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Original Research: Diffuse Lung Disease |

CT Imaging Phenotypes of Pulmonary Fibrosis in the MUC5B Promoter Site Polymorphism

Jonathan H. Chung, MD; Anna L. Peljto, PhD; Ashish Chawla, MD; Janet L. Talbert, MS; David F. McKean, MS; Byung-Hak Rho, MD; Tasha E. Fingerlin, PhD; Marvin I. Schwarz, MD; David A. Schwartz, MD; David A. Lynch, MBBS
Author and Funding Information

Dr Chung is currently at The University of Chicago Medicine (Chicago, IL).

FUNDING/SUPPORT: This research was funded by R01 HL097163 (PI D. A. Schwartz), 1I01BX001534 (D. A. Schwartz), P01 HL092870 (PD D. A. Schwartz), and R01 HL095393 (PI D.A. Schwartz).

CORRESPONDENCE TO: Jonathan H. Chung, MD, Thoracic Radiology, The University of Chicago Medicine, 5841 S Maryland Ave, Chicago, IL 60637


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


Chest. 2016;149(5):1215-1222. doi:10.1016/j.chest.2015.11.009
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Background  To determine the effect of the MUC5B promoter polymorphism (rs35705950) on the CT imaging appearance of pulmonary fibrosis.

Methods  High-resolution CT scans of 1,764 subjects were scored as part of a, genomewide association study with institutional review board approval; 1,491 of these had pulmonary fibrosis on CT scans and were included in the study. Two thoracic radiologists independently scored CT scans systematically. Discrepancies were resolved by a third thoracic radiologist. All patients were genotyped specifically for the rs35705950 single-nucleotide polymorphism (SNP). Two-tailed Fisher exact or χ2 tests and Student t tests or Mann-Whitney U tests were used to compare proportions and means, respectively.

Results  The major and minor alleles at the rs35705950 SNP are guanine (G) and thymine (T), respectively: 514 were homozygous for the major allele (G group), and 977 were heterozygous or homozygous for the minor allele (T group). The G group had a higher proportion than the T group with ground-glass opacity (62.1% vs 54.2%; P = .04). There was no significant difference between the G and T groups regarding presence of honeycombing. The T group showed a significantly higher subpleural axial distribution of fibrosis than did the G group (62.3% vs 42.2%; P < .0001). The T group showed a lower proportion of diagnoses inconsistent with usual interstitial pneumonitis (UIP; 20.3% compared with 30.5% for the G group) and a greater proportion of confident (probable UIP and UIP) UIP diagnoses (43.8% compared with 32.6% for the G group).

Conclusions  The MUC5B promoter polymorphism identifies a pattern of fibrosis that is different from other causes of fibrosis and may respond differently to potential therapies.

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