Bone mineral density in children and adolescents with perinatal HIV infection

DiMeglio, Linda A.a; Wang, JiaJiab; Siberry, George K.c; Miller, Tracie L.d; Geffner, Mitchell E.e; Hazra, Rohanc; Borkowsky, Williamf; Chen, Janet S.g; Dooley, Laurieh; Patel, Kunjali; van Dyke, Russell B.j; Fielding, Roger A.k; Gurmu, Yaredl; Jacobson, Denise L.b; for the Pediatric HIVAIDS Cohort Study (PHACS)

AIDS:
doi: 10.1097/QAD.0b013e32835a9b80
Clinical Science
Abstract

Objective: To estimate prevalence of low bone mineral density (BMD) in perinatally HIV-infected (HIV+) and HIV-exposed but uninfected (HEU) children, and to determine predictors of BMD in HIV+.

Design: Cross-sectional analysis within a 15-site United States and Puerto Rico cohort study.

Methods: Total body and lumbar spine BMD were measured using dual energy-X-ray absorptiometry. BMD Z-scores accounted for bone age and sex. Multiple linear regression was used to evaluate differences in Z-scores by HIV status and for predictors of BMD in HIV+.

Results: 350 HIV+ and 160 HEU were enrolled. Mean age was 12.6 and 10.7 years for HIV+ and HEU, respectively. Most (87%) HIV+ were receiving HAART. More HIV+ than HEU had total body and lumbar spine Z-scores less than −2.0 (total body: 7 vs. 1%, P = 0.008; lumbar spine: 4 vs. 1%, P = 0.08). Average differences in Z-scores between HIV+ and HEU were attenuated after height and/or weight adjustment. Among HIV+, total body Z-scores were lower in those with higher CD4% and in those who ever used boosted protease inhibitors or lamivudine. Lumbar spine Z-scores were lower with higher peak viral load and CD4%, more years on HAART, and ever use of indinavir.

Conclusion: Rates of low BMD in HIV+ children were greater than expected based on normal population distributions. These differences were partially explained by delays in growth. As most HIV+ children in this study had not entered their pubertal growth spurt, prepubertal factors associated with BMD, magnified or carried forward, may result in sub-optimal peak BMD in adulthood.

Author Information

aSection of Pediatric Endocrinology and Diabetology, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana

bCenter for Biostatistics in AIDS Research, Harvard School of Public Health, Boston, Massachusetts

cPediatric Adolescent Maternal AIDS Branch, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland

dDivision of Pediatric Clinical Research, Department of Pediatrics, Miller School of Medicine at the University of Miami, Miami, Florida

eSaban Research Institute, Children's Hospital Los Angeles, Los Angeles, California

fNew York University Langone Medical Center, New York, New York

gDepartment of Pediatrics, Drexel University College of Medicine, Philadelphia, Pennsylvania

hFrontier Science and Technology Research Foundation, Amherst, New York

iDepartment of Epidemiology, Harvard School of Public Health, Boston, Massachusetts

jDepartment of Pediatrics, Tulane University Health Sciences Center, New Orleans, Los Angeles

kBody Composition Analysis Center, Friedman School of Nutrition Science and Policy, Tufts University

lDepartment of Biostatistics, Harvard School of Public Health, Boston, Massachusetts, USA.

Correspondence to Linda DiMeglio, MD, MPH, Room 5960, 705 Riley Hospital Drive, Indianapolis, IN 46202-5225, USA. E-mail: dimeglio@iupui.edu

Received 3 May, 2012

Revised 26 July, 2012

Accepted 20 September, 2012

© 2013 Lippincott Williams & Wilkins, Inc.