Peripheral alveolar nitric oxide concentration reflects alveolar inflammation in autoimmune pulmonary alveolar proteinosis. Issue 1 (23rd March 2018)

• Record Type: Journal Article
• Authors: Hirano, Taizou; Ohkouchi, Shinya; Tode, Naoki; Kobayashi, Makoto; Ono, Manabu; Satoh, Teruyuki; Mitsuishi, Yoichiro; Watanabe, Akira; Tabata, Masao; Irokawa, Toshiya; Ogawa, Hiromasa; Sugiura, Hisatoshi; Kikuchi, Toshiaki; Akasaka, Keiichi; Tazawa, Ryushi; Inoue, Yoshikazu; Nakata, Koh; Kurosawa, Hajime; Ichinose, Masakazu
• Is Part Of: ERJ open research. Volume 4:Issue 1(2018)
• Publication Date: 2018-03-23
• Subjects: Respiratory organs -- Diseases -- Periodicals; Respiration -- Periodicals; Respiration; Respiratory organs -- Diseases; Respiratory organs -- Diseases -- Treatment; Respiratory Tract Diseases; Electronic journals; Fulltext; Internet Resources; Periodicals; Periodical; 616.2005
• DOI: 10.1183/23120541.00071-2017
• Languages: English
• ISSNs: 2312-0541

Abstract

Autoimmune pulmonary alveolar proteinosis (aPAP) is caused by an excess of autoantibodies against granulocyte-macrophage colony-stimulating factor (GM-CSF). In this situation, the clearance of intracellular debris in alveolar macrophages is impaired, and the alveolar spaces are occupied by excessive surfactant sediments. Several serum markers (lactate dehydrogenase (LDH), KL-6, carcinoembryonic antigen and surfactant protein D), alveolar–arterial oxygen difference ( P A–aO2 ) and the percentage diffusing capacity of the lung for carbon monoxide (% D LCO ) have a correlation with the disease severity and are used to evaluate the severity of aPAP [1]. Nitric oxide and alveolar macrophage inflammation http://ow.ly/czCx30i12n8