Serum S100A8 and S100A9 as prognostic biomarkers in acute exacerbation of idiopathic pulmonary fibrosis.


Journal

Respiratory investigation
ISSN: 2212-5353
Titre abrégé: Respir Investig
Pays: Netherlands
ID NLM: 101581124

Informations de publication

Date de publication:
Nov 2021
Historique:
received: 05 01 2021
revised: 16 04 2021
accepted: 19 05 2021
pubmed: 23 6 2021
medline: 26 11 2021
entrez: 22 6 2021
Statut: ppublish

Résumé

Acute exacerbation of idiopathic pulmonary fibrosis (AE-IPF) is a devastating and life-threatening condition during its clinical course. Biomarkers for precisely anticipating the prognosis of AE-IPF remain to be fully established. The objective of this study was to clarify whether S100A8 and S100A9, which are calcium-binding proteins mainly produced by activated neutrophils, are significant prognostic biomarkers in AE-IPF. Thirty-seven patients with AE-IPF who were diagnosed and treated at our hospital were retrospectively evaluated. The serum levels of S100A8 and S100A9 were measured using enzyme-linked immunosorbent assay, and the relationships between these levels and clinical parameters or prognosis were evaluated. The serum levels of S100A8 (median 386.5 ng/mL) and S100A9 (median 60.2 ng/mL) in patients with AE-IPF were significantly higher than those in age-matched healthy controls and in patients at IPF diagnosis (p < 0.001 for all combinations). The serum levels of S100A8 negatively correlated with percent forced vital capacity (r = -0.356, p = 0.049) and positively correlated with peripheral white blood cell number (r = 0.509, p = 0.002). Immunohistochemical staining of autopsy lung specimens showed that neutrophils, present mainly in the alveolar septum, were positive for S100A8 and S100A9. Patients with AE-IPF with higher levels of S100A8 or S100A9 showed significantly worse 3-month survival than those with lower levels (log-rank test, both p = 0.028). Finally, in multivariate analysis, the serum levels of both S100A8 and S100A9 were significant prognostic factors (hazard ratio 4.032, p = 0.023 and hazard ratio 4.327, p = 0.012). The serum levels of S100A8 and S100A9 at AE were significant prognostic biomarkers in patients with AE-IPF.

Sections du résumé

BACKGROUND BACKGROUND
Acute exacerbation of idiopathic pulmonary fibrosis (AE-IPF) is a devastating and life-threatening condition during its clinical course. Biomarkers for precisely anticipating the prognosis of AE-IPF remain to be fully established. The objective of this study was to clarify whether S100A8 and S100A9, which are calcium-binding proteins mainly produced by activated neutrophils, are significant prognostic biomarkers in AE-IPF.
METHODS METHODS
Thirty-seven patients with AE-IPF who were diagnosed and treated at our hospital were retrospectively evaluated. The serum levels of S100A8 and S100A9 were measured using enzyme-linked immunosorbent assay, and the relationships between these levels and clinical parameters or prognosis were evaluated.
RESULTS RESULTS
The serum levels of S100A8 (median 386.5 ng/mL) and S100A9 (median 60.2 ng/mL) in patients with AE-IPF were significantly higher than those in age-matched healthy controls and in patients at IPF diagnosis (p < 0.001 for all combinations). The serum levels of S100A8 negatively correlated with percent forced vital capacity (r = -0.356, p = 0.049) and positively correlated with peripheral white blood cell number (r = 0.509, p = 0.002). Immunohistochemical staining of autopsy lung specimens showed that neutrophils, present mainly in the alveolar septum, were positive for S100A8 and S100A9. Patients with AE-IPF with higher levels of S100A8 or S100A9 showed significantly worse 3-month survival than those with lower levels (log-rank test, both p = 0.028). Finally, in multivariate analysis, the serum levels of both S100A8 and S100A9 were significant prognostic factors (hazard ratio 4.032, p = 0.023 and hazard ratio 4.327, p = 0.012).
CONCLUSION CONCLUSIONS
The serum levels of S100A8 and S100A9 at AE were significant prognostic biomarkers in patients with AE-IPF.

Identifiants

pubmed: 34154976
pii: S2212-5345(21)00089-7
doi: 10.1016/j.resinv.2021.05.008
pii:
doi:

Substances chimiques

Biomarkers 0
Calgranulin A 0
Calgranulin B 0
S100A8 protein, human 0
S100A9 protein, human 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

827-836

Informations de copyright

Copyright © 2021 The Japanese Respiratory Society. Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Conflict of Interest All authors do not have any potential conflicts of interest. This research was not funded.

Auteurs

Kazuki Tanaka (K)

Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.

Noriyuki Enomoto (N)

Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan; Health Administration Center, Hamamatsu University School of Medicine, Hamamatsu, Japan. Electronic address: norieno@hama-med.ac.jp.

Hironao Hozumi (H)

Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.

Takuya Isayama (T)

Medical & Biological Laboratories Co., Ltd., Nagoya, Japan.

Hyogo Naoi (H)

Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.

Yuya Aono (Y)

Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.

Mineo Katsumata (M)

Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.

Hideki Yasui (H)

Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.

Masato Karayama (M)

Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.

Yuzo Suzuki (Y)

Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.

Kazuki Furuhashi (K)

Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.

Tomoyuki Fujisawa (T)

Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.

Naoki Inui (N)

Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan; Department of Clinical Pharmacology and Therapeutics, Hamamatsu University School of Medicine, Hamamatsu, Japan.

Yutaro Nakamura (Y)

Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.

Takafumi Suda (T)

Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.

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Classifications MeSH