Involvement of pulmonary endothelial cell injury in the pathogenesis of pulmonary fibrosis: clinical assessment by 123I-MIBG lung scintigraphy
Involvement of pulmonary endothelial cell injury in the pathogenesis of pulmonary fibrosis: clinical assessment by 123I-MIBG lung scintigraphy
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DOI：
10.1007/s00259-004-1663-1
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发表时间：
2005-02
影响因子：
9.1
通讯作者：
N. Takabatake;T. Arao;M. Sata;S. Abe;S. Inoue;Y. Shibata;Y. Takeishi;I. Kubota
中科院分区：
文献类型：
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作者：
N. Takabatake;T. Arao;M. Sata;S. Abe;S. Inoue;Y. Shibata;Y. Takeishi;I. Kubota
目的肺微血管内皮损伤可能参与了肺纤维化（PF）的发病过程。本研究的目的是评估肺血管状况与PF患者的肺动脉造影评估of 123 I-间碘苄胍（123 I-MIBG），这反映了潜在的内皮细胞lesions.MethodsWe评估肺123 I-MIBG动力学和临床指标在23 PF患者和16个对照。计算静脉注射123 I-MIBG后30 min（早期显像）和270 min（延迟显像）肺与纵隔平均摄取比值（L/M）。结果PF组早期显像L/M比值（1.41 ± 0.14vs1.53 ± 0.10，P <0.01）显著低于对照组（1.28 ± 0.10vs1.33 ± 0.07，P =NS），延迟显像L/M比值（1.33± 0.07，P <0.01）与对照组无显著性差异。PF组WR为28.6%±3.1%，对照组为34.2%± 5.1%，P <0.001。研究受试动物中（PF患者加对照组）123 I-MIBG肺WR与PF严重程度的其他诊断参数（如肺活量）之间存在显著相关性（r= 0.625，p <0.0001），肺总量（r= 0.691，p <0.0001），一氧化碳弥散量（r= 0.622，P <0.0001），血清血管紧张素转换酶活性（r= 0.422，p <0.01）、糖链抗原KL-6水平（r=-0.495，p <0.01）和表面活性蛋白D水平（r=-0.461，p <0.01）。当对照组被排除在外时，观察到WR和%TLC之间存在类似的显著相关性（r= 0.508，p <0.05），DLCO（r= 0.593，p <0.01）与血清ACE活性结论内皮细胞损伤在PF发病中起重要作用，123 I-MIBG的肺WR，作为内皮损伤的特异性标志物，可作为评价PF功能严重程度的一种新的诊断工具。
PurposePulmonary microvascular endothelial injury may be involved in the pathogenesis of pulmonary fibrosis (PF). The aim of this study was to evaluate the pulmonary vascular status in patients with PF by lung scintigraphic assessment of123I-metaiodobenzylguanidine (123I-MIBG), which reflects latent endothelial cell lesions.MethodsWe assessed lung123I-MIBG kinetics and clinical indices in 23 PF patients and 16 controls. Mean uptake ratios of lung to mediastinum (L/M) were calculated in anterior planar images at 30 (early image) and 270 (delayed image) min after intravenous injection of123I-MIBG. The pulmonary mean washout rate (WR) of123I-MIBG was also calculated.ResultsTheL/Mratio in early images, but not in delayed images, was significantly lower in the PF patients than in the controls (L/Mearly1.41±0.14 vs 1.53±0.10,p<0.01;L/Mdelayed1.28±0.10 vs 1.33±0.07,p=NS). WR was significantly reduced in the PF patients compared with the controls (28.6%±3.1% vs 34.2%±5.1%,p<0.001). In the study subjects (PF patients plus controls) there were significant relationships between lung WR of123I-MIBG and other diagnostic parameters for the severity of PF, such as vital capacity (r=0.625,p<0.0001), total lung capacity (r=0.691,p<0.0001), carbon monoxide diffusing capacity (r=0.622,p<0.0001), serum angiotensin-converting enzyme activity (r=0.422,p<0.01), carbohydrate antigen KL-6 levels (r=−0.495,p<0.01) and surfactant protein-D levels (r=−0.461,p<0.01). When control subjects were excluded, similar significant correlations were observed between WR and %TLC (r=0.508,p<0.05), DLCO(r=0.593,p<0.01) and serum ACE activity (r=0.515,p<0.05) in the PF patients.ConclusionThese results suggest that endothelial cell injury plays a significant role in the pathogenesis of PF, and that lung WR of123I-MIBG, which is a specific marker of endothelial damage, can serve as a novel diagnostic tool to evaluate the functional severity of PF.