BMD alterations in HIV-infected pregnant women and in their infants

In both HIV-infected adults and children skeletal abnormalities, including decreased bone mineral content and bone mineral density are frequently reported (1,2,3,4), although the mechanisms of the pathogenesis of these alterations have not completely assessed. Several studies have concluded that, at least in infected adults, bone disorders are strongly associated with HIV itself that can infect ostoblasts or indirectly alter osteoclasts and osteoblast function through T-cell activation and increased production of bone-resorbing cytokines like IL-1, IL-6 and TNF-alfa (5,6,7). Besides, the duration of infection, often causing physical inactivity and poor nutrition, can contribute to decrease bone mineral content and increase bone turnover in HIV- infected patients (8,9,10). On the other hand, in HAART (Hihgly Active Antiretroviral Therapy) era many reports on bone disorders in HIV-infected adults and all of those in children suggest that prolonged administration of protease inhibitor (PI)-containing regimens plays a role in the pathogenesis of abnormal bone metabolism, by inducing osteoclast and osteoblast dysfunction . With regard to HIV-infected HAARTtreated pregnant women, the evolution of bone mineralization and metabolism has not thoroughly studied yet. The lack of data about the bone changes occurring over time in these subjects and about the risk of consequences in their newborns and infants (infected or not) who are exposed “in utero” to the same antiretroviral drugs prompted us to study the bone strength in a cohort of HIV-infected pregnant women treated with different therapeutic protocols and in their children, followed from birth to the end of the first year of life with bone density measurements.