Statin Therapy Does Not Reduce Liver Fat Scores in Patients Receiving Antiretroviral Therapy for HIV Infection.
Adolescent
Adult
Aged
Aged, 80 and over
Anti-Retroviral Agents
/ administration & dosage
Antiretroviral Therapy, Highly Active
/ adverse effects
Double-Blind Method
Fatty Liver
/ pathology
Female
HIV Infections
/ drug therapy
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors
/ administration & dosage
Male
Middle Aged
Placebos
/ administration & dosage
Prospective Studies
Treatment Outcome
Viral Load
Young Adult
ART
Fatty Liver
Hepatosteatosis
Virus Infection
Journal
Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
ISSN: 1542-7714
Titre abrégé: Clin Gastroenterol Hepatol
Pays: United States
ID NLM: 101160775
Informations de publication
Date de publication:
02 2019
02 2019
Historique:
received:
22
03
2018
revised:
17
05
2018
accepted:
26
05
2018
pubmed:
17
6
2018
medline:
1
4
2020
entrez:
17
6
2018
Statut:
ppublish
Résumé
Therapies are needed to limit progression of fatty liver diseases in patients with human immunodeficiency virus (HIV) infection. We analyzed data from a prospective study of the effects of rosuvastatin (a statin) on hepatic steatosis in HIV-positive adults. We performed a secondary analysis of data from a double-blind trial of adult patients with HIV infection (78% male; 68% African American; mean age, 46 y; body mass index, 29 kg/m The placebo and rosuvastatin groups each had significant increases in LFS, compared with baseline, at 96 weeks (P = .01 and P < .01; P = .49 for difference increase between groups). Baseline LFS was independently associated with blood level of C-X-C motif chemokine ligand 10 (P = .04) and the soluble CD163 molecule (P = .01). After we adjusted for baseline characteristics, an increase in LFS over time was significantly associated with the blood level of C-X-C motif chemokine ligand 10 (P = .04), insulin resistance (P < .01), and viral load (P = .02), but not rosuvastatin use (P = .06). In a secondary analysis of data from a trial of patients receiving treatment for HIV infection, hepatic steatosis increased over time, regardless of statin treatment, and was independently associated with markers of immune activation. Patients who received rosuvastatin appeared to have a nonsignificant increase in hepatic steatosis over 96 weeks. Despite their ability to reduce the risk of cardiovascular disease, statins do not appear to reduce hepatic steatosis. Clinicaltrials.gov no: NCT01218802.
Sections du résumé
BACKGROUND & AIMS
Therapies are needed to limit progression of fatty liver diseases in patients with human immunodeficiency virus (HIV) infection. We analyzed data from a prospective study of the effects of rosuvastatin (a statin) on hepatic steatosis in HIV-positive adults.
METHODS
We performed a secondary analysis of data from a double-blind trial of adult patients with HIV infection (78% male; 68% African American; mean age, 46 y; body mass index, 29 kg/m
RESULTS
The placebo and rosuvastatin groups each had significant increases in LFS, compared with baseline, at 96 weeks (P = .01 and P < .01; P = .49 for difference increase between groups). Baseline LFS was independently associated with blood level of C-X-C motif chemokine ligand 10 (P = .04) and the soluble CD163 molecule (P = .01). After we adjusted for baseline characteristics, an increase in LFS over time was significantly associated with the blood level of C-X-C motif chemokine ligand 10 (P = .04), insulin resistance (P < .01), and viral load (P = .02), but not rosuvastatin use (P = .06).
CONCLUSIONS
In a secondary analysis of data from a trial of patients receiving treatment for HIV infection, hepatic steatosis increased over time, regardless of statin treatment, and was independently associated with markers of immune activation. Patients who received rosuvastatin appeared to have a nonsignificant increase in hepatic steatosis over 96 weeks. Despite their ability to reduce the risk of cardiovascular disease, statins do not appear to reduce hepatic steatosis. Clinicaltrials.gov no: NCT01218802.
Identifiants
pubmed: 29908359
pii: S1542-3565(18)30612-8
doi: 10.1016/j.cgh.2018.05.058
pmc: PMC6294718
mid: NIHMS975108
pii:
doi:
Substances chimiques
Anti-Retroviral Agents
0
Hydroxymethylglutaryl-CoA Reductase Inhibitors
0
Placebos
0
Banques de données
ClinicalTrials.gov
['NCT01218802']
Types de publication
Journal Article
Randomized Controlled Trial
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
536-542.e1Subventions
Organisme : NHLBI NIH HHS
ID : K23 HL116209
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR002548
Pays : United States
Organisme : NHLBI NIH HHS
ID : R00 HL108743
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR000439
Pays : United States
Organisme : NINR NIH HHS
ID : R01 NR012642
Pays : United States
Informations de copyright
Copyright © 2019 AGA Institute. Published by Elsevier Inc. All rights reserved.
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