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Reduced bone density in HIV-infected women

Dolan, Sara Ea; Huang, Jeannie Sb; Killilea, Kathleen Ma; Sullivan, Meghan Pa; Aliabadi, Negara; Grinspoon, Stevena

Clinical Science

Objectives: Although bone density has been previously investigated in HIV-infected men, little is known regarding bone density in HIV-infected women.

Methods and design: Bone density was measured by dual-energy X-ray absorptiometry in 84 ambulatory, HIV-infected females and 63 healthy female control subjects similar in age (41 ± 1 versus 41 ± 1 years, P = 0.83), body mass index (26.0 ± 0.6 versus 27.0 ± 0.5 kg/m2, P = 0.44) and racial background (% non-Caucasian, 61 versus 51%; P = 0.24, HIV-infected versus control).

Results: Lumbar spine (1.02 ± 0.02 versus 1.07 ± 0.02 g/cm2, P = 0.03) and total hip (0.93 ± 0.01 versus 0.99 ± 0.01 g/cm2, P = 0.004) bone density were reduced in HIV-infected compared with control subjects. Osteopenia was demonstrated in 54 versus 30% (P = 0.004) of HIV-infected versus control subjects and was 2.5 times more likely in a multivariate model accounting for age, race, menstrual function and body mass index. Urinary N-telopeptides of type 1 collagen (NTx) (39.6 ± 3.5 versus 29.9 ± 2.0 nM/mM urine creatinine, P = 0.03) and osteoprotegerin (4.76 ± 0.23 versus 3.39 ± 0.17 pmol/l, P ≤ 0.0001) were increased in HIV-infected compared with control subjects. Among the HIV-infected women, bone density correlated with weight (r = 0.41, P < 0.001) and inversely with urinary NTx (r = −0.28, P = 0.01). Bone density did not differ by current or past protease inhibitor, nucleoside reverse trancriptase inhibitor, or non-nucleoside reverse transcriptase inhibitor exposure.

Conclusions: HIV-infected women demonstrate reduced bone density. Altered nutritional status, hormonal function and body composition may contribute to lower bone density in HIV-infected women. Consideration should be given to testing bone density in HIV-infected women with risk factors for osteopenia.

From the aNeuroendocrine Unit and Program in Nutritional Metabolism,

Massachusetts General Hospital, Boston, Massachusetts, USA and the bProgram in Pediatric Gastroenterology and Nutrition, University of California San Diego, San Diego, California, USA.

Correspondence to Steven Grinspoon, MD, Neuroendocrine Unit and Program in Nutritional Metabolism, Massachusetts General Hospital, 55 Fruit Street, LON207, Boston, MA 02114, USA.

Tel: +1 617 726 3870; fax: +1 617 724-8998; e-mail: sgrinspoon@partners.org

Received: 25 July 2003; revised: 13 August 2003; accepted: 8 September 2003.

© 2004 Lippincott Williams & Wilkins, Inc.