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糖皮质激素与破骨细胞

Glucocorticoids and the osteoclast.

作者信息

Teitelbaum Steven L

机构信息

Washington University School of Medicine, St. Louis Missouri, USA.

出版信息

Clin Exp Rheumatol. 2015 Jul-Aug;33(4 Suppl 92):S37-9. Epub 2015 Oct 12.

Abstract

Glucocorticoid-induced osteoporosis uniformly represents suppression of bone formation. The steroid's effects on osteoclasts are, however, controversial. While glucocorticoid administration to patients with inflammatory diseases accelerates bone resorption, osteoclast function falls below normal with prolonged treatment. Thus, administration of anti-resorptive agents, such as bisphosphonates, is justified during early glucocorticoid therapy, but further suppression of osteoclasts, by these drugs, in chronically treated patients will dampen bone remodelling and may compromise skeletal quality, predisposing to fracture.

摘要

糖皮质激素诱导的骨质疏松症始终表现为骨形成受抑制。然而,该类固醇对破骨细胞的作用存在争议。虽然给炎症性疾病患者使用糖皮质激素会加速骨吸收,但长期治疗后破骨细胞功能低于正常水平。因此,在糖皮质激素治疗早期使用抗吸收药物(如双膦酸盐)是合理的,但在长期治疗的患者中,这些药物进一步抑制破骨细胞会抑制骨重塑,并可能损害骨骼质量,增加骨折风险。

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