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Reduced Bone Mineral Density in HCV- or HBV-co-infected Patients: 2-year Follow-up, ANRS CO3 Aquitaine Cohort, France
Charles Cazanave*1,2, M Dupon1,2, V Lavignolle-Aurillac3, N Barthe2, S Lawson-Ayayi1,2,3, N Mehsen2, D Lacoste1,2, J L Pellegrin1,2, D Neau1,2,3, F Dabis1,2,3, and for the Groupe d'Epidemiologie Clinique du SIDA en Aquitaine (GECSA)
1COREVIH-Aquitaine, France; 2Bordeaux Univ Hosp, France; and 3INSERM U593, Inst for Publ Hlth, Epi and Devt, Univ Victor Segalen, Bordeaux, France
Background: Chronic viral
hepatopathy is a risk factor of bone demineralization. Little is known
about the temporal changes of bone abnormalities in HIV-infected patients. We
examined the 2-year progression of bone mineral density and body composition in
a cohort of HIV-infected patients and estimated the prevalence
of osteoporosis/osteopenia according to the hepatitis co-infection status.
Methods: Patients were consecutively screened for bone
mineral density and hepatitis co-infection from November 2004 to May 2005. The
prevalence of osteoporosis was 26.8%. We repeated the bone
mineral density assessment 2
years later in patients who had no bone abnormality or osteopenia diagnosis
at baseline (WHO criteria). We expanded in 2007 the enrolment
of hepatitis co-infected patients to estimate the bone
mineral density prevalence in this group. Bone mineral density of whole
body, lumbar spine, and femoral neck was measured by dual energy X-ray absorptiometry
(DEXA), as well as bone mineral content and fat and lean body mass.
Results: We
repeatedly assessed 208 patients in the longitudinal study (67.8% male; median
age 46 years; 26.7% with normal bone mineral density and 73.3% with osteopenia
at baseline). After 2 years, 39 patients (18.7%) remained free of bone abnormality;
osteopenia was diagnosed in 147 patients (70.7%) and osteoporosis in 22
(10.6%). Osteopenia predominated at the femoral neck in both men and women, and
osteoporosis at the femoral neck in men. A fat mass significant decline (median
–2.9%) was observed in those acquiring osteopenia compared to those remaining
normal (+7.5%) (p = 0.01). Osteopenic patients at baseline presented a
significant femoral neck bone mineral density decline when becoming
osteoporotic (–4.2%) compared to those who remained osteopenic (–1.9%) (p
<10–3). Bone mineral density was investigated in 103 hepatitis
co-infected patients (66% hepatitis C virus [HCV], 31% hepatitis B virus [HBV],
3% both; 71.8% male; 28.2% AIDS stage; 88.2% treated by HAART; 11% with
cirrhosis). Prevalence of osteopenia was 52.5% in men (95%CI 40.0 to 65.0%),
and 58.3% among women (38.6 to 78.0%). Osteoporosis was diagnosed in 34.4% of
men (22.5 to 46.3%) and 8.3% of women (2.7 to 19.3%). These prevalence
estimates of bone demineralization were not significantly different from those
documented in patients with HIV monoinfection 2 years earlier.
Conclusions: This study confirms
our earlier findings of a high prevalence of bone mineral disorders in HIV patients.
However, we did not observe any association with viral hepatitis co-infection. Bone
metabolism is rapidly evolving in 2 years among HIV-infected patients and
underlying biological mechanisms need further investigation.
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