Faculty Opinions recommendation of Serum CC-chemokine ligand 18 concentration predicts outcome in idiopathic pulmonary fibrosis.

Author(s):  
Vincent Cottin ◽  
Lize Kiakouama
2009 ◽  
Vol 179 (8) ◽  
pp. 717-723 ◽  
Author(s):  
Antje Prasse ◽  
Corinna Probst ◽  
Elena Bargagli ◽  
Gernot Zissel ◽  
Galen B. Toews ◽  
...  

2007 ◽  
Vol 29 (6) ◽  
pp. 1082-1093 ◽  
Author(s):  
E. M. Pierce ◽  
K. Carpenter ◽  
C. Jakubzick ◽  
S. L. Kunkel ◽  
H. Evanoff ◽  
...  

2020 ◽  
Vol 9 (6) ◽  
pp. 1993
Author(s):  
Canay Caliskan ◽  
Benjamin Seeliger ◽  
Benedikt Jäger ◽  
Jan Fuge ◽  
Tobias Welte ◽  
...  

Idiopathic pulmonary fibrosis (IPF) is a progressive disease with high mortality. CC-chemokine ligand 18 (CCL18) is predictive of survival in IPF. We described correlation of CCL18 serum levels with the genotype of rs2015086 C > T polymorphism the CCL18-gene, which was associated with survival in a pre-antifibrotic cohort (Part-A). Herein (Part-B), we aimed to validate these findings and to study the effects of antifibrotics. Two cohorts were prospectively recruited, cohort-A (n = 61, pre-antifibrotic) and cohort B (n = 101, received antifibrotics). Baseline CCL18 serum level measurement by enzyme-linked immunosorbent assay (ELISA, serially in cohort B) and genotyping of rs2015086 was performed and correlated with clinical outcomes. The CT genotype was present in 15% and 31% of patients. These patients had higher CCL18 levels compared to the TT-genotype (cohort-A: 234 vs. 115.8 ng/mL, p < 0.001; cohort B: 159.5 vs. 120 ng/mL, p = 0.0001). During antifibrotic therapy, CCL18 increased (p = 0.0036) regardless of rs2015086-genotype and antifibrotic-agent. In cohort-A, baseline CCL18-cutoff (>120 ng/mL) and CT-genotype were associated with mortality (p = 0.041 and p = 0.0051). In cohort-B, the CCL18-cutoff (>140 ng/mL) was associated with mortality (p = 0.003) and progression (p = 0.004), but not the CT/CC-genotype. In conclusion, we validated the correlation between rs2015086-genotype and CCL18 serum levels, which was predictive of (progression-free)-survival in two prospective validation cohorts.


Respiration ◽  
2009 ◽  
Vol 78 (3) ◽  
pp. 285-292 ◽  
Author(s):  
Hiromi Shinoda ◽  
Sadatomo Tasaka ◽  
Seitaro Fujishima ◽  
Wakako Yamasawa ◽  
Keisuke Miyamoto ◽  
...  

2015 ◽  
Vol 46 (6) ◽  
pp. 1740-1750 ◽  
Author(s):  
Ganesh Raghu ◽  
Fernando J. Martinez ◽  
Kevin K. Brown ◽  
Ulrich Costabel ◽  
Vincent Cottin ◽  
...  

The objective of this study was to determine the safety and efficacy of carlumab in the treatment of idiopathic pulmonary fibrosis (IPF).A phase 2, randomised, double-blind placebo-controlled dose-ranging study was conducted in patients with IPF (n=126). Patients were randomised to carlumab (1 mg·kg−1, 5 mg·kg−1, or 15 mg·kg−1) or placebo every 4 weeks. The primary endpoint was the rate of percentage change in forced vital capacity (FVC). Secondary endpoints were time to disease progression, absolute change in FVC, relative change in diffusing capacity of the lung for carbon monoxide (DLCO), and St George's Respiratory Questionnaire (SGRQ) total score.Due to a pre-planned, unfavourable interim benefit–risk analysis, dosing was suspended. The rate of percentage change in FVC showed no treatment effect (placebo −0.582%, 1 mg·kg−1−0.533%, 5 mg·kg−1−0.799% and 15 mg·kg−1−0.470%; p=0.261). All active treatment groups showed a greater decline in FVC (1 mg·kg−1−290 mL, 5 mg·kg−1−370 mL and 15 mg·kg−1−320 mL) compared with placebo (−130 mL). No effect on disease progression,DLCO, infection rates or mortality was observed. SGRQ scores showed a nonsignificant trend toward worsening with active treatment. Unexpectedly, free CC-chemokine ligand 2 levels were elevated above baseline at both 24 and 52 weeks. A higher proportion of patients with one or more serious adverse events was observed in the 5 mg·kg−1group (53.1%) compared with 1 mg·kg−1(15.2%), 15 mg·kg−1(21.9%) and placebo (46.4%), although no unexpected serious adverse events were noted.Although dosing was stopped prematurely, it is unlikely that carlumab provides benefit to IPF patients.


2021 ◽  
Author(s):  
Sanja Stankovic ◽  
Mihailo Stjepanovic ◽  
Milika Asanin

Numerous published papers are investigating the utility of biomarkers in Idiopathic Pulmonary Fibrosis (IPF) diagnosis, treatment, and outcome prediction. This chapter will summarize our current knowledge about biomarkers associated with alveolar epithelial cell damage and dysfunction (Krebs von den Lungen, surfactant proteins, the mucin MUC5B, CA 15-3, CA 125, CA 19-9, defensins, Clara cell protein (CC16), telomere shortening), biomarkers associated with fibrogenesis, fibroproliferation and extracellular matrix (ECM) remodeling (MMPs and their inhibitors, osteopontin, periostin, insulin-like growth factors, fibulin-1, heat shock protein 47, lysyl oxidase-like 2, circulating fibroblasts, extracellular matrix neoepitopes) and biomarkers related to immune dysfunction and inflammation (C-C chemokine ligand-18, C-C chemokine 2, YKL-40, C-X-C motif chemokine 13, S100A4, S100A8/9, S100A12, autoantibodies to heat shock protein 72, toll-like receptor 3, soluble receptor for advanced glycosylated end products, endothelial damage (vascular endothelial growth factor, interleukin 8, endothelin 1). The future directions in incorporating IPF biomarkers into clinical practice will be reviewed.


2004 ◽  
Vol 173 (7) ◽  
pp. 4692-4698 ◽  
Author(s):  
John A. Belperio ◽  
Maria Dy ◽  
Lynne Murray ◽  
Marie D. Burdick ◽  
Ying Y. Xue ◽  
...  

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