Study finds HIV-infected have osteopenia & osteoporosis more than HIV uninfected. Treatment naive had less osteopenia then those taking HAART. The same rates of osteopenia were found whether a person was taking a PI or a NNRTI regimen.
Osteopenia in HIV-infected
patients: is it the disease or is it the treatment?
Hernando Knobel; Ana Guelar; Gabriel Vallecillo; Xavier Nogués; Adolfo Díez
AIDS 2001;15:807-808 >
Full text PDF attached [lipodystrophysex.pdf]
Bone loss is a normal feature of aging. Accelerated bone demineralization is a multifactorial process; recent reports have suggested that HIV infection, perhaps in association with protease inhibitor (PI) therapy, is an additional risk factor for osteopenia [1,2]. However, changes in bone mineral metabolism, bone histomorphometry or bone mineral density had been described in HIV-infected patients before the era of highly active antiretroviral therapy (HAART) .
The aim of this study is to define the role of HIV infection and antiretroviral therapy in the development of bone mineral loss. A cross-sectional study was performed with the following patients enrolled: 80 HIV-infected patients [58 men, 22 women, mean age (SD) 41 years (± 8)]; 26 did not receive treatment; 37 were on HAART that included a PI; 17 were on HAART without a PI (two nucleoside reverse transcriptase inhibitors plus one non-nucleoside reverse transcriptase inhibitor). One hundred healthy seronegative adults matched by age and sex served as controls. Patients with known factors of osteopenia were excluded (recent history of extended bed rest, previous diagnosis of metabolic bone disease, renal insufficiency, hepatic failure, diabetes mellitus or previous diagnosis of other endocrine disease, moderate or severe nutritional alteration, and severe alcohol consumption).
Hologic QDR-4500 SL dual energy X-ray absorptiometry was used to determine the bone mineral density (BMD) of the lumbar spine (L1L4) and proximal femur, with T and Z scores (T score represents a SD in BMD within the mean of the population at 30; Z score represents a SD in BMD within the mean of the same age and sex group). Using World Health Organization definitions of osteopenia and osteoporosis, we classified the patients into the following categories: normal: T score greater than 1; osteopenic: T score from 1 to 2.5; and osteoporotic: T score less than 2.5.
Non-parametric statistical tests (KruskalWallis) were used to compare Z scores for spinal and hip BMD between groups. Normally distributed variables were compared using an analysis of variance. Chi-square and Fisher's exact test were used for categorical variables. Pearson's correlation coefficient was used to evaluate weight, body mass index, duration of therapy, CD4 cell count, and viral load in relation to BMD.
No differences were found in HIV-infected patients, irrespective of the treatment or type of treatment; however, the HIV-infected patients have lower BMD compared with healthy adults; the difference in BMD Z score between healthy adults and HIV patients was: in the lumbar spine: 0.43 [P = 0.001; 95% confidence interval (CI) 0.7 to 0.2]; in the femoral neck: 0.68 (P = 0.0001; 95% CI 0.91 to 0.44).
BMD was not correlated with HIV categories, viral load, CD4 cell count, duration of therapy, or the presence of lipodystrophy, and was correlated with weight and body mass index (r = 0.3; P = 0.02).
In relation to the potential role of individual antiretroviral agents on decreased BMD, we found that patients exposed to indinavir (17 patients, as the only PI used) have lower Z scores in the femoral neck compared with treated patients who have not been exposed to indinavir (1.4 versus 0.7; P = 0.02).
Osteopenia was present in 25% of healthy adults and in 67.5% of HIV-infected patients [P = 0.00001; odds ratio (OR) 6.2; 95% CI 3.112.6]. Osteoporosis was present in 5% of healthy adults and in 21.2% of HIV-infected patients (P= 0.00009; OR 5.1; 95% CI 1.718.5). Differences in osteopenia or osteoporosis did not reach statistical significance among the HIV patient groups.
In our study, a decrease in BMD and a higher rate of osteopenia and osteoporosis was found in HIV-infected patients compared with non-HIV patients. No clear association was found in relation to the use of HAART or the type of HAART used.
Studies made before the HAART era and a more recent study obtained similar conclusions . The hypothesis that the systemic activation of T cells in vivo leads to an osteoprotegerin ligand-mediated increase in osteoclastogenesis and boneloss  may explain the interaction of HIV infection and bone mineralization. The lack of differences in the rate of osteopenia and osteoporosis found in HIV-infected patients irrespective of the treatment received has the limitation of the relatively small population included in the study. The difference observed in patients exposed to indinavir with respect to other patients treated in the femoral neck is a very preliminary observation; however, indinavir is the only PI known to alter the activity of osteoblast alkaline phosphatase in vitro .
The aetiology of bone loss in HIV-infected patients, the role of specific class toxicity, the clinical implications and the therapeutic or preventative strategies require further investigation.
* Department of Internal Medicine-Infectious Diseases, Hospital del Mar, Autonomous University of Barcelona, Passeig Marítim 2529, E-08003 Barcelona, Spain.
Received: 6 December 2000; accepted: 18 January 2001.