Evidence map›Paper›PMID 30033951›Full record

ReviewJournal of atherosclerosis and thrombosis2018

Sitosterolemia, Hypercholesterolemia, and Coronary Artery Disease.

Hayato Tada, Atsushi Nohara, Akihiro Inazu, Nagahiko Sakuma, Hiroshi Mabuchi, Masa-Aki Kawashiri

Abstract readReview
In one paragraph

Review in Journal of atherosclerosis and thrombosis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

69 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Current and Future Perspectives of LDL-C Lowering Therapies 2026.Journal of atherosclerosis and thrombosis · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Observational
  9. Article
  10. NovelHuman mutation · 2026
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
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  18. Article
  19. Article
  20. Article

9 more citing papers are in PubMed but not listed here.

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

6 authors.

Hayato TadaDepartment of Cardiovascular and Internal Medicine, Kanazawa University Graduate School of Medical Science.
Atsushi NoharaDepartment of Cardiovascular and Internal Medicine, Kanazawa University Graduate School of Medical Science.
Akihiro InazuDepartment of Laboratory Science, Molecular Biochemistry and Molecular Biology, Graduate School of Medical Science, Kanazawa University.
Nagahiko SakumaDepartment of Cardio-Renal Medicine and Hypertension, Nagoya City University Graduate School of Medical Sciences.
Hiroshi MabuchiDepartment of Cardiovascular and Internal Medicine, Kanazawa University Graduate School of Medical Science.
Masa-Aki KawashiriDepartment of Cardiovascular and Internal Medicine, Kanazawa University Graduate School of Medical Science.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sitosterolemia is a rare inherited disease characterized by increased levels of plant sterols, such as sitosterol. The cause of this disease is ATP-binding cassette (ABC) subfamily G member 5 or member 8 (ABCG5 or ABCG8, respectively) gene mutations. Recent advances in genetics have revealed that the prevalence of subjects with deleterious mutations in ABCG5 and/or ABCG8 genes could be more than 1 in ~200,000 individuals among the general population. Furthermore, accumulated evidence, including infantile cases exhibiting progression/regression of systemic xanthomas associated with LDL cholesterol levels, have shown that the elevation of LDL cholesterol seems to be the major cause of development of atherosclerosis and not the elevation of sitosterol. Regarding therapies, LDL apheresis, as well as proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, could be useful for sitosterolemia, in addition to ezetimibe and/or colestimide. In this study, we provide the current understanding and future perspectives of sitosterolemia, which is currently considered an extremely rare disorder but is expected to be much more prevalent in clinical settings.

Indexed as

ATP Binding Cassette Transporter, Subfamily G, Member 5ATP Binding Cassette Transporter, Subfamily G, Member 8Coronary Artery DiseaseHeterozygoteHumansHypercholesterolemiaIntestinal DiseasesLipid Metabolism, Inborn ErrorsLipoproteinsMutationPhenotypePhytosterolsPolymorphism, GeneticProprotein Convertase 9SitosterolsABCG5 protein, humanABCG8 protein, humanATP Binding Cassette Transporter, Subfamily G, Member 5ATP Binding Cassette Transporter, Subfamily G, Member 8gamma-sitosterolLipoproteinsPCSK9 protein, humanPhytosterolsProprotein Convertase 9SitosterolsABCG5ABCG8Familial hypercholesterolemiaSitosterolemia

Identifiers

PMID30033951
PMCPMC6143779

What OpenQuestion holds

Textmetadata
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Registered trials

None linked

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.