Over the past few years we have become more aware of the wide range of metabolic complications, including bone pathology, that are caused not only by the natural progression of HIV, but also by currently available HIV treatments. Specifically, osteopenia and osteoporosis have been increasingly reported in HIV-infected persons.

The precipitating factors associated with the progression of bone abnormality in HIV infection include:

• reduced bone mineral density associated with age and hormonal deficiencies;

• HIV's direct effect on bone cells;

• chronic T-cell activation;

• cytokines affecting osteoclast and osteoblast function; and

• direct toxicity from antiretrovirals.

In this study, Aronson et al from the Uniformed Services University of the Health Sciences in Bethesda, Md., reported the results of a cross-sectional analysis on bone mineral density in HIV-infected patients. For this study, a subgroup of patients already participating in a natural history study at Walter Reed Army Medical Center completed a DEXA scan looking at the proximal femur and the lumbar spine. The World Health Organization's definitions of osteopenia [t scores between -1 and -2.5] and osteoporosis [t score <-2.5] were used to define the cases.

Of the 267 patients enrolled in the study, 85% were male and 61% were African American. The median age was 41 (range 20-70) and the median duration of HIV infection was 3,654 days (range 86 to 6,209). The investigators determined the amount of bone loss using a multivariate analysis, and correlated this with multiple variables, including prior antiretroviral therapy, gender, duration of HIV infection, viral burden, current and nadir CD4+ cell counts and age. No significant correlations were seen with any of these parameters.

The investigators identified an incidence of 6% for osteoporosis and 40% for osteopenia in this cohort of predominantly African-American men. They were able to establish a correlation between race and weight, but no correlation was observed with the duration of HIV infection or the use of antiretroviral therapy.

Less bone loss was seen on the hip than on the spine, and this was not associated with race. A strong association with race was found at the spine, however; African Americans were 2 to 3 times more likely to have spinal bone loss than other races, even when controlling for smoking.

This is yet another study looking to establish a correlation between osteoporosis/osteopenia and factors that we might be able to either control or predict. So far, the correlations identified between bone loss and other characteristics have been the same as the factors that affect the general population, such as hormonal deficiency, smoking and nutritional issues. The correlations related to the natural progression and treatment of HIV infection itself have been modest at best and not very useful, given the current limitations that we have to select antiretroviral therapy for our patients.

There are several factors in this study that may have influenced the results observed, including the small sample size, the predominantly male population and even the current definitions of osteopenia and osteoporosis, which may not be standardized for all demographic groups.

However, I agree with the authors that the results of this study suggest that spinal bone loss may occur differently in racial groups, but this association needs further investigation. I suspect that a more comprehensive analysis like this will require the use of matched controls -- at least by gender, age and race.