Background: Osteopenia and osteoporosis are frequent complications of HIV infection and/or its treatment. Alendronate is the only bisphosphonate approved for the treatment of osteoporosis in men and women. We conducted a 48-week prospective, randomized, open-label study to evaluate the effects of alendronate, vitamin D, and calcium supplementation on bone mineral density (BMD) in patients with HIV infection.
Methods: Thirty-one HIV-infected subjects with lumbar spine BMD t-scores less than −1.0 on antiretroviral therapy for a minimum of 6 months were randomized to receive (n = 15) or not to receive (n = 16) 70 mg of alendronate weekly for 48 weeks. All subjects received calcium (1000 mg daily as calcium carbonate) and vitamin D supplementation (400 IU daily). The study was powered to detect 3% changes in BMD in the lumbar spine within arms at 48 weeks.
Results: Thirty-one patients were enrolled; most were male, with an average length of HIV infection of 8 years. Eighty-four percent had an HIV RNA load below 400 copies/mL, with a current median CD4+ T-cell count of 561 cells/mm3 (median nadir CD4 cell count of 167 cells/mm3). At baseline, the median t-score in the lumbar spine was −1.52 and the median t-score in the hip was −1.02. Alendronate in combination with vitamin D and calcium increased lumbar spine BMD by 5.2% (95% confidence interval [CI]: 1.3-6.4) at 48 weeks compared with an increase of 1.3% (95% CI: −2.4 to 4.0) in subjects receiving vitamin D and calcium alone. One subject discontinued treatment in each arm. There were no serious adverse events.
Conclusions: Alendronate, vitamin D, and calcium are safe and potentially useful in the treatment of osteopenia/osteoporosis associated with HIV infection.
From the *Washington University School of Medicine, Division of Infectious Diseases, St. Louis, MO; †Washington University School of Medicine, Division of Endocrinology, St. Louis, MO; and ‡University of Pennsylvania, School of Medicine, Division of Infectious Diseases, Philadelphia, PA.
Received for publication May 13, 2004; accepted September 2, 2004.
Supported in part by AI25903, AI032783, and AI01612 and a grant from the Campbell Foundation. Dr. Tebas is a recipient of the Glaxo SmithKline Development Partners Junior Faculty.
Reprints: Pablos Tebas, University of Pennsylvania, Division of Infectious Diseases, 502 Johnson Pavilion, 3610 Hamilton Walk, Philadelphia, PA 19104-6073 (e-mail: Pablo.Tebas@uphs.upenn.edu).