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Clinical significance of anti-GM-CSF antibodies in idiopathic pulmonary alveolar proteinosis
  1. F-C Lin1,
  2. G-D Chang2,
  3. M-S Chern4,
  4. Y-C Chen3,
  5. S-C Chang3,5
  1. 1Department of Internal Medicine, Yuan Shan Veteran Hospital and Institute of Clinical Medicine, National Yang-Ming University, Taiwan
  2. 2Graduate Institute of Biochemical Sciences, National Taiwan University, Taiwan
  3. 3Chest Department, Taipei Veterans General Hospital, Taipei, Taiwan
  4. 4Department of Radiology, Taipei Veterans General Hospital
  5. 5Emergency and Critical Care Medicine, National Yang-Ming University, Taiwan
  1. Correspondence to:
    Dr S-C Chang
    Chest Department, Taipei Veterans General Hospital, #201 Section 2, Shih-Pai Road, Shih-Pai, Taipei 112, Taiwan; scchang{at}vghtpe.gov.tw

Abstract

Background: The role of anti-granulocyte-macrophage colony stimulating factor (GM-CSF) antibodies as a diagnostic marker in idiopathic pulmonary alveolar proteinosis (iPAP) remains unclear.

Methods: Anti-GM-CSF antibodies were detected in blood and bronchoalveolar lavage fluid (BAL) fluid in 13 patients with iPAP. Three patients with secondary PAP, 35 with other pulmonary disorders, and 10 subjects without lung lesions acted as controls. Blood samples only were obtained from 30 healthy medical personnel. Anti-GM-CSF antibodies were detected using immunoblotting and measured semi-quantitatively by serial dilution or concentration methods. The relationship between antibodies and reported severity indicators for iPAP was analysed.

Results: Anti-GM-CSF antibodies could be detected in both blood and BAL fluid samples in 12 of 13 iPAP patients and were undetectable in blood and/or BAL fluid from the other subjects studied. BAL fluid levels of anti-GM-CSF antibodies were highly correlated with the severity indicators for iPAP, including serum lactate dehydrogenase (LDH) levels, arterial oxygen tension, alveolar-arterial oxygen tension difference, (AaPo2), lung carbon monoxide transfer factor, and some lesion scores on chest radiographs and computed tomographic scans. In contrast, blood anti-GM-CSF antibodies were not significantly correlated with the severity indicators evaluated. In addition, patients with iPAP who required subsequent therapeutic lung lavage had significantly higher values of serum LDH, AaPO2, and BAL fluid anti-GM-CSF antibodies, and significantly lower values of Pao2.

Conclusions: In addition to serum LDH levels, Pao2 and AaPo2, BAL fluid levels of anti-GM-CSF antibodies might reflect disease severity in patients with iPAP and predict the need for subsequent therapeutic lung lavage. These findings may expand the role of anti-GM-CSF antibodies in iPAP.

  • AaPo2, alveolar-arterial oxygen tension difference
  • BAL, bronchoalveolar lavage
  • GM-CSF, granulocyte-macrophage colony stimulating factor
  • iPAP, idiopathic pulmonary alveolar proteinosis
  • LDH, lactate dehydrogenase
  • Pao2, arterial oxygen tension
  • Tlco, carbon monoxide transfer factor
  • anti-granulocyte-macrophage colony stimulating factor antibodies
  • granulocyte-macrophage colony stimulating factor
  • lactate dehydrogenase
  • pulmonary alveolar proteinosis
  • pulmonary function
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Footnotes

  • Published Online First 3 March 2006

  • This work was supported by grants from the Taipei Veterans General Hospital (TVGH91-323 and TVGH93-288)

  • Competing interests: none.

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