enriched with walnuts or pecans Decrement by 15% and 6% to 15%, respectively [102,105] Dietary supplements (L-carnitine, and coenzyme Q10) Modest reduction between 10% and 30% [101,106] Specific foods (coffee, tea, and alcoholic beverages, especially red wine) Modest reduction between 10% and 30% [101,106] Vitamin C Neutral effect on plasma Lp(a) levels [107,108] Bariatric surgery Significant increase in Lp(a) plasma levels [111] Table 2. Potential mechanisms of action of current and emerging lipoprotein(a) (Lp(a))-lowering therapies.…”

mentioning

confidence: 99%

Effects of Lipid-Modifying and Other Drugs on Lipoprotein(a) Levels—Potent Clinical Implications

et al. 2023

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The past few years have shown an ongoing interest in lipoprotein(a) (Lp(a)), a lipid molecule that has been proven to have atherogenic, thrombogenic, and inflammatory properties. Several lines of evidence, indeed, have demonstrated an increased risk of cardiovascular disease as well as calcific aortic valve stenosis in patients with elevated Lp(a) levels. Statins, the mainstay of lipid-lowering therapy, slightly increase Lp(a) levels, while most other lipid-modifying agents do not significantly alter Lp(a) concentrations, except for proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors. The latter have been shown to reduce Lp(a) levels; however, the clinical significance of this effect has not been clearly elucidated. Of note, the pharmaceutical lowering of Lp(a) may be achieved with novel treatments specifically designed for this purpose (i.e., antisense oligonucleotides (ASOs) and small interfering RNAs (siRNAs)). Large clinical trials with cardiovascular outcomes with these agents are ongoing, and their results are eagerly awaited. Furthermore, several non-lipid-modifying drugs of various classes may influence Lp(a) concentrations. We have searched MEDLINE, EMBASE, and CENTRAL databases up to 28 January 2023 and summarized the effects of established and emerging lipid-modifying drugs and other medications on Lp(a) levels. We also discuss the potent clinical implications of these alterations.

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Effect of antiretroviral therapy on allele-associated Lp(a) level in women with HIV in the Women's Interagency HIV Study

Cited by 9 publications

References 51 publications

Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement

Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement

Heritability of apolipoprotein (a) traits in two-generational African-American and Caucasian families

Effects of Lipid-Modifying and Other Drugs on Lipoprotein(a) Levels—Potent Clinical Implications

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