Otolin-1用于鉴别急性持续性头晕的中枢性与周围性病因

文献信息

中文摘要

背景： 孤立性急性起病持续性头晕（iAOCD）患者常见于急诊科（ED）。区分周围性前庭疾病与中枢性病因仍具挑战性。现有诊断工具，包括床旁检查和神经影像学，均存在重要局限性。Otolin-1是一种内耳特异性糖蛋白，已被提出作为周围性前庭病理的生物标志物。本研究评估otolin-1能否作为区分二者的诊断性生物标志物。
方法： 本研究分析了来自一项前瞻性多中心队列的样本，对象为因急性起病、持续性头晕且无局灶性神经功能缺损而就诊于ED的成年患者。患者在症状发作24小时内纳入。采用酶联免疫吸附试验测定血浆otolin-1浓度。最终诊断（中枢性 versus 周围性）由专家小组根据临床评估、弥散加权磁共振成像及3个月随访确定。
结果： 我们分析了245例患者（179例周围性，66例中枢性）。周围性与中枢性病因之间的otolin-1浓度中位数无显著差异（517.6 [IQR 443.7-592.8] pg/mL vs 487.9 [424.9-644.4] pg/mL；p = 0.349）。在超急性期（症状发作后<4.5小时）或急性期（症状发作后4.5-24小时）亚组中均未观察到显著差异。同样，中枢性iAOCD与特定周围性诊断之间的otolin-1浓度也无差异。在所有比较中均观察到浓度范围存在大量重叠。受试者工作特征分析同样显示无有用区分能力（AUC 0.539，95% CI 0.455-0.623）。
结论： 在ED环境中，otolin-1不能区分iAOCD的中枢性与周围性病因。尽管其在生物学上与内耳病理相关，但otolin-1作为独立诊断性生物标志物缺乏足够的区分价值。

英文摘要

BACKGROUND: Patients with isolated acute-onset continuous dizziness (iAOCD) are commonly seen at the emergency department (ED). Distinguishing peripheral vestibular disorders from central causes remains challenging. Existing diagnostic tools, including bedside examination and neuroimaging, have important limitations. Otolin-1, an inner ear-specific glycoprotein, has been proposed as a biomarker of peripheral vestibular pathology. This study evaluated whether otolin-1 could serve as a diagnostic biomarker for this differentiation.
METHODS: This study analyzed samples from a prospective multicenter cohort of adult patients who were seen at the ED with acute onset, continuous dizziness without focal neurological deficits. Patients were included within 24 hours of symptom onset. Otolin-1 plasma concentrations were measured using an enzyme-linked immunosorbent assay. Final diagnoses (central versus peripheral) were determined by an expert panel based on clinical assessment, diffusion-weighted magnetic resonance imaging and 3-month follow-up.
RESULTS: We analyzed 245 patients (179 peripheral, 66 central). Median otolin-1 concentrations did not differ significantly between peripheral and central causes (517.6 [IQR 443.7-592.8] pg/mL vs 487.9 [424.9-644.4] pg/mL; p = 0.349). No significant differences were observed in hyperacute (<4.5 hours after symptom onset) or acute (4.5-24 hours after symptom onset) subgroups. Similarly, otolin-1 concentrations did not differ between central iAOCD and specific peripheral diagnoses. Substantial overlap in concentration ranges was observed across all comparisons. Receiver operating characteristic analysis similarly showed no useful discrimination (AUC 0.539, 95% CI 0.455-0.623).
CONCLUSIONS: Otolin-1 does not differentiate between central and peripheral causes of iAOCD in the ED setting. Although biologically linked to inner ear pathology, otolin-1 lacks sufficient discriminatory value as a stand-alone diagnostic biomarker.