Evidence map›Paper›PMID 38390468›Full record

ArticleAtherosclerosis plus2024

Changing from lipoprotein apheresis to evolocumab treatment lowers circulating levels of arachidonic acid and oxylipins.

Chaoxuan Wang, Anne Kaufmann, Nadja Kampschulte, Ulf Elbelt, Ursula Kassner, Elisabeth Steinhagen-Thiessen, Anne Pietzner, Christoph Schmöcker, Dev Datta, Tiziana Sanpietro and 3 more

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In one paragraph

Article in Atherosclerosis plus, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 97% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 5 institutions in 3 countries.

Chaoxuan WangMedical Department B, Division of Hepatology, Gastroenterology, Oncology, Hematology, Palliative Care, Endocrinology and Diabetes, University Hospital Ruppin-Brandenburg, Brandenburg Medical School, Neuruppin, Germany.
Anne KaufmannChair of Food Chemistry, Faculty of Mathematics and Natural Sciences, University of Wuppertal, Wuppertal, Germany.
Nadja KampschulteChair of Food Chemistry, Faculty of Mathematics and Natural Sciences, University of Wuppertal, Wuppertal, Germany.
Ulf ElbeltMedical Department B, Division of Hepatology, Gastroenterology, Oncology, Hematology, Palliative Care, Endocrinology and Diabetes, University Hospital Ruppin-Brandenburg, Brandenburg Medical School, Neuruppin, Germany.
Ursula KassnerMedical Department, Division of Hepatology and Gastroenterology (including Metabolic Diseases), Campus Virchow Klinikum, Charité-Universitätsmedizin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Elisabeth Steinhagen-ThiessenMedical Department, Division of Hepatology and Gastroenterology (including Metabolic Diseases), Campus Virchow Klinikum, Charité-Universitätsmedizin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Anne PietznerMedical Department B, Division of Hepatology, Gastroenterology, Oncology, Hematology, Palliative Care, Endocrinology and Diabetes, University Hospital Ruppin-Brandenburg, Brandenburg Medical School, Neuruppin, Germany.
Christoph SchmöckerMedical Department B, Division of Hepatology, Gastroenterology, Oncology, Hematology, Palliative Care, Endocrinology and Diabetes, University Hospital Ruppin-Brandenburg, Brandenburg Medical School, Neuruppin, Germany.
Dev DattaDepartment of Metabolic Medicine, University Hospital Llandough, Cardiff, United Kingdom.
Tiziana SanpietroLipoapheresis Unit, Reference Center for Diagnosis and Treatment of Inherited Dyslipidemias, Fondazione Toscana Gabriele Monasterio, Pisa, Italy.
Nils Helge SchebbChair of Food Chemistry, Faculty of Mathematics and Natural Sciences, University of Wuppertal, Wuppertal, Germany.
Karsten-H WeylandtMedical Department B, Division of Hepatology, Gastroenterology, Oncology, Hematology, Palliative Care, Endocrinology and Diabetes, University Hospital Ruppin-Brandenburg, Brandenburg Medical School, Neuruppin, Germany.
Nadine RohwerMedical Department B, Division of Hepatology, Gastroenterology, Oncology, Hematology, Palliative Care, Endocrinology and Diabetes, University Hospital Ruppin-Brandenburg, Brandenburg Medical School, Neuruppin, Germany.
University of Potsdam · DEUniversity of Wuppertal · DEHumboldt-Universität zu Berlin · DEFondazione Toscana Gabriele Monasterio · ITUniversity Hospital Llandough · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background and aims: Previous studies have shown that lipoprotein apheresis can modify the plasma lipidome and pro-inflammatory and pro-thrombotic lipid mediators. This has not been examined for treatment with protein convertase subtilisin/kexin type 9 inhibitors such as evolocumab, which are increasingly used instead of lipoprotein apheresis in treatment-resistant familial hypercholesterolemia. The aim of this study was to compare the effects of evolocumab treatment and lipoprotein apheresis on the fatty acid profile and on formation of lipid mediators in blood samples. Methods: We analyzed blood samples from 37 patients receiving either lipoprotein apheresis or evolocumab treatment as part of a previous study. Patients were stratified according to receiving lipoprotein apheresis (n = 19) and evolocumab treatment (n = 18). Serum fatty acid analysis was performed using gas chromatography flame ionization detection and plasma oxylipin analysis was done using liquid chromatography tandem mass spectrometry. Results: Changing from lipoprotein apheresis to evolocumab treatment led to lower levels of omega-6 polyunsaturated fatty acid (n-6 PUFA) including arachidonic acid, dihomo-γ-linolenic acid and linoleic acid. Moreover, several n-6 PUFA-derived oxylipins were reduced after evolocumab treatment. Conclusions: Given that arachidonic acid, either directly or as a precursor, is associated with the development of inflammation and atherosclerosis, evolocumab-mediated reductions of arachidonic acid and its metabolites might have an additional beneficial effect to lower cardiovascular risk.

Indexed as

Arachidonic acidCardiovascular diseaseEvolocumabLipid mediatorLipoprotein apheresisOxylipinPolyunsaturated fatty acid

Identifiers

PMID38390468
PMCPMC10881432
OpenAlexW4391756137

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.