Osteopenia in Patients with HIV Infection Is Not Associated with Elevated sTNFR2 Levels

Bone health in HIV infection

“…24 Gibellini et al 25 recently reported that levels of RANKL were higher in HIV-infected men and correlated with reduced BMD. However, in the study of Chirch et al, 26 BMD in seven HIV-positive individuals was not associated with levels of soluble TNF receptor 2.…”

“…28 Using gene chip microarray analysis, Malizia et al 29 recently showed that exposure to the PIs nelfinavir and ritonavir increased the expression by osteoblastic cells of the inflammatory cytokines MCP-1 and IL-8. PIs may also inhibit 1-a-hydroxylase and reduce serum 1,25(OH) 2 D levels, 26 which could have a detrimental effect on BMD. In addition, LRP5, a positive regulator of bone formation, is inhibited by PIs.…”

Bone Metabolism and HIV Infection

“…gp120 also stimulates RANKL (42). ARV naïve HIV-positive individuals have increased serum RANKL levels and reduced OPG/RANKL ratios, which correlate negatively with the www.intechopen.com HIV viral load and the Z-score obtained by densitometry (43). RANKL is not only produced by osteoblasts but also by activated T-cells, which represent a likely source of enhanced RANKL expression in light of their increased numbers during HIV infection.…”

Aging, human immunodeficiency virus, and bone health

“…During the asymptomatic phase of HIV infection, levels of inflammatory cytokines, such as interleukin-1, interleukin-6, and TNF-α are increased, and these cytokines can also stimulate bone resorption 43. RANKL levels have been found to be higher in HIV-infected men and correlated with lower bone mineral density,44 although another study found that bone mineral density was not associated with soluble TNF receptor 2 levels 45. Well-controlled studies have not been performed to date to demonstrate a connection between altered expression of cytokines due to HIV infection and changes in bone mineral density.…”

“…Recent gene expression profiling has indicated that exposure of osteoblastic cells to nelfinavir and ritonavir increases gene expression of the inflammatory cytokines, MCP-1, and interleukin-8 51. Protease inhibitors have also been suggested to inhibit 1-alpha-hydroxylase, as well as to reduce 1,25(OH) 2 D levels, which could reduce bone mineral density 45. LRP5, a positive regulator of bone formation, is inhibited by protease inhibitors 51,52…”