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10/09/2013

Osteoporosis and Inflammation Linked at ID Week 2013


Chronic diseases of aging are increasingly common in HIV. As use of antiretroviral therapy (ART) extends life expectancy and the HIV-infected population ages, these comoribid conditions will be seen even more often. Osteoporosis is one of the most common comorbidities in HIV. Traditional risk factors like smoking, alcohol and steroid use, activity level and possibly vitamin D deficiency are important risk factors. Because patients with other chronic inflammatory conditions, such as rheumatoid arthritis and inflammatory bowel disease also have increased risk for osteoporosis, the pathogenesis of bone mineral density (BMD) loss in HIV is presumed to be related to chronic inflammation as well. However, the mechanism is complex and incompletely understood. Initiation of ART reduces many components of inflammation but accelerates BMD loss. To better understand the relation between BMD and inflammation Hileman et al. performed DEXA and measured inflammatory markers over one year in 47 untreated individuals with early HIV (CD4>400) and 41 age, race and gender matched HIV-negative controls. At baseline, BMD of the femoral neck, trochanter, total hip and spine was remarkably similar between groups, despite more smoking, hepatitis C, and higher levels of the inflammatory markers IL-6, sTNFR-II, sVCAM-1 and sICAM-1 in the HIV-infected group. Vitamin D and hsCRP levels were similar in both groups. After 48 weeks, there were no significant changes in the HIV-negative group and the differences between groups did not reach statistical significance. However, HIV-infected patients experienced losses from baseline of about 0.6% and 1.4% for total hip and trochanter BMD, which were statistically significant. More HIV-infected than uninfected individuals had BMD loss at the trochanter (73% vs. 49%, p=o.03) and more progressed to osteopenia or osteoporosis (21% vs. 6%, p=0.09) at any site. Multivariable analysis showed that among HIV-infected individuals, white race and elevated IL-6 were the only factors independently associated with progression. For the entire study population, HIV infection conferred a 2.8-fold risk of BMD loss at the trochanter (p=0.03). Adding inflammatory markers to the model partially attenuated the risk. The study findings prompt some additional questions. The average age of study participants was around 40. Is bone loss more significant in older HIV patients? Since HIV-infection was already present for a median of 4 years at baseline, why were the baseline BMD values so similar? Does the course of BMD loss accelerate over time? Since IL-6 appeared to be the marker best correlated with BMD loss, why does IL-6 decline while BMD loss worsens after ART initiation? This study confirms that modest BMD loss occurs over a one year time period in HIV-infected individuals not receiving ART and also suggests that inflammation is at least partly to blame. Because of its small size, the power to detect significant difference between groups and bone loss at other sites was limited. Larger studies with longer follow-up may help clarify the picture, although studies of untreated patients will be increasingly hard to do given the trend toward universal ART initiation.

Reference:
HIleman CO, Labbato DE, Storer NJ, McComsey GA. Inflammation, Vitamin D and Change in Bone Mineral Density (BMD) in Antiretroviral Therapy (ART)-Naive HIV-infected and Uninfected Adults—A 48-Week Matched Prospective Cohort Study, ID Week 2013, San Francisco, CA, October 2-6, 2013, abstract 674.


Source: Reporting from San Francisco for PRN News: David H Shepp, MD