Objective: To characterize total body bone mineral content (BMC) and total body and spinal bone mineral density (BMD) in perinatally HIV-infected and uninfected children/youth across puberty.
Design: HIV-infected (7–24 years) were randomly selected from six strata based on Tanner stage/protease inhibitor use. HIV-uninfected were frequency-matched by Tanner group and sociodemographic background to the HIV-infected.
Methods: Dual-energy X-ray absorptiometry (DXA) measured BMC and BMD. Linear regression models tested differences in bone outcomes by HIV and the interaction of HIV by Tanner group (1–2, 3–4, 5). Models were performed separately by sex and adjusted for DXA scanner, race/ethnicity, height, age and lean body mass.
Results: HIV-infected (N = 236) and uninfected (N = 143) were comparable on sex and race/ethnicity. HIV-infected were slightly older (median 12.6 versus 11.9 years). In adjusted models, HIV-infected males had significantly lower total body BMC and total body and spinal BMD at Tanner 5, lower BMC at Tanner 3–4 and similar BMC and BMD at Tanner 1–2, compared to HIV-uninfected males. HIV-infected and uninfected girls did not differ significantly on any bone outcome, but there was a marginally significant interaction of HIV and Tanner group for spinal BMD. Kaletra/ritonavir was associated with lower BMC and total body BMD and nevirapine was associated with higher spinal BMD in a model with all HIV-infected.
Conclusions: Perinatally HIV-infected males showed more evidence of lower bone density especially in the final stage of pubertal development than HIV-infected girls and they may be at increased risk for bone disease during adulthood.
aCenter for Biostatistics in AIDS Research, Harvard School of Public Health, Boston, USA
bDepartments of Adolescent Medicine and Endocrinology, Children's Hospital Boston, Boston, Massachusetts, USA
cNational Institute of Child Health and Human Development, Bethesda, Maryland, USA
dNationwide Children's Hospital, Columbus, Ohio, USA
eSan Francisco General Hospital, University of California, San Francisco, San Francisco, USA
fChildrens Hospital Los Angeles, Pediatric Infectious Diseases, Los Angeles, California, USA.
*D.L.J., J.C.L., K.M., and G.A. contributed equally to the writing of this article.
Received 6 August, 2009
Revised 20 November, 2009
Accepted 30 November, 2009
Correspondence to Denise Jacobson, PhD, MPH, Center for Biostatistics in AIDS Research, Harvard School of Public Health, 651 Huntington Ave, Boston, MA 02115, USA. E-mail: firstname.lastname@example.org