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[糖皮质激素性骨质疏松——机制与预防]

[Glucocorticoid-induced osteoporosis--mechanisms and preventions].

作者信息

Tomita A

机构信息

Department of Laboratory Medicine, Aichi Medical University.

出版信息

Nihon Rinsho. 1998 Jun;56(6):1574-8.

PMID:9648484
Abstract

It has been well known that patients with Cushing's syndrome have frequently osteoporosis or bone loss due to excess endogenous glucocorticoids and also osteopenia or osteoporosis is commonly observed in patients with long-term glucocorticoid therapy. In this paper, the mechanisms involved in bone loss in Cushing's syndrome and glucocorticoid-induced osteoporosis were demonstrated. In the patients with Cushing's syndrome, excess endogenous glucocorticoids increase bone resorption and decrease bone formation and also act to depress intestinal calcium absorption and increase urinary calcium excretion, leading to compensatory stimulation of parathyroid hormone secretion. Then, parathyroid hormone stimulates bone resorption. Thus, secondary osteoporosis is commonly observed due to excess glucocorticoid. Finally, preventions and managements for glucocorticoid-induced osteoporosis were discussed.

摘要

众所周知,库欣综合征患者常因内源性糖皮质激素过多而出现骨质疏松或骨质流失,长期接受糖皮质激素治疗的患者也普遍存在骨质减少或骨质疏松的情况。本文阐述了库欣综合征和糖皮质激素诱导的骨质疏松中骨质流失所涉及的机制。在库欣综合征患者中,过多的内源性糖皮质激素会增加骨吸收、减少骨形成,还会抑制肠道钙吸收并增加尿钙排泄,从而导致甲状旁腺激素分泌的代偿性刺激。然后,甲状旁腺激素刺激骨吸收。因此,糖皮质激素过多常导致继发性骨质疏松。最后,本文讨论了糖皮质激素诱导的骨质疏松的预防和管理措施。

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