Secondary Logo

Journal Logo

Institutional members access full text with Ovid®

HIV and Bone Metabolism

Huang, Jeannie S. M.D.*; Grinspoon, Steven M.D.*

CME Review Articles: Bone & Mineral

Reduced bone density and abnormal bone turnover has recently been reported in HIVinfected patients receiving antiretroviral therapy. In addition, recent data suggest that individuals infected with HIV are at an increased risk for avascular necrosis. A number of factors, including potential medication toxicity, undernutrition, hypogonadism, abnormalities in calcium homeostasis, or HIV infection itself, may be contributing to the bone pathology in this population. However, the specific mechanisms of the disordered bone turnover and reduced bone density in HIVinfected patients have not yet been identified. Moreover, the associated vertebral fracture risk of this newly identified osteopenia in the HIV-infected population has yet to be fully assessed. This paper reviews the literature to date on bone metabolism in HIV-infected patients, highlighting possible etiologies and contributors to the observed reduction in bone density in this population.

Learning Objectives:

* Recognize the occurrence of osteopenia in HIVinfected persons and how it is related to highly active antiretroviral therapy (HAART).

* Describe the relationship between osteopenia and both AIDS wasting syndrome and avascular necrosis of the femoral head

* Explain ways in which HIV infection and/or HAART might predispose to osteopenia, and how osteopenia relates to lipodystrophy.

Clinical Research Fellow, Combined Program in Gastroenterology and Nutrition (J.S.H), Children’s Hospital, Assistant Professor of Medicine, Neuroendocrine Unit (S.G.), Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114.


This article is the 19th of 36 that will be published in 2001 for which a total of up to 36 Category 1 CME credits can be earned. Instructions for how credits can be earned appear following the Table of Contents.

Address correspondence to: Steven Grinspoon, M.D., Neuroendocrine Unit, Massachusetts General Hospital, BUL457B, 55 Fruit Street, Boston, MA 02114. Phone: 617–726-3890; Fax: 617–726-5072; E-mail:

This work was supported in part by National Institutes of Health grant M01-RR01066, T32 DK 07477, and R01-DK54167.

*The authors have disclosed that they have no significant relationships with or financial interest in any commercial companies that pertain to this educational activity.

© 2001 Lippincott Williams & Wilkins, Inc.