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High Concentration of (1→3)-β-D-Glucan in BAL Fluid in Patients With Acute Eosinophilic Pneumonia*

Tomotaka Kawayama; Rei Fujiki; Junichi Honda; Toru Rikimaru; Hisamichi Aizawa
Author and Funding Information

*From the First Department of Internal Medicine, Kurume University School of Medicine, Fukuoka, Japan.

Correspondence to: Hisamichi Aizawa, MD, First Department of Internal Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume-City, Fukuoka 830-0011, Japan; e-mail: aizawa@med.kurume-u.ac.jp



Chest. 2003;123(4):1302-1307. doi:10.1378/chest.123.4.1302
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Our aim in the study was to investigate the pathogenesis of eosinophilic inflammation in patients with acute eosinophilic pneumonia (AEP), and to determine the levels of (1→3)-β-D-glucan, which is one of the major components of the cell wall of most fungi, in the BAL fluid (BALF) of those patients with AEP. Six patients with AEP and five patients with chronic eosinophilic pneumonia (CEP) that was in the acute stage and had been newly diagnosed, and nine healthy subjects from the Kurume University School of Medicine and the Social Institute Tagawa Hospital between 1995 and 2001 were entered into the study. In AEP patients, (1→3)-β-D-glucan was detected in BALF, and these findings were compared with BALF findings in patients with CEP as well as with those in healthy subjects. In the BALF of AEP patients, the mean concentration of (1→3)-β-D-glucan was significantly higher (p < 0.05) than that of CEP patients as well as healthy subjects. In patients with AEP, the mean concentration of (1→3)-β-D-glucan in BALF was significantly higher (p < 0.05) than that in the blood. In four of six patients with AEP, we measured serial changes in (1→3)-β-D-glucan levels, and the level of (1→3)-β-D-glucan in the BALF decreased with clinical improvement at follow-up. We concluded that inhaled (1→3)-β-D-glucan may be involved in the mechanisms of pulmonary inflammation in patients with AEP.

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