Bone Metabolism and HIV Infection
نویسنده
چکیده
Osteoporosis (OP) is the most widely spread metabolic osteopathy in the Western world, and is defined as a generalised state of the skeletal structure, characterised by a low bone mass and microarchitectural alterations, with an increase in bone fragility and risk of fracture (1). OP is now considered as an evolutive disorder affecting both the mineral and organic components leading to a progressive reduction in bone density, due to an imbalance in the regulation of hormones, which normally regulates the skeletal tissues (2). There are numerous classifications of OP in existence based on its pathogenesis , age of onset, association with other pathologies and pharmacological treatment or skeletal districts involved. Alongside primary OP is the heterogeneous group of secondary OP, which is either the consequence of the core disease or of the use of drugs. HIV infection has been shown to play an important role in the development of OP (3) and high prevalence of both osteopenia (OPe) and OP have been reported in subjects with chronic HIV infection (4). Loss of body weight, low body mass index (BMI) and diminished functional capacity are among some of the risk factors which, to a large extent, contribute to the loss of bone tissues in subjects suffering from chronic HIV infection (2-8).Furthermore, the drugs used to treat HIV+ patients can also interfere with bone metabolism and contribute to loss of bone mass (16). A reduction in bone mineral density (BMD) was observed in both HIV+ patients with hypogonadism and in those without (9-11). OP seems to be most frequently observed in subjects undergoing intense antiretroviral therapy, however, the mechanism by which antiretroviral treatments interfere with bone metabolism has not yet been clearly demonstrated. The success of highly active antiretroviral therapy (HAART) has dramatically increased the life expectancy of HIV+ patients in the developed world, however, their use has been associated with a range of side effects and complications. As people with HIV now live longer, bone disease is among the metabolic complications presenting physicians with new challenges in the management of the HIV+ patients (12). Although, OP is the most common bone disease described in HIV, but osteomalacia, usually in association with Fanconi’s syndrome or in patients treated with tenofovir, is also reported (15). The reduction in bone mass and the disruption of bone architecture increases the risk of bone fracture leading to disability, morbidity and mortality especially in the older population. One in two women and one in five men over the age of 50 years will suffer a fracture due to OP during their lifetime (13). There are concerns that as the HIV+ population ages, increased rates of bone loss may give rise to an ‘epidemic’ of fragility fractures (17).
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