Increased arteriovenous carboxyhemoglobin differences in patients with inflammatory pulmonary diseases.
Increased arteriovenous carboxyhemoglobin differences in patients with inflammatory pulmonary diseases.
复制标题
炎症性肺部疾病患者的动静脉碳氧血红蛋白差异增加。
DOI：
10.1378/chest.125.6.2160
复制
发表时间：
2004
期刊：
影响因子：
9.6
通讯作者：
Hidetada Sasaki
中科院分区：
文献类型：
--
作者：
H. Yasuda;Takahiko Sasaki;M. Yamaya;S. Ebihara;M. Maruyama;A. Kanda;Hidetada Sasaki
目的
炎症性肺病患者呼出的一氧化碳和动脉血碳氧血红蛋白浓度增加。本研究旨在阐明动静脉碳氧血红蛋白（a-vHb-CO）浓度差异是否也可用于确定炎症部位，无论是在肺或肺以外的器官。
材料和方法
我们检测了包括支气管哮喘（n = 18）和肺炎（n = 33）在内的急性肺部炎症患者以及包括急性肾盂肾炎（n = 28）和活动性类风湿关节炎（n = 16）在内的肺外炎症患者的动脉和外周静脉血以及呼出气中一氧化碳的碳氧血红蛋白浓度。
结果
肺和肺外炎症患者的动脉血和外周静脉血中碳氧血红蛋白值均显著高于对照组（n = 22）。此外，a-vHb-CO的差异在炎症性肺部疾病患者高于急性肾盂肾炎患者和类风湿性关节炎患者，并比对照组。肺炎患者a-vHb-CO差值与外周静脉血WBC计数相关。在支气管哮喘患者中，a-vHb-CO差值与FEV（1）呈负相关，尽管它们与外周静脉血WBC计数无关。急性肾盂肾炎患者的a-vHb-CO差值高于活动性类风湿关节炎患者。
结论
本研究表明，a-vHb-CO的差异可能是一个有用的手段来定义炎症的网站，无论是在肺或器官以外的肺，在患者的发热原因不明。大的a-vHb-CO差异可能是由肺部炎症中的一氧化碳产生引起的。
PURPOSE
Exhaled carbon monoxide and arterial blood carboxyhemoglobin concentrations increase in inflammatory pulmonary diseases. The present study was undertaken to elucidate whether arteriovenous carboxyhemoglobin (a-vHb-CO) concentration differences are also useful to define the site of inflammation, either in the lung or organs other than the lung.
MATERIALS AND METHODS
We examined concentrations of carboxyhemoglobin in both arterial and peripheral venous blood and exhaled carbon monoxide in patients with acute pulmonary inflammation including bronchial asthma (n = 18) and pneumonia (n = 33), and those in patients with extrapulmonary inflammatory diseases, including acute pyelonephritis (n = 28) and active rheumatoid arthritis (n = 16).
RESULTS
The values of carboxyhemoglobin in both arterial and peripheral venous blood were significantly higher in patients with pulmonary and extrapulmonary inflammation compared with those in control subjects (n = 22). Furthermore, a-vHb-CO differences in patients with inflammatory pulmonary diseases were higher than those in patients with acute pyelonephritis and patients with rheumatoid arthritis, and than those in control subjects. The a-vHb-CO differences correlated with the WBC count of peripheral venous blood in patients with pneumonia. In patients with bronchial asthma, the a-vHb-CO differences inversely correlated with FEV(1), although they did not correlate with WBC count of peripheral venous blood. The a-vHb-CO differences in patients with acute pyelonephritis were higher than those in patients with active rheumatoid arthritis.
CONCLUSION
The present study suggests that a-vHb-CO differences may be a useful means to define the site of inflammation, either in the lung or organs other than the lung, in patients with a fever of unknown origin. The large a-vHb-CO differences may be caused by carbon monoxide production in pulmonary inflammation.