Objectives
To determine the incidence and age-related fracture risk among HIV-infected (HIV+) and uninfected men (HIV−). To evaluate factors independently associated with fracture risk.
Design
Prospective, multicenter cohort study of men with or at risk for HIV.
Methods
Outcome measures: 1) all fractures (excluding skull, face, digits) and 2) fragility fractures (vertebral column, femur, wrist, humerus) were collected semiannually in 1221 HIV+ and 1408 HIV− men ≥ age 40. Adjusted incident rate ratios (aIRR) with an interaction term for age (40–49, 50–59, ≥60 years) and HIV serostatus were estimated with Poisson regression models accounting for additional risk factors.
Results
Fracture incidence increased with age among both HIV+ and HIV− men. While there was no significant difference in fracture incidence by HIV serostatus among men aged 40–49 years, the HIV+ men aged 50–59 years had a significantly higher incidence of all fractures (aIRR=2.06 [1.49, 2.84]) and fragility fractures (aIRR=2.06 [1.21, 3.50]) compared with HIV− participants of similar age. HIV modified the effect of age on all fractures (p=0.002) but did not significantly modify the effect for fragility fractures (p=0.135). Hypertension increased the rate of all fractures by 32% after adjustment for covariates (aIRR=1.32 [1.04, 1.69]).
Conclusions
Fracture incidence increased with age among HIV+ and HIV− men but was higher among HIV+ men. A significant increase in fracture incidence was found among 50–59-year-old HIV+ men, highlighting the importance of osteoporosis screening for HIV infected men above the age of 50.
Adding to its well-known roles in locomotion and calcium balance, the skeleton has recently been appreciated as a true endocrine organ. Bone remodeling, a highly dynamic process, requires synchronized activities and crosstalk between bone cells. Discovery and characterization of the Wnt/β catenin pathway in bone formation, FGF23 regulation of phosphate homeostasis and osteocalcin in energy and glucose homeostasis have reframed our view of the skeleton from simply a target tissue of the endocrine system to an endocrine tissue itself. This comprehensive review provides an overview of these complex pathways, their application to human bone disorders and implications for developing diagnostic and therapeutic targets.
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