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目的探讨超体质量、肥胖成人肺通气功能与炎性因子的相关性。方法 90例成人体检者按体质量指数分为正常组、超体质量组、肥胖组各30例。采用ELISA法检测3组肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-6(interleukin-6,IL-6)、细胞间黏附分子-1(intercellular cell adhesion molecule-1,ICAM-1)水平,并进行肺通气功能检测;分析肺通气功能与TNF-α、IL-6、ICAM-1的相关性。结果肥胖组肺活量(vital capacity,VC)(92.37±6.45)%、用力肺活量(forced vital capacity,FVC)(93.27±7.78)%、第1秒用力呼气容积(forced expiratory volume in one second,FEV1)(89.87±9.43)%、最高呼气流速(peak expiratory flow,PEF)(78.00±11.18)%均较正常组(VC(96.43±5.99)%、FVC(101.4±15.41)%、FEV1(98.90±13.85)%、PEF(87.40±10.98)%)明显降低(P<0.05或P<0.01),超体质量组上述指标(VC(93.07±7.30)%、FVC(96.27±6.91)%、FEV1(95.10±10.77)%、PEF(80.03±21.62)%)与正常组、肥胖组比较差异均无统计学意义(P>0.05);肥胖组中TNF-α((0.82±0.05)μg/L)、IL-6((86.86±3.80)ng/L)较正常组(TNF-α为(0.79±0.05)μg/L、IL-6(84.82±2.86)ng/L)明显增高(P<0.05),超体质量组上述指标(TNF-α(0.80±0.05)μg/L、IL-6(85.22±3.79)ng/L)与正常组、肥胖组比较差异均无统计学意义(P>0.05),各组间ICAM-1水平比较差异无统计学意义(P>0.05);TNF-α与FVC、FEV1呈负相关(r=-0.285,P=0.006;r=-0.269,P=0.010),ICAM-1与VC呈负相关(r=-0.230,P=0.042)。结论肥胖者存在肺功能受损及部分炎症介质改变;炎症介质与肥胖通气功能受损相关。
Objective To explore the correlation between lung function and inflammatory factors in overweight and obesity adults. Methods Ninety adult adults were divided into normal group, overweight group and obesity group according to body mass index. The levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), intercellular cell adhesion molecule- 1, ICAM-1) were measured and lung ventilation was tested. The correlation between pulmonary ventilation and TNF-α, IL-6 and ICAM-1 was analyzed. Results In the obese group, the vital capacity (VC) was 92.37 ± 6.45%, the forced vital capacity (FVC) was 93.27 ± 7.78%, and the forced expiratory volume in one second (FEV1) (89.87 ± 9.43)%, peak expiratory flow (PEF) (78.00 ± 11.18)% were significantly higher than those in the normal group (VC 96.43 ± 5.99%, FVC 101.4 ± 15.41%, FEV 1 98.90 ± 13.85 ), PEF (87.40 ± 10.98)%, P <0.05 or P <0.01). The above indexes in the overweight group (VC: 93.07 ± 7.30%, FVC (96.27 ± 6.91)%, FEV1 (P <0.05). The levels of TNF-α (0.82 ± 0.05) μg / L and IL-10 in the obese group were significantly lower than those in the obese group 6 in the control group was significantly higher than that in the control group (P <0.05), and the level of IL-6 (86.86 ± 3.80) ng / L was significantly higher than that of the normal group (0.79 ± 0.05 vs 0.84 ± 2.86 ng / L, There were no significant differences in the above indexes (TNF-α (0.80 ± 0.05) μg / L and IL-6 (85.22 ± 3.79) ng / L vs the normal group and obesity group) There was no significant difference in the levels of ICAM-1 between the two groups (P> 0.05). TNF-α was negatively correlated with FVC and FEV1 (r = -0.285, P = 0.006; r = -0.269, Negative with VC (R = -0.230, P = 0.042). Conclusion Obese patients have impaired pulmonary function and some inflammatory mediators. Inflammatory mediators are associated with impaired ventilatory function.