原发性干燥综合征中肺功能障碍对夜间低氧血症的贡献超出阻塞性睡眠呼吸暂停严重程度

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中文摘要

背景/目的： 肺部受累是原发性干燥综合征（pSS）常见的腺外表现，可能损害肺气体交换。尽管已有pSS中阻塞性睡眠呼吸暂停（OSA）的报道，但夜间低氧血症与肺功能障碍之间的关系仍不清楚。我们研究了pSS中的夜间氧合异常是否与超出OSA严重程度的肺功能损害相关。方法：在这项对照横断面研究中，44例pSS患者和88名对照接受了整夜多导睡眠监测。所有pSS患者均具备肺功能检查，包括肺一氧化碳弥散量（DLCO），以及胸部计算机断层扫描。采用相关性分析评估夜间低氧血症参数与肺功能指标之间的关联。采用多变量线性回归评估夜间最低血氧饱和度的预测因素，并校正年龄、体重指数和呼吸暂停低通气指数。结果：除pSS组REM睡眠比例较低外，pSS患者与对照之间的睡眠呼吸障碍严重程度和夜间氧合特征相当。在pSS队列内，夜间最低血氧饱和度与DLCO、DLCO占预计值百分比、DLCO/VA和FVC占预计值百分比呈正相关。校正年龄、BMI和AHI后，DLCO占预计值百分比仍与夜间最低血氧饱和度独立相关。然而，在额外校正FVC后，该关联减弱，提示弥散功能损害和限制性通气功能障碍对夜间氧合的贡献存在重叠。结论：尽管总体夜间氧合与匹配对照无差异，但在pSS队列内肺功能损害与更差的夜间氧合相关。这些发现提示，pSS中的夜间低氧血症反映的是肺功能障碍多个相互关联的方面，而不仅仅是OSA严重程度。因此，在评估pSS患者夜间氧合异常时，评估肺功能（包括DLCO和FVC）可能提供具有临床意义的信息。

英文摘要

Background/Objectives: Pulmonary involvement is a common extraglandular manifestation of primary Sjögren syndrome (pSS) and may impair pulmonary gas exchange. Although obstructive sleep apnea (OSA) has been reported in pSS, the relationship between nocturnal hypoxemia and pulmonary dysfunction remains unclear. We investigated whether nocturnal oxygenation abnormalities in pSS are associated with pulmonary functional impairment beyond OSA severity. Methods: In this controlled cross-sectional study, 44 patients with pSS and 88 controls underwent overnight polysomnography. Pulmonary function testing, including diffusing capacity of the lung for carbon monoxide (DLCO), and thoracic computed tomography were available for all pSS patients. Associations between nocturnal hypoxemia parameters and pulmonary function indices were assessed using correlation analyses. Predictors of minimum nocturnal oxygen saturation were evaluated using multivariable linear regression adjusted for age, body mass index, and apnea-hypopnea index. Results: Sleep-disordered breathing severity and nocturnal oxygenation profiles were comparable between patients with pSS and controls, with the exception of a lower proportion of REM sleep in the pSS group. Within the pSS cohort, minimum nocturnal oxygen saturation correlated positively with DLCO, DLCO% predicted, DLCO/VA, and FVC% predicted. DLCO% predicted remained independently associated with minimum nocturnal oxygen saturation after adjustment for age, BMI, and AHI. However, this association was attenuated after additional adjustment for FVC, suggesting overlapping contributions of diffusion impairment and restrictive ventilatory dysfunction to nocturnal oxygenation. Conclusions: Although overall nocturnal oxygenation did not differ from that of matched controls, pulmonary functional impairment was associated with worse nocturnal oxygenation within the pSS cohort. These findings suggest that nocturnal hypoxemia in pSS reflects multiple interrelated aspects of pulmonary dysfunction rather than OSA severity alone. Assessment of pulmonary function, including both DLCO and FVC, may therefore provide clinically relevant information when evaluating nocturnal oxygenation abnormalities in patients with pSS.