1.解放军总医院耳鼻咽喉头颈外科医学部/听觉与平衡觉全国重点实验室/国家耳鼻咽喉疾病临床医学研究中心 北京 100853
2.深圳龙岗区耳鼻咽喉医院 深圳 518172
刘兴健 本科 助理研究员;研究方向:听觉和前庭觉干预研究,E-mail: xingjianliu301@126.com
收稿:2026-02-03,
纸质出版:2026-05-15
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刘兴健,李娟娟,杜一等.肥胖与良性阵发性位置性眩晕的关联机制综述[J].中国听力语言康复科学杂志,2026,24(03):267-271.
LIU Xing-jian,LI Juan-juan,DU Yi,et al.Mechanistic Links Between Obesity and Benign Paroxysmal Positional Vertigo: A Review[J].Chinese Scientific Journal of Hearing and Speech Rehabilitation,2026,24(03):267-271.
刘兴健,李娟娟,杜一等.肥胖与良性阵发性位置性眩晕的关联机制综述[J].中国听力语言康复科学杂志,2026,24(03):267-271. DOI: 10.3969/j.issn.1672-4933.2026.03.010.
LIU Xing-jian,LI Juan-juan,DU Yi,et al.Mechanistic Links Between Obesity and Benign Paroxysmal Positional Vertigo: A Review[J].Chinese Scientific Journal of Hearing and Speech Rehabilitation,2026,24(03):267-271. DOI: 10.3969/j.issn.1672-4933.2026.03.010.
良性阵发性位置性眩晕(benign paroxysmal positional vertigo,BPPV)是临床常见的外周前庭眩晕疾病,终身患病率约2.4%。其核心病理基础为耳石脱位,但全身代谢与营养状态等系统性因素对疾病发生、复发及预后的影响日益受到重视。在全球肥胖流行背景下,肥胖与BPPV的关系成为研究热点,现有证据不支持二者存在稳定的直接因果联系。本文整合流行病学、病理生理及临床研究结果显示,横断面研究多提示肥胖/超重与BPPV患病率相关,但多变量校正后关联常减弱或消失,孟德尔随机化研究亦未证实肥胖为独立危险因素。机制层面肥胖更可能通过代谢综合征相关微血管障碍、慢性低度炎症与氧化应激、维生素D/钙稳态紊乱及肌肉减少症等间接通路,破坏内耳微环境与耳石稳定性,从而增加发病与复发倾向,并影响治疗获益。临床应在规范复位基础上,采用代谢干预+前庭保护的综合管理策略,包括代谢共病筛查与控制、维生素D/钙优化补充、抗阻训练与肌肉功能维护,并依托多学科协作进行长期随访。
Benign paroxysmal positional vertigo (BPPV) is the most common peripheral vestibular disorder in clinical practice
with an estimated lifetime prevalence of approximately 2.4%. Although otoconial dislodgement is the fundamental pathological basis
increasing attention has been paid to the contribution of systemic factors-particularly metabolic and nutritional status-to disease onset
recurrence
and clinical outcomes. Against the backdrop of the global obesity epidemic
the association between obesity and BPPV has become a focus of investigation; however
current evidence does not support a consistent direct causal relationship. By synthesizing available epidemiological
pathophysiological
and clinical data
this review shows that most cross-sectional studies report an association between overweight/obesity and BPPV prevalence
yet the association often attenuates or disappears after multivariable adjustment
and Mendelian randomization analyses have not identified obesity as an independent risk factor. Mechanistically
obesity is more likely to influence BPPV through indirect pathways
including metabolic syndrome-related microvascular dysfunction
chronic low-grade inflammation and oxidative stress
disrupted vitamin D/calcium homeostasis
and sarcopenia
thereby destabilizing the inner-ear microenvironment and otoconia and ultimately increasing susceptibility to onset and recurrence while reducing therapeutic benefit. Clinically
in addition to standardized canalith repositioning procedures
a comprehensive strategy integrating "metabolic intervention plus vestibular protection" is warranted. This includes screening and control of metabolic comorbidities
optimized vitamin D/calcium supplementation
resistance training with preservation of muscle function
and long-term follow-up within a multidisciplinary care model. Future work should prioritize large prospective cohorts
refined body-composition phenotyping
and targeted interventional trials to clarify key links and optimize individualized management.
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