阐明抗精神病药和抗抑郁药介导的骨折的机制。

Karen L Houseknecht, C C Bouchard, C A Black
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引用次数: 8

摘要

情绪谱系障碍和用于治疗这些障碍的药物,如非典型抗精神病药物(AA),与代谢和内分泌副作用有关,包括肥胖、血脂异常、高血糖和骨折风险增加。抗抑郁药物,包括选择性5 -羟色胺再摄取抑制剂(SSRI),也被报道会增加一些患者骨折的风险。骨折风险增加的药理学机制目前尚不清楚。可能的机制包括多巴胺能和/或血清素能信号通路的改变。由于这些药物分布到骨髓和大脑,药物性骨折可能是由于中枢介导的作用以及对骨转换的直接影响。考虑到越来越多的患者在标签上和标签外适应症下使用这些药物,了解药物性骨折的风险水平和机制对于告知处方和患者监测实践非常重要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Elucidating the Mechanism(s) Underlying Antipsychotic and Antidepressant-Mediated Fractures.

Mood spectrum disorders and medications used to treat these disorders, such as atypical antipsychotic drugs (AA), are associated with metabolic and endocrine side effects including obesity, dyslipidemia, hyperglycemia and increased risk of fractures. Antidepressant medications, including selective serotonin reuptake inhibitors (SSRI), have also been reported to increase fracture risk in some patients. The pharmacology underlying the increased risk of fractures is currently unknown. Possible mechanisms include alternations in dopaminergic and/or serotonergic signaling pathways. As these medications distribute to the bone marrow as well as to the brain, it is possible that drug-induced fractures are due to both centrally mediated effects as well as direct effects on bone turnover. Given the growing patient population that is prescribed these medications for both on- and off-label indications, understanding the level of risk and the mechanisms underlying drug-induced fractures is important for informing both prescribing and patient monitoring practices.

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