TY - JOUR
T1 - Changes in plasma RANKL-osteoprotegerin in a prospective, randomized clinical trial of initial antiviral therapy
T2 - A5260s
AU - Kelesidis, Theodoros
AU - Moser, Carlee B.
AU - Johnston, Elizabeth
AU - Stein, James H.
AU - Dube, Michael P.
AU - Yang, Otto O.
AU - McComsey, Grace A.
AU - Currier, Judith S.
AU - Brown, Todd T.
N1 - Funding Information:
Supported by NIH grants HL095132, HL095126, AI068636, AI068634, AI69471, AI069501, and AI56933. T.T.B. is supported in part by K24 AI120834. T.K. is supported by NIH Grant #K08AI08272, NIH/NCATS Grant # UL1TR000124. The study received additional financial support from Gilead, Merck, Bristol Myers Squibb, Janssen. The project described was supported by Award Number UM1 AI068634, UM1 AI068636, and UM1 AI106701 from the National Institute of Allergy and Infectious Diseases. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institute of Allergy and Infectious Diseases or the National Institutes of Health or any of the funders.
Funding Information:
T.T.B. has served as a consultant for BMS, GSK, Merck, Abbott, Gilead, ViiV Healthcare and has received research funding from Merck and GSK. J.S.C. has served as a consultant for Gilead and has received research funding from Merck. J.H.S. served on a Data Safety Monitoring Board for Lilly. G.A.M. has served as consultant or received research grants from BMS, Pfizer, Gilead, ICON, and GSK/ViiV. C.B.M. and E.J. have no Duality of Interest disclosures. M.P.D. has served as a consultant for Gilead and Astra Zeneca and receives research funding from Gilead, ViiV, and Merck. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed.
Publisher Copyright:
Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
PY - 2018
Y1 - 2018
N2 - Background: The contributions of the receptor activator of nuclear factor kappa-B ligand (RANKL)/osteoprotegerin (OPG) axis to cardiovascular and bone disease in treated HIV-1 infection are not well defined. Setting: Prospective, observational, longitudinal study. Methods: In a subset analysis of a prospective randomized clinical trial, 234 HIV-1–infected antiretroviral therapy–naive participants received tenofovir–emtricitabine plus either atazanavir/ritonavir, darunavir/ritonavir, or raltegravir and achieved plasma HIV-1 RNA,50 copies per milliliter by week 24 and thereafter. Associations between plasma RANKL, OPG, or RANKL/OPG ratio levels with total, hip, and spine bone mineral density (BMD) loss or progression of carotid artery intima-media thickness were assessed longitudinally over 96 weeks. Results: Over 96 weeks, all treatment groups had similar and sustained declines in plasma RANKL, increases in plasma OPG, and subsequently, decreases in the RANKL/OPG ratio. There were no associations between plasma RANKL or RANKL/OPG ratio levels with total, hip, and spine BMD loss or progression of carotid artery intima-media thickness; however, plasma OPG in successfully treated HIV-infected patients (week 48 and 96) was associated with spine BMD loss. Conclusions: In virologically suppressed HIV-infected patients, the evolution of bone disease could be linked to plasma OPG levels; however, the role of plasma levels of RANKL and RANKL/OPG ratio in the prediction of morbidity in treated HIV-1 infection may be limited.
AB - Background: The contributions of the receptor activator of nuclear factor kappa-B ligand (RANKL)/osteoprotegerin (OPG) axis to cardiovascular and bone disease in treated HIV-1 infection are not well defined. Setting: Prospective, observational, longitudinal study. Methods: In a subset analysis of a prospective randomized clinical trial, 234 HIV-1–infected antiretroviral therapy–naive participants received tenofovir–emtricitabine plus either atazanavir/ritonavir, darunavir/ritonavir, or raltegravir and achieved plasma HIV-1 RNA,50 copies per milliliter by week 24 and thereafter. Associations between plasma RANKL, OPG, or RANKL/OPG ratio levels with total, hip, and spine bone mineral density (BMD) loss or progression of carotid artery intima-media thickness were assessed longitudinally over 96 weeks. Results: Over 96 weeks, all treatment groups had similar and sustained declines in plasma RANKL, increases in plasma OPG, and subsequently, decreases in the RANKL/OPG ratio. There were no associations between plasma RANKL or RANKL/OPG ratio levels with total, hip, and spine BMD loss or progression of carotid artery intima-media thickness; however, plasma OPG in successfully treated HIV-infected patients (week 48 and 96) was associated with spine BMD loss. Conclusions: In virologically suppressed HIV-infected patients, the evolution of bone disease could be linked to plasma OPG levels; however, the role of plasma levels of RANKL and RANKL/OPG ratio in the prediction of morbidity in treated HIV-1 infection may be limited.
KW - Bone disease
KW - CVD
KW - HIV
KW - OPG
KW - RANKL
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UR - http://www.scopus.com/inward/citedby.url?scp=85064109812&partnerID=8YFLogxK
U2 - 10.1097/QAI.0000000000001679
DO - 10.1097/QAI.0000000000001679
M3 - Article
C2 - 29533303
AN - SCOPUS:85064109812
SN - 1525-4135
VL - 78
SP - 362
EP - 366
JO - Journal of Acquired Immune Deficiency Syndromes
JF - Journal of Acquired Immune Deficiency Syndromes
IS - 3
ER -