Introduction: Peak bone mass (PBM) is the amount of bone present at the end of skeletal maturation. It is an important determinant of osteoporotic fracture risk. Data on the PBM in the HIV-infected population are lacking.
Design and Methods: We performed a multicenter (6 centers in Spain), case–control study to assess PBM using dual-energy x-ray absorptiometry. We studied HIV-infected patients aged 20–30 years and compared them with age- and gender-matched non–HIV-infected controls. We also assessed the predictive factors for a low PBM.
Results: We included 307 subjects: 232 HIV-infected patients and 75 non–HIV-infected controls. Bone mineral density was similar in both groups although differences were seen in the total femur T-score (−0.15SD versus +0.50SD, respectively, P = 0.018). The percentage of osteopenia and osteoporosis was higher in the HIV-infected patients (56.5% and 10.7%, respectively) than in the controls (50.7% and 4%, respectively; P = 0.019). Osteoporosis was more frequent in HIV-infected men than in control men and HIV-infected women (12.2% versus 5.5% and 4.8%, P = 0.033). Protease inhibitors and nadir CD4 T-cells were negatively associated with PBM, whereas fat and lean mass were positively associated with PBM.
Conclusions: Bone mineral density was similar between HIV-infected patients aged 20–30 years than in age- and gender-matched controls. However, lower femoral T-scores and higher rate of osteopenia and osteoporosis were seen in HIV-infected men. Therapy with protease inhibitors, nadir CD4 counts, and fat and lean mass were predictive factors of PBM. Given that these patients will be living with HIV infection for many years, every effort should be made to modify risk factors.
*Lluita Contra la Sida Foundation, Internal Medicine Department, Germans Trias i Pujol University Hospital, Autonomous University of Barcelona, Barcelona, Spain;
†Internal Medicine Department, Hospital Sant Pau, Barcelona, Spain;
‡Internal Medicine Department, Hospital Bellvitge, Barcelona, Spain;
§Internal Medicine Department, Hospital Clínico San Carlos, Madrid, Spain;
‖Internal Medicine Department, Hospital Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain;
¶CETIR, Grup Mèdic, Barcelona, Spain;
#Statistics and Operations Research, Technical University of Catalunya, Barcelona, Spain; and
**Irsicaixa Foundation, Germans Trias i Pujol University Hospital, Autonomous University of Barcelona, Barcelona, Spain.
Correspondence to: Eugènia Negredo, MD, PhD, Lluita Contra la SIDA Foundation, Germans Trias i Pujol 08916 Badalona, Catalonia, Spain (e-mail: firstname.lastname@example.org).
D.P. received payment for consultation educational lectures of Boerhinger-Ingelheim ,ViiV, BMS, Abbott, Gilead, Jannsen-Cilag, Merck Sharp and Dohme (MSD), GlaxoSmithKline and Pfizer. A.N. received payment for lectures from Gilead. V.E. received fees for consultancy, grants or educational presentations from Abbott, MSD, Gilead, Abbott, Jannsen, MSD and GlaxoSmithKline. B.C. received payments for grants or consultancy from MSD, ViiV, Gilead, BMS, Jannsen and MSD. E.N. received payments for consultancy from Abbott, Pfizer, MSD, GlaxoSmithKline, Roche and Jannsen. A.C. received payment for lectures from Viiv, Jannsen, BMS, ViiV and Boerhinger ingelheim. A.B. received payment for consultation from Roche, Abbott, Merck and GlaxoSmithKline. All other authors have no other funding or conflicts of interest to disclose.
Received June 11, 2013
Accepted August 27, 2013