HPA轴相关的帕金森病与骨质疏松症的共病机制研究进展

帕金森病 （Parkinson''s Disease，PD） 是骨质疏松症的独立风险因素。PD合并骨质疏松患者在临床上数量较多， 预后较差，给患者生活和公共卫生带来极大的负担。然而，目前依然缺乏对PD与骨质疏松共病机制的探索，为疾病的防治带来困难。下丘脑-垂体-肾上腺轴 （Hypothalamic-Pituitary-Adrenal axis，HPA） 活性异常在 PD患者中已有多年的研究，被认为参与了 PD 的发病机制。HPA 轴的激活与慢性压力相关，并且可以导致血浆皮质醇、糖皮质激素等固醇类激素水平上升。而慢性压力应激已被报道可以导致骨质流失，且糖皮质激素在临床上的应用也被认为与骨质疏松有关。这提示HPA轴的活性异常可能是PD共患骨质疏松症的重要机制。本综述针对PD患者中的HPA轴活性功能异常的病理过程，提出HPA轴活性异常可能通过导致固醇类激素水平异常上升、甲状旁腺激素水平异常以及交感神经系统异常三个方面影响骨代谢水平， 对PD和骨质疏松共患机制进行探索，以期为临床上PD患者的治疗提供线索和启示。

HPA axis participates in the osteoporosis symptoms of Parkinson's disease

Parkinson''s disease (PD) is considered as an independent risk factor of osteoporosis, which reveals a common pathology within the two disorders. The dysfunction of hypothalamic-pituitary-adrenal axis (HPA axis), which has been frequently reported in PD patients. The overactivated HPA axis is also considered as a key reason of bone loss induced by chronic stress, as well as glucocorticoid treatment of disorders including autoimmune, pulmonary, and gastrointestinal diseases. Therefore, the HPA axis overactivation in PD probably participates in the osteoporosis symptoms of PD, by elevating steroid hormone levels, suppressing parathyroid function, and affecting sympathetic nervous system, which all leads to decreased plasma calcium levels and increased bone loss. The role of HPA axis participating in the coexistence of PD and osteoporosis may provide insights and targets for the treatment of PD patients in clinical practice.