Studies among HIV-uninfected persons (mostly in their sixth decade of life) show that detectable coronary artery calcium (CAC) is independently associated with low bone mineral density (BMD), suggesting a possible common pathogenic mechanism.
We assessed the relationship between CAC and BMD, which has not been well described among younger to middle-aged HIV-infected persons.
We studied participants with baseline CAC and BMD measures from a prospective cohort of HIV-infected persons enrolled in the Study to Understand the Natural History of HIV/AIDS in the Era of Effective Therapy (SUN) during 2004–2006. We used logistic regression to assess the association between detectable CAC (>0 Agatston score) and BMD (g/cm2, T-score), and adjusted for known traditional and HIV-related risk factors.
Among 472 participants (76% male, 30% non-Hispanic black, median age 41 years, and 71% with HIV RNA < 400 copies/mL), the majority had no detectable CAC (82%), but had baseline osteopenia (53%) or osteoporosis (10%). In univariate analysis, participants with detectable CAC had lower femoral neck/total hip T-scores, lower femoral neck/total hip/lumbar spine BMD, and higher rates of osteopenia/osteoporosis. After adjustment for age, all associations were no longer significant; adjustment for traditional risk factors excluding age and HIV-related variables failed to attenuate these associations.
We found aging attenuates the association between detectable CAC and BMD in this cohort. Aging remains an important contributor to non–AIDS-defining illnesses. These data reinforce the importance of developing screening and prevention strategies for aging HIV-infected persons given their excess risk across a wide spectrum of end-organ complications.
aDivision of Infectious Diseases, Washington University School of Medicine, Saint Louis, MO;
bDepartment of Infectious Diseases, Hennepin County Medical Center, University of Minnesota, Minneapolis, MN;
cDivision of HIV/AIDS Prevention, Centers for Disease Control and Prevention, Atlanta, GA; and
dDivision of Infectious Diseases, University of Alabama School of Medicine, Birmingham, AL.
Correspondence to: Gerome Escota, MD, Division of Infectious Diseases, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110 (e-mail: email@example.com).
Centers for Disease Control and Prevention contract numbers 200-2002-00610, 200-2002-00611, 200-2002-00612, 200-2002-00613, 200-2007-23633, 200-2007-23634, 200-2007-23635, and 200-2007-23636.
The findings and conclusions from this review are those of the authors and do not necessarily represent the views of the Centers for Disease Control and Prevention.
E.T.O. has received honoraria from Merck & Co. and GlaxoSmithKline. W.P. is a member of the Advisory Boards for Merck & Co. and Gilead Sciences and has received Research Support from Merck & Co. The remaining authors have no conflicts of interest to disclose.
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Received December 19, 2018
Accepted April 08, 2019