ReviewThe pharmacogenomics journal2011
High-density lipoprotein (HDL) cholesterol: leveraging practice-based biobank cohorts to characterize clinical and genetic predictors of treatment outcome.
Review in The pharmacogenomics journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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.
Who cites it
5 citing papers in PubMed.
- Secondary use of clinical data: the Vanderbilt approach.Journal of biomedical informatics · 2014Article
- CYP4A11 variant is associated with high-density lipoprotein cholesterol in women.The pharmacogenomics journal · 2013Article
- Article
- 'Triglyceride effect' on the dynamics of plasma lipoproteins and its possible link to atherogenesis.The Libyan journal of medicine · 2012Article
- Mapping genes that predict treatment outcome in admixed populations.The pharmacogenomics journal · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
Over the past decade, large multicenter trials have unequivocally demonstrated that decreasing low-density lipoprotein (LDL) cholesterol can reduce both primary and secondary cardiovascular events in patients at risk. However, even in the context of maximal LDL lowering, there remains considerable residual cardiovascular risk. Some of this risk can be attributed to variability in high-density lipoprotein (HDL) cholesterol. As such, there is tremendous interest in defining determinants of HDL homeostasis. Risk prediction models are being constructed based upon (1) clinical contributors, (2) known molecular determinants and (3) the genetic architecture underlying HDL cholesterol levels. To date, however, no single resource has combined these factors within the context of a practice-based data set. Recently, a number of academic medical centers have begun constructing DNA biobanks linked to secure encrypted versions of their respective electronic medical record. As these biobanks combine resources, the clinical community is in a position to characterize lipid-related treatment outcome on an unprecedented scale.
Indexed as
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What OpenQuestion holds
Registered trials
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.