Metabolic bone disease in HIV infection.

The advent and widespread use of highly active antiretroviral therapy (HAART) in the last two decades has led to a marked improvement in the treatment of HIV disease even though viral infection cannot be eradicated because HAART does not completely eliminate the viral reservoirs [2]. HAART has dramatically changed the course of HIV infection from a fatal infection to a chronic and relatively manageable disease. The increased life expectancyof HIVpatients and the effects of HAART have changed the management of HIV infection. Nowadays medical treatment is no longer focused solely on HIV infection, opportunistic diseases and monitoring immune derangement, but also includes the control of metabolic, cardiovascular, liver, bone and kidney complications. In particular, bone alterations have been observed in the course of HIV disease representing a pivotal clinical problem in themanagement of HIVpatients especially for a possible development of bone fractures [3]. The major bone lesions detectable in HIV patients are related to bone demineralization (osteopenia/osteoporosis and osteomalacia) and osteonecrosis ([4] for a review).