肥胖和炎症反应在中重度急性呼吸窘迫综合征:一项单中心试点研究

Adriano Peris, Marzia Del Re, Manuela Bonizzoli, Chiara Lazzeri, Eleonora Rofi, Gabriella Di Lascio, Lorenzo Fontanelli, Morena Cozzolino, Romano Danesi
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引用次数: 0

摘要

背景:在急性呼吸窘迫综合征(ARDS)中,肥胖与较低的死亡率相关,但其机制尚未阐明。方法:我们旨在评估20例连续入院的中重度ARDS患者在基线和3天后血浆生物标志物白介素-8 (IL-8)、基质金属蛋白酶-7 (MMP-7)、toll样受体2 (TLR-2)、肿瘤坏死因子-α (TNF-α)和降钙素原(PCT)水平。结果:我们的人群包括20例连续机械通气的中重度ARDS患者。肥胖发生率为40%(8/20)。肥胖患者和正常患者在基线特征上没有发现差异。特别是,ICU死亡率在两个亚组之间具有可比性。两个亚组在基线和72小时后的生物标志物血浆水平没有检测到差异。当检查每个生物标志物的行为时,肥胖患者在72小时内的MMP7和TLR-2值相对于基线显著增加,与正常患者不同。结论:我们的数据强烈提示,肥胖合并中重度ARDS患者对急性肺损伤的炎症反应发生了改变,因为只有这些患者在72小时内才检测到MMP-7和TLR-2的显著增加。需要进一步的调查以在更大的队列中证实我们的结果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Obesity and inflammatory response in moderate-to-severe acute respiratory distress syndrome: a single center pilot study.

Background: In acute respiratory distress syndrome (ARDS) obesity is associated with lower mortality but the mechanism(s) have not been elucidated.

Methods: We aimed at assessing plasma biomarker levels interleukin-8 (IL-8), matrix metalloproteinase-7 (MMP-7), Toll-like receptor 2 (TLR-2), tumor necrosis factor-α (TNF-α) and procalcitonin (PCT) at baseline and 3 days later in 20 consecutive moderate-severe ARDS consecutively admitted to our Center.

Results: Our population includes 20 consecutive mechanically ventilated patients with moderate-to severe ARDS. The incidence of obesity was 40% (8/20). No differences were detectable between obese and normal patients in baseline characteristics. In particular, ICU mortality was comparable between the two subgroups. No differences were detectable between the two subgroups at baseline and after 72 hours in biomarker plasma levels. When examining the behavior of each biomarker, obese patients showed a significant increase in MMP7 and TLR-2 values at 72 hours in respect to baseline, differently from normal patients.

Conclusions: Our data strongly suggest that obese patients with moderate to severe ARDS have an altered inflammatory response to acute lung injury, since a significant increase in MMP-7 and TLR-2 was detectable at 72 hours only in these patients. Further investigations are needed to confirm our results in larger cohorts.

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