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神经性厌食症中骨质流失的机制及治疗选择

Mechanisms and treatment options for bone loss in anorexia nervosa.

作者信息

Grinspoon S, Herzog D, Klibanski A

机构信息

Neuroendocrine Unit, Massachusetts General Hospital, Boston 02114, USA.

出版信息

Psychopharmacol Bull. 1997;33(3):399-404.

PMID:9550884
Abstract

Osteoporosis is present in over half of all patients with anorexia nervosa. Bone loss often occurs at a young age and may persist even after recovery, predisposing patients to debilitating spinal crush fractures. The pathogenesis of bone loss in anorexia nervosa is not completely understood and may result from a number of mechanisms, including estrogen deficiency, inadequate vitamin and calcium intake, and nutritional effects on bone formation. Recent studies demonstrate that estrogen itself is inadequate to increase bone density in a majority of patients with anorexia nervosa and suggest that nutritionally dependent factors such as insulin-like growth factor-I (IGF-I), a potent bone trophic hormone, may be important in maintaining bone mass. IT is hoped that new anabolic strategies to increase osteoblast function will become available in the future. In the interim, weight gain, restoration of gonadal function, and calcium supplementation remain the cornerstones of treatment in this disease.

摘要

超过半数的神经性厌食症患者存在骨质疏松。骨质流失往往在年轻时就会发生,甚至在康复后仍可能持续存在,使患者易患导致身体衰弱的脊椎压缩性骨折。神经性厌食症骨质流失的发病机制尚未完全明确,可能由多种机制引起,包括雌激素缺乏、维生素和钙摄入不足以及营养对骨形成的影响。最近的研究表明,雌激素本身不足以增加大多数神经性厌食症患者的骨密度,并提示营养依赖性因素,如胰岛素样生长因子-I(IGF-I,一种强大的骨营养激素),可能在维持骨量方面具有重要作用。人们希望未来能有新的促进成骨细胞功能的合成代谢策略。在此期间,体重增加、性腺功能恢复和补充钙剂仍然是该病治疗的基石。

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