Evidence map›Paper›PMID 28945911›Full record

Trial reportThe Journal of clinical endocrinology and metabolism2017

HDL Cholesterol Efflux Capacity in Newly Diagnosed HIV and Effects of Antiretroviral Therapy.

Mabel Toribio, Min Hi Park, Markella V Zanni, Gregory K Robbins, Tricia H Burdo, Kenneth C Williams, Meghan N Feldpausch, Lauren Stone, Kathleen Melbourne, Steven K Grinspoon and 1 more

Open access · bronzeAbstract readClinical Trial
In one paragraph

Trial report in The Journal of clinical endocrinology and metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

5 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
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

11 authors at 4 institutions in 1 country.

Mabel ToribioProgram in Nutritional Metabolism, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114.
Min Hi ParkLipid Metabolism Unit/Center for Computational and Integrative Biology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114.
Markella V ZanniProgram in Nutritional Metabolism, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114.
Gregory K RobbinsMassachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114.
Tricia H BurdoDepartment of Biology, Boston College, Chestnut Hill, Massachusetts 02467.
Kenneth C WilliamsDepartment of Biology, Boston College, Chestnut Hill, Massachusetts 02467.
Meghan N FeldpauschProgram in Nutritional Metabolism, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114.
Lauren StoneProgram in Nutritional Metabolism, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114.
Kathleen MelbourneGilead Sciences, Foster City, California 99404.
Steven K GrinspoonProgram in Nutritional Metabolism, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114.
Michael L FitzgeraldLipid Metabolism Unit/Center for Computational and Integrative Biology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114.
Harvard University · USMassachusetts General Hospital · USBoston College · USGilead Sciences (United States) · US

Funding

ROLE OF DIETARY CONSTITUENTS ON GENE EXPRESSION IN INTESTINAL EPITHELIUMP30DK040561 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI Takara Leah Stanley · 1994 to 2026
$31.6M
TRAINING PROGRAM IN ENDOCRINOLOGY AND DIABETEST32DK007028 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI Karen K Miller · 1986 to 2026
$18.5M
HIV Disease and Impairement of High Density Lipoprotein MetabolismR01HL101274 · NHLBI · GEORGE WASHINGTON UNIVERSITY · PI BUKRINSKY, MICHAEL ILYA, FITZGERALD, MICHAEL LEO · 2010 to 2015
$4.0M
HDL prevention of cholesterol crystal inflammation in HIV diseaseR01HL112661 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI FITZGERALD, MICHAEL LEO, LATZ, EICKE · 2012 to 2016
$3.1M
Harvard Clinical and Translational Science Center (KL2)KL2TR000168 · NCATS · HARVARD MEDICAL SCHOOL · PI NADLER, LEE MARSHALL · 2012 to 2013
$965k
Novel Macrophage Specific Strategy for Imaging of Arterial Inflammation in HIVF32AI129700 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI TORIBIO, MABEL · 2017 to 2017
$21k
NCATS NIH HHS KL2 TR000168NHLBI NIH HHS R01 HL101274NHLBI NIH HHS R01 HL112661NIAID NIH HHS F32 AI129700NIDDK NIH HHS P30 DK040561NIDDK NIH HHS T32 DK007028
6 · The paper itself

Abstract

Context: In the general population, high-density lipoprotein (HDL) cholesterol efflux capacity (HCEC) relates inversely to incident cardiovascular events. Previous studies have suggested that HCEC is decreased in HIV and that antiretroviral therapy (ART) initiation might improve HCEC. Objective: To evaluate HCEC in the context of ART initiation and immune activation in HIV. Design and Outcome Measures: Baseline HCEC from 10 ART-naive HIV-infected males and 12 prospectively matched non-HIV-infected males were analyzed. In the HIV cohort, HCEC 6 months after elvitegravir/cobicistat/emtricitabine/tenofovir disoproxil fumarate (E/C/F/TDF) therapy was evaluated. HCEC served as the primary outcome and was measured by the ability of J774 mouse macrophages to efflux cholesterol. Our ex vivo assay used two cholesterol acceptors [apolipoprotein B (apoB)-depleted sera or purified HDL] and modulation of cellular efflux pathways using a liver X receptor (LXR) agonist. Results: The median age was 34 years [interquartile range (IQR), 27 to 51], and baseline HDL was 46 mg/dL (IQR, 38 to 61). HCEC was significantly greater in the non-HIV-infected subjects than in the HIV-infected subjects at baseline. HCEC, assessed using apoB-depleted sera, significantly increased after ART (no LXR agonist, baseline: median, 8.1%; IQR, 7.0% to 11.9%; after ART: median, 12.9%; IQR, 10.4% to 21.1%; P = 0.006; LXR agonist, baseline, 1.3% ± 1.3%; after ART, 2.5% ± 1.0%; P = 0.02), although not to the levels in the non-HIV-infected subjects (no LXR agonist: median, 14.9%; IQR, 11.5% to 19.1%; LXR agonist: 5.8% ± 1.3%). HCEC, assessed using purified HDL, did not significantly increase after ART. The change in HCEC with ART related inversely to the change in the percentage of CD14-CD16+ (nonclassical) monocytes (ρ = -0.74, P = 0.04) and directly to the change in the percentage of CD14+CD16- (classical) monocytes (ρ = 0.72, P = 0.045). Conclusions: Our data suggest improvement of HCEC with E/C/F/TDF and a relationship between the ART-induced decrease in immune activation and ART-induced improvement in HCEC.

Indexed as

AdultAnimalsAnticholesteremic AgentsAnti-HIV AgentsAnti-Retroviral AgentsBenzenesulfonamidesBiological TransportCase-Control StudiesCells, CulturedCholesterol, HDLFluorocarbonsHIVHIV InfectionsHumansHydrocarbons, FluorinatedImmunity, InnateAnticholesteremic AgentsAnti-HIV AgentsAnti-Retroviral AgentsBenzenesulfonamidesCholesterol, HDLFluorocarbonsHydrocarbons, FluorinatedLiver X ReceptorsSulfonamidesT0901317

Identifiers

PMID28945911
PMCPMC5673269
OpenAlexW2754880109

What OpenQuestion 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 OpenQuestion graph.