Effect of evolocumab on fasting and post fat load lipids and lipoproteins in familial dysbetalipoproteinemia

Heidemann, Britt E; Koopal, Charlotte; Lennep, Jeanine Roeters van; Stroes, Erik S.G.; Riksen, Niels P.; Mulder, Monique; Zee, Leonie van Vark van C. der; Blackhurst, Dee; Marais, A. David; Visseren, Frank L.J.

doi:10.1016/j.jacl.2022.10.006

Cited by 5 publications

(4 citation statements)

References 42 publications

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“…Both same‐target inhibitors and small nucleic acid drugs have shown similar hypolipidemic effects. It is worth noting that PCSK9 monoclonal antibodies need to be administered every 2 weeks and PCSK9 small nucleic acid drugs can be administered semiannually, suggesting PCSK9 small nucleic acid drugs are more convenient for patients (Heidemann et al, 2023; Luo et al, 2023). Moreover, patient compliance is improved with the long‐term effect characteristics of small nucleic acid drugs (Liu et al, 2022).…”

Section: Application Of Small Nucleic Acid Drugs In Chronic Diseasesmentioning

confidence: 99%

The current perspective and opportunities of small nucleic acid‐based therapeutics

Chen,

Li,

et al. 2024

Drug Development Research

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Compared to traditional small molecule and antibody drugs, RNA‐based drugs offer a simple design, short research and development cycles, high specificity, broad treatment fields, and long‐term efficacy. As a result, RNA‐based drugs are extensively used to treat genetic diseases, tumors, viral infections, and other illnesses, suggesting that they have the potential to become the third‐largest drug class after small molecule and antibody drugs. Currently, more than 10 small nucleic acid drugs have gained regulatory approval. The commercialization successes of small nucleic acid drugs will stimulate the development of RNA‐based drugs. Small nucleic acid drugs primarily target liver diseases, metabolic diseases, genetic diseases, and tumors, and there is also significant potential for expanding indications in the future. This review provides a brief overview of the advantages and development of small nucleic acid‐based therapeutics and shows a focus on platform technologies such as chemical modifications and delivery systems that have enabled the clinical translation of small nucleic acid‐based therapeutics. Additionally, we summarize the latest clinical progress in small nucleic acid‐based therapeutics for the treatment of various diseases, including rare diseases, liver diseases, metabolic diseases, and tumors. Finally, we highlight the future prospects for this promising treatment approach.

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Section: Application Of Small Nucleic Acid Drugs In Chronic Diseasesmentioning

confidence: 99%

The current perspective and opportunities of small nucleic acid‐based therapeutics

Chen,

Li,

et al. 2024

Drug Development Research

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“…Therefore, an elevation in CMR and IDL (VLDLR) is observed in patients with familial type III hyperlipoproteinemia. In such patients, serum TG levels reached a peak at 6–8 h after the OFL, and did not return to initial levels even after 8 h [ 31 ], suggesting that familial type III hyperlipoproteinemia causes postprandial hyperlipidemia.…”

Section: Pathological Factors That Induce Postprandial Hyperlipidemiamentioning

confidence: 99%

Postprandial Hyperlipidemia: Its Pathophysiology, Diagnosis, Atherogenesis, and Treatments

Yanai,

Adachi,

Hakoshima

et al. 2023

IJMS

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Postprandial hyperlipidemia showing postprandial increases in serum triglyceride (TG) is associated with the development of atherosclerotic cardiovascular disease (ASCVD). To diagnose postprandial hyperlipidemia, the oral fat loading test (OFLT) should be performed; however, this test is very time-consuming and is difficult to perform. Elevated serum TG levels reflect an increase in TG-rich lipoproteins (TRLs), such as chylomicrons (CM), very low-density lipoproteins (VLDL), and their remnants (CM remnants [CMRs] and VLDL remnants [VLDLRs]). Understanding of elevation in CMR and/or VLDLR can lead us to understand the existence of postprandial hyperlipidemia. The measurement of apo B48, which is a constituent of CM and CMR; non-fasting TG, which includes TG content in all lipoproteins including CM and CMR; non-high-density lipoprotein cholesterol (non-HDL-C), which includes TRLs and low-density lipoprotein; and remnant cholesterol are useful to reveal the existence of postprandial hyperlipidemia. Postprandial hyperlipidemia is observed in patients with familial type III hyperlipoproteinemia, familial combined hyperlipidemia, chronic kidney disease, metabolic syndrome and type 2 diabetes. Postprandial hyperlipidemia is closely related to postprandial hyperglycemia, and insulin resistance may be an inducing and enhancing factor for both postprandial hyperlipidemia and postprandial hyperglycemia. Remnant lipoproteins and metabolic disorders associated with postprandial hyperlipidemia have various atherogenic properties such as induction of inflammation and endothelial dysfunction. A healthy diet, calorie restriction, weight loss, and exercise positively impact postprandial hyperlipidemia. Anti-hyperlipidemic drugs such pemafibrate, fenofibrate, bezafibrate, ezetimibe, and eicosapentaenoic acid have been shown to improve postprandial hyperlipidemia. Anti-diabetic drugs including metformin, alpha-glucosidase inhibitors, pioglitazone, dipeptidyl-peptidase-4 inhibitors and glucagon-like peptide 1 analogues have been shown to ameliorate postprandial hyperlipidemia. Although sodium glucose cotransporter-2 inhibitors have not been proven to reduce postprandial hyperlipidemia, they reduced fasting apo B48 and remnant lipoprotein cholesterol. In conclusion, it is important to appropriately understand the existence of postprandial hyperlipidemia and to connect it to optimal treatments. However, there are some problems with the diagnosis for postprandial hyperlipidemia. Postprandial hyperlipidemia cannot be specifically defined by measures such as TG levels 2 h after a meal. To study interventions for postprandial hyperlipidemia with the outcome of preventing the onset of ASCVD, it is necessary to define postprandial hyperlipidemia using reference values such as IGT.

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“…The design and rationale of the EVOLVE-FD study were previously described. [11] In short, this was a multicenter, randomized, placebocontrolled, double-blind, crossover study (Supplementary Fig. 1).…”

Section: Study Design and Patientsmentioning

confidence: 99%

“…A complete list of in-and exclusion criteria was previously described. [11] During the study patients received an oral fat load that consisted of unsweetened fresh cream. Venous blood samples were collected before and up to 8 h after the oral fat load.…”

Section: Study Design and Patientsmentioning

confidence: 99%

Low-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol measurement in Familial Dysbetalipoproteinemia

Heidemann

Koopal

Lennep

et al. 2023

Clinica Chimica Acta

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Effect of evolocumab on fasting and post fat load lipids and lipoproteins in familial dysbetalipoproteinemia

Cited by 5 publications

References 42 publications

The current perspective and opportunities of small nucleic acid‐based therapeutics

The current perspective and opportunities of small nucleic acid‐based therapeutics

Postprandial Hyperlipidemia: Its Pathophysiology, Diagnosis, Atherogenesis, and Treatments

Low-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol measurement in Familial Dysbetalipoproteinemia

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