RESUMO
Patients with rheumatoid arthritis are predisposed to systemic bone loss, and they are at an increased risk of fractures. Although there are similarities in the patient demographics between rheumatoid arthritis patients and the general population of osteoporosis patients, there are factors, particularly the use of glucocorticoids, which are specific to rheumatoid arthritis. These factors can lead to an increased risk of bone loss and fracture. Given that fractures are often very debilitating, especially in elderly patients, it is of paramount importance for the practicing rheumatologist to be aware of ways to reduce the risk of fracture in patients with rheumatoid arthritis. This review discusses currently available modalities for fracture risk assessment as well as pharmacologic and lifestyle interventions available to treat and prevent bone loss in rheumatoid arthritis patients.
Assuntos
Artrite Reumatoide/complicações , Fraturas Ósseas/diagnóstico , Fraturas Ósseas/prevenção & controle , Antirreumáticos/uso terapêutico , Artrite Reumatoide/tratamento farmacológico , Reabsorção Óssea/diagnóstico , Reabsorção Óssea/etiologia , Reabsorção Óssea/prevenção & controle , Fraturas Ósseas/etiologia , Glucocorticoides/uso terapêutico , Humanos , Estilo de Vida , Osteoporose/diagnóstico , Osteoporose/etiologia , Osteoporose/prevenção & controle , Medição de RiscoRESUMO
We previously reported a role for the IZH2 gene product in metal ion metabolism. Subsequently, Izh2p was also identified as a member of the PAQR family of receptors and, more specifically, as the receptor for the plant protein osmotin. In this report, we investigate the effect of Izh2p on iron homeostasis. We show that overproduction of Izh2p prevents the iron-dependent induction of the Fet3p component of the high-affinity iron-uptake system and is deleterious for growth in iron-limited medium. We demonstrate that the effect of Izh2p requires cAMP-dependent kinase and AMP-dependent kinase and is not mediated by general inhibition of the Aft1p iron-responsive transcriptional activator. We also show that Izh2p-overproduction negatively regulates Nrg1p/Nrg2p- and Msn2p/Msn4p-dependent reporters. Furthermore, we show that the Nrg1p/Nrg2p and Msn2p/Msn4p pairs are epistatic to each other with respect to their effects on FET3 expression. Finally, we show that the mechanism by which PAQR receptors activate signal transduction pathways is likely to be conserved from yeast to humans.
