Evidence map›Paper›PMID 19159124›Full record

ReviewAmerican journal of cardiovascular drugs : drugs, devices, and other interventions2008

Statin adverse effects : a review of the literature and evidence for a mitochondrial mechanism.

Beatrice A Golomb, Marcella A Evans

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in American journal of cardiovascular drugs : drugs, devices, and other interventions, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 273 papers, 11 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
273citing papers in PubMed, 11 pooled it
18.7field-weighted citation impact, top 1% 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

273 citing papers in PubMed, 11 syntheses or guidelines pooled it, 667 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Statins in Healthy Adults: A Meta-Analysis.Medicina (Kaunas, Lithuania) · 2021
    Pooled it
  5. Pooled it
  6. Pooled it
  7. Pooled it
  8. Pooled it
  9. Pooled it
  10. THE IMPACT OF CARDIOVASCULAR DRUGS ON GLYCEMIC CONTROL: A REVIEW.Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2017
    Pooled it
  11. Pooled it
  12. Trial
  13. Trial
  14. Trial
  15. Trial
  16. Trial
  17. Trial
  18. Article
  19. Cholesterol in Mitochondrial Diseases-Friend or Foe?International journal of molecular sciences · 2026
    Review
  20. Review

213 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

2 authors at 1 institution in 1 country.

Beatrice A GolombDepartment of Medicine, University of California, San Diego, California 92093-0995, USA. bgolomb@ucsd.edu
Marcella A Evans
University of California, San Diego · US

Funding

STATINS AND NON-CARDIAC ENDPOINTSR01HL063055 · UNIVERSITY OF CALIFORNIA SAN DIEGO · 1999 to 2003
$4.8M
NHLBI NIH HHS R01 HL063055
6 · The paper itself

Abstract

HMG-CoA reductase inhibitors (statins) are a widely used class of drug, and like all medications, have potential for adverse effects (AEs). Here we review the statin AE literature, first focusing on muscle AEs as the most reported problem both in the literature and by patients. Evidence regarding the statin muscle AE mechanism, dose effect, drug interactions, and genetic predisposition is examined. We hypothesize, and provide evidence, that the demonstrated mitochondrial mechanisms for muscle AEs have implications to other nonmuscle AEs in patients treated with statins. In meta-analyses of randomized controlled trials (RCTs), muscle AEs are more frequent with statins than with placebo. A number of manifestations of muscle AEs have been reported, with rhabdomyolysis the most feared. AEs are dose dependent, and risk is amplified by drug interactions that functionally increase statin potency, often through inhibition of the cytochrome P450 3A4 system. An array of additional risk factors for statin AEs are those that amplify (or reflect) mitochondrial or metabolic vulnerability, such as metabolic syndrome factors, thyroid disease, and genetic mutations linked to mitochondrial dysfunction. Converging evidence supports a mitochondrial foundation for muscle AEs associated with statins, and both theoretical and empirical considerations suggest that mitochondrial dysfunction may also underlie many nonmuscle statin AEs. Evidence from RCTs and studies of other designs indicates existence of additional statin-associated AEs, such as cognitive loss, neuropathy, pancreatic and hepatic dysfunction, and sexual dysfunction. Physician awareness of statin AEs is reportedly low even for the AEs most widely reported by patients. Awareness and vigilance for AEs should be maintained to enable informed treatment decisions, treatment modification if appropriate, improved quality of patient care, and reduced patient morbidity.

Indexed as

Drug InteractionsHumansHydroxymethylglutaryl-CoA Reductase InhibitorsMeta-Analysis as TopicMitochondriaMitochondria, MuscleMuscular DiseasesRandomized Controlled Trials as TopicRhabdomyolysisRisk FactorsHydroxymethylglutaryl-CoA Reductase Inhibitors

Identifiers

PMID19159124
PMCPMC2849981
OpenAlexW1963958736

What Socratic holds

Textmetadata
Read underepoch 390

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 Socratic graph.