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GLUCOCORTICOID EXCESS IN BONE AND MUSCLE.
Sato, Amy Y; Peacock, Munro; Bellido, Teresita.
Afiliação
  • Sato AY; Department of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, Indiana, 46202.
  • Peacock M; Department of Medicine, Division of Endocrinology, Indiana University School of Medicine, Indianapolis, Indiana, 46202.
  • Bellido T; Department of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, Indiana, 46202.
Clin Rev Bone Miner Metab ; 16(1): 33-47, 2018 Mar.
Article em En | MEDLINE | ID: mdl-29962904
ABSTRACT
Glucocorticoids (GC), produced and released by the adrenal glands, regulate numerous physiological processes in a wide range of tissues. Because of their profound immunosuppressive and anti-inflammatory actions, GC are extensively used for the treatment of immune and inflammatory conditions, the management of organ transplantation, and as a component of chemotherapy regimens for cancers. However, both pathologic endogenous elevation and long-term use of exogenous GC are associated with severe adverse effects. In particular, excess GC has devastating effects on the musculoskeletal system. GC increase bone resorption and decrease formation leading to bone loss, microarchitectural deterioration and fracture. GC also induce loss of muscle mass and strength leading to an increased incidence of falls. The combined effects on bone and muscle account for the increased fracture risk with GC. This review summarizes the advance in knowledge in the last two decades about the mechanisms of action of GC in bone and muscle and the attempts to interfere with the damaging actions of GC in these tissues with the goal of developing more effective therapeutic strategies.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Clin Rev Bone Miner Metab Ano de publicação: 2018 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Clin Rev Bone Miner Metab Ano de publicação: 2018 Tipo de documento: Article