Children living with HIV demonstrate deficits in bone architecture and reductions in bone strength, compared with uninfected children, according to results of a study published in the Journal of Acquired Immune Deficiency Syndromes.
Previous cross-sectional and longitudinal studies among children living with HIV receiving antiretroviral (ART) therapy have reported decreased bone mass compared with children without HIV, even when weight, height, and pubertal stage are adjusted for. Most of these prior studies used dual x-ray absorptiometry (DXA) to demonstrate low bone mass by measuring bone mineral content and bone mineral density (BMD). The DXA approach has many limitations including that it estimates a 2-dimensional areal BMD by taking the ratio of the amount of bone and area scanned, instead of a 3-dimensional volumetric BMD, which allows data to be affected by bone size.
Because children living with HIV commonly experience poor somatic growth and delays in puberty, peripheral quantitative computed tomography (pQCT) can be advantageous compared with DXA; the former imaging can provide data on volumetric BMD, information on bone geometry and trabecular structure, has good accuracy and precision, and involves little ionizing radiation exposure. Currently, no studies of pQCT imaging in children living with HIV have been focused in sub-Saharan Africa, which is the most affected region of the pediatric HIV epidemic. Therefore, this study compared bone architecture and strength in black South African children living with HIV with uninfected control children using peripheral quantitative computed tomography.
In total, 172 children living with HIV who were receiving ART and 98 control children in the CHANGES Bone Study in South Africa were included in the study. Of the children living with HIV, 51% were boys and of the control children, 63% were boys. The average age of all children in the study cohort was 10.4 years. Among the children living with HIV, the mean duration of ART was 9.5 years: 70.9% were receiving efavirenz-based ART, 28.5% were receiving lopinavir/ritonavir-based therapy, and 1 child was receiving atazanavir/ritonavir-based ART.
All but 4 children received pQCT scans of their radius and tibia with measurements that included trabecular and cortical volumetric bone mineral density and bone strength, estimated by polar strength strain index, which is a validated measure of fracture risk.
Results demonstrated that compared with control children, children living with HIV have deficits in bone architecture and reductions in bone strength as detected by pQCT. Compared with boys in the control group, boys with HIV had lower radial length (P=.018), tibial length (P <.001) trabecular volumetric BMD at the radius (P =.018). Though trabecular volumetric BMD at the radius and tibia did not differ between girls with HIV and those without, the former group had lower measures of radial length, tibial length (P = .002 and <.001, respectively). Cortical thickness was lower in boys and girls with HIV compared with those without (P = .003 and .004, respectively).
In addition, compared with controls, children living with HIV had lower bone strength measured by polar strength strain index (972 vs 778 mm3; P <.01). Compared with children with HIV receiving an efavirenz-based ART, those receiving an lopinavir/ritonavir-based ART regimen had lower trabecular volumetric BMD (222 vs 199 mg/cm3; P <.001) and cortical volumetric BMD (1093 vs 1074 mg/cm3; P =.004). There were no notable differences observed between children with HIV and control children in bone strength by polar strength strain index.
Follow-up data of these children are needed to determine whether the differences observed remain clinically significant as the children age. Overall, the study authors concluded that, “[S]tudies of interventions to normalize bone growth and homeostasis and mitigate fracture risk, during childhood and adolescence, which are critical periods for none mineralization and skeletal development, are warranted.”
Shiau S, Yin MT, Strehlau R, et al. Deficits in bone architecture and strength in children living with HIV on antiretroviral therapy. J Acquir Immune Defic Syndr. 2020;84:101-106.
This article originally appeared on Infectious Disease Advisor