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Original Research: Diffuse Lung Disease |

High Level of Chemokine CCL18 Is Associated With Pulmonary Function Deterioration, Lung Fibrosis Progression, and Reduced Survival in Systemic Sclerosis

Anna-Maria Hoffmann-Vold, MD, PhD; Anders Heiervang Tennøe, MD; Torhild Garen; Øyvind Midtvedt, MD; Aurelija Abraityte; Trond Mogens Aaløkken, MD, PhD; May Britt Lund, MD, PhD; Cathrine Brunborg; Pål Aukrust, MD, Prof; Thor Ueland, MD, Prof; Øyvind Molberg, MD, Prof
Author and Funding Information

Drs Hoffmann-Vold and Tennøe contributed equally to this manuscript.

FUNDING/SUPPORT: This work was supported by grants from the Norwegian Women’s Public Health Association and the Norwegian Rheumatology Foundation.

aDepartment of Rheumatology, Oslo University Hospital, Oslo, Norway

bResearch Institute for Internal Medicine, Oslo University Hospital, Oslo, Norway

cDepartment of Radiology and Nuclear Medicine, Oslo University Hospital, Oslo, Norway

dDepartment of Respiratory Medicine, Oslo University Hospital, Oslo, Norway

eOslo Centre for Biostatistics and Epidemiology, Research Support Services, Oslo University Hospital, Oslo, Norway

fInstitute of Clinical Medicine, University of Oslo, Oslo, Norway

CORRESPONDENCE TO: Anna-Maria Hoffmann-Vold, MD, PhD, Oslo University Hospital—Rikshospitalet, Pb 4950 Nydalen, 0424 Oslo, Norway


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;150(2):299-306. doi:10.1016/j.chest.2016.03.004
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Objective  Markers for early identification of progressive interstitial lung disease (ILD) in systemic sclerosis (SSc) are in demand. Chemokine CCL18, which has been linked to pulmonary inflammation, is an interesting candidate, but data have not been consistent. We aimed to assess CCL18 levels in a large, prospective, unselected SSc cohort with longitudinal, paired data sets on pulmonary function and lung fibrosis.

Methods  Sera from the Oslo University Hospital SSc cohort (n = 298) and healthy control subjects (n = 100) were analyzed for CCL18 by enzyme immunoassay. High CCL18 (>53 ng/mL) was defined using the mean value plus 2 SD in sera obtained from healthy control subjects as the cutoff.

Results  High serum CCL18 was identified in 35% (105 of 298). Annual decline in FVC differed significantly between high and low CCL18 subsets (13.3% and 4.7%; P = .016), as did the annual progression rate of lung fibrosis (0.9% [SD, 2.9] and 0.2% [SD, 1.9]). Highest rates of annual FVC decline > 10% (21%) and annual fibrosis progression (1.2%) were seen in patients with high CCL18 and early disease (< 3 years). In multivariate analyses, CCL18 was associated with annual FVC decline > 10% (OR, 1.1; 95% CI, 1.01-1.11) and FVC < 70% at follow-up (OR, 3.1; 95% CI, 1.08-8.83). Survival analyses showed that patients with high CCL18 had reduced 5- and 10-year cumulative survival compared with patients with low CCL18 (85% and 74%, compared with 97% and 89%, respectively; P = .001).

Conclusions  The results from this prospective cohort reinforce the notion that high CCL18 may serve as a marker for early identification of progressive ILD in SSc.

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