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( Bo Hyung Kang ),( Joyce S Lee ),( Brett M Elicker ),( Thomas Urbania ),( Jay H Ryu ),( Talmadge E King ),( Harold R Collard ),( Dong Soon Kim ) 대한결핵 및 호흡기학회 2012 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.114 No.-
Introduction: Definite usual interstitial pneumonia (UIP) pattern on high-resolution computed tomography (HRCT) is very specific, but not sensitive, for UIP pattern on surgical lung biopsy in patients suspected of having idiopathic pulmonary fibrosis (IPF). We investigated whether definite UIP pattern on HRCT was specific for UIP pattern on histopathology in patients with rheumatoid arthritis associated interstitial lung disease (RA-ILD). Methods: Two radiologists reviewed HRCT scans patients with biopsy proven RA-ILD. The radiologists categorized the HRCT scans as definite, possible or inconsistent with UIP pattern using the ATS/ERS/JRS/ALAT criteria. We also determined the sensitivity and specificity of definite UIP pattern on HRCT to UIP pattern onhistopathology. Results: There were 69 patients with RA-ILD included in this study and were collected from 3 tertiary care centers: University of California San Francisco, Mayo Clinic, and Asan Medical Center. The frequency of histopathologic UIP pattern in this cohort was 61%. Men were more likely than women to have a UIP pattern on histopathology (p 0.02). The agreement between the 2 radiologists for definite UIP pattern was 87% (kappa 0.67, p value <0.0001). The specificity of UIP pattern on HRCT for histopathologic UIP pattern was 96% (95% CI 81%-100%), with a positive predictive value of 95%. The sensitivity of UIP pattern on HRCT for histopathologic UIP pattern was 45% (95% CI 30%-61%), with a negative predictive value of 53%. Conclusion: Definite UIP pattern on HRCT in patients with RA-ILD is highly specific, but not sensitive, to UIP pattern on histopathology. This is consistent with the literature in IPF.
Acute exacerbation of idiopathic pulmonary fibrosis associated with air pollution exposure
Johannson, Kerri A.,Vittinghoff, Eric,Lee, Kiyoung,Balmes, John R.,Ji, Wonjun,Kaplan, Gilaad G.,Kim, Dong Soon,Collard, Harold R. ERS Journals Ltd 2014 The European respiratory journal Vol.43 No.4
<P>Acute exacerbations of idiopathic pulmonary fibrosis are associated with high mortality and are of unknown cause. The effect of air pollution on exacerbations of interstitial lung disease is unknown. This study aims to define the association of air pollution exposure with acute exacerbation of idiopathic pulmonary fibrosis.</P><P>Patients with idiopathic pulmonary fibrosis and corresponding air pollution data were identified from a longitudinal cohort. Air pollution exposures were assigned to each patient for ozone, nitrogen dioxide, particulate matter, sulfur dioxide and carbon monoxide based on geo-coded residential addresses. Cox proportional hazards models were used to estimate the association of air pollution exposures and acute exacerbations.</P><P>Acute exacerbation was significantly associated with antecedent 6-week increases in mean level, maximum level and number of exceedances above accepted standards of ozone (hazard ratio (HR) 1.57, 95% CI 1.09–2.24; HR 1.42, 95% CI 1.11–1.82; and HR 1.51, 95% CI 1.17–1.94, respectively) and nitrogen dioxide (HR 1.41, 95% CI 1.04–1.91; HR 1.27, 95% CI 1.01–1.59; and HR 1.20, 95% CI 1.10–1.31, respectively).</P><P>Increased ozone and nitrogen dioxide exposure over the preceding 6 weeks was associated with an increased risk of acute exacerbation of idiopathic pulmonary fibrosis, suggesting that air pollution may contribute to the development of this clinically meaningful event.</P>
( Eun Kyung Kim ),( Seung Ick Cha ),( Aaron V Schroeder ),( Jasleen Kukreja ),( Kirk D Jones ),( Jeffrey A Golden ),( Michael A Matthay ),( David J Erle ),( Harold R Collard ),( Paul J Wolters ) 대한결핵 및 호흡기학회 2012 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.114 No.-
Background: The prevalence of idiopathic pulmonary fibrosis (IPF) increases with age. Recent reports have demonstrated that mutations in TERT or TERC and short telomeres are risk factors for the development of IPF. Because short telomeres induce cellular senescence, these findings suggest senescence may occur in IPF lung. Methods: To evaluate for cellular senescence, we compared microRNA (miRNA) expression by miRNA arrays in type II epi-thelial cells. Senescence-associated β-galactosidase staining and immunohistochemical detection of p16, p21 and p53 were examined in sections of lung obtained from IPF patients and normal controls. Results: Expression of miR34-a, -b, and -c, which reportedly induce senescence in human epithelial cells are increased in IPF type II epithelial cells. β-Galactosidase activity is detectable on type II epithelial cells of IPF, but not normal lung. p16, p21 and p53 were detectable by immunostaining in IPF epithelial cells. Conclusions: IPF epithelial cells express several markers of senescence. These results suggest that the senescence of alveolar epithelial cells is accelerated in patients with IPF and may play a role in the pathogenesis of IPF.