Collagen biomarkers and subclinical interstitial lung disease: The Multi-Ethnic Study of Atherosclerosis.
Collagen biomarkers and subclinical interstitial lung disease: The Multi-Ethnic Study of Atherosclerosis.
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DOI：
10.1016/j.rmed.2018.06.001
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发表时间：
2018-07
影响因子：
4.3
通讯作者：
Lederer DJ
中科院分区：
文献类型：
--
作者：
Madahar P;Duprez DA;Podolanczuk AJ;Bernstein EJ;Kawut SM;Raghu G;Barr RG;Gross MD;Jacobs DR Jr;Lederer DJ
Lung fibrosis is attributed to derangements in extracellular matrix remodeling, a process driven by collagen turnover. We examined the association of two collagen biomarkers, carboxy-terminal telopeptide of collagen type I (ICTP) and amino-terminal propeptide of type III procollagen (PIIINP), with subclinical interstitial lung disease (ILD) in adults. We performed a cross-sectional analysis of 3244 participants age 45–84 years in the Multi-Ethnic Study of Atherosclerosis. Serum ICTP and PIIINP levels were measured at baseline by radioimmunoassay. Subclinical ILD was defined as high attenuation areas (HAA) in the lung fields on baseline cardiac CT scans. Interstitial lung abnormalities (ILA) were measured in 1082 full-lung CT scans at 9.5 years median follow-up. We used generalized linear models to examine the associations of collagen biomarkers with HAA and ILA. Median (IQR) for ICTP was 3.2 μg/L (2.6–3.9 μg/L) and for PIIINP was 5.3 μg/L (4.5–6.2 μg/L). In fully adjusted models, each SD increment in ICTP was associated with a 1.3% increment in HAA (95% CI 0.2–2.4%, p = 0.02) and each SD increment in PIIINP was associated with a 0.96% increment in HAA (95% CI 0.06–1.9%, p = 0.04). There was no association between ICTP or PIIINP and ILA. There was no evidence of effect modification by gender, race, smoking status or eGFR. Higher levels of collagen biomarkers are associated with greater HAA independent of gender, race and smoking status. This suggests that extracellular matrix remodeling may accompany subclinical ILD prior to the onset of clinically evident disease.
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影响因子：
30.8
作者：
Fingerlin, Tasha E.;Murphy, Elissa;Zhang, Weiming;Peljto, Anna L.;Brown, Kevin K.;Steele, Mark P.;Loyd, James E.;Cosgrove, Gregory P.;Lynch, David;Groshong, Steve;Collard, Harold R.;Wolters, Paul J.;Bradford, Williamson Z.;Kossen, Karl;Seiwert, Scott D.;du Bois, Roland M.;Garcia, Christine Kim;Devine, Megan S.;Gudmundsson, Gunnar;Isaksson, Helgi J.;Kaminski, Naftali;Zhang, Yingze;Gibson, Kevin F.;Lancaster, Lisa H.;Cogan, Joy D.;Mason, Wendi R.;Maher, Toby M.;Molyneaux, Philip L.;Wells, Athol U.;Moffatt, Miriam F.;Selman, Moises;Pardo, Annie;Kim, Dong Soon;Crapo, James D.;Make, Barry J.;Regan, Elizabeth A.;Walek, Dinesha S.;Daniel, Jerry J.;Kamatani, Yoichiro;Zelenika, Diana;Smith, Keith;McKean, David;Pedersen, Brent S.;Talbert, Janet;Kidd, Raven N.;Markin, Cheryl R.;Beckman, Kenneth B.;Lathrop, Mark;Schwarz, Marvin I.;Schwartz, David A.
通讯作者：
Schwartz, David A.
DOI：
10.1016/j.jchf.2014.03.013
发表时间：
2014-08
期刊：
JACC. Heart failure
影响因子：
--
作者：
Safdar Z;Tamez E;Chan W;Arya B;Ge Y;Deswal A;Bozkurt B;Frost A;Entman M
通讯作者：
Entman M
影响因子：
24
作者：
Chirinos, Julio A.;Kips, Jan G.;Jacobs, David R., Jr.;Brumback, Lyndia;Duprez, Daniel A.;Kronmal, Richard;Bluemke, David A.;Townsend, Raymond R.;Vermeersch, Sebastian;Segers, Patrick
通讯作者：
Segers, Patrick
DOI：
10.1056/nejmoa1007285
发表时间：
2011-03-10
期刊：
The New England journal of medicine
影响因子：
--
作者：
Washko GR;Hunninghake GM;Fernandez IE;Nishino M;Okajima Y;Yamashiro T;Ross JC;Estépar RS;Lynch DA;Brehm JM;Andriole KP;Diaz AA;Khorasani R;D'Aco K;Sciurba FC;Silverman EK;Hatabu H;Rosas IO;COPDGene Investigators
通讯作者：
COPDGene Investigators
影响因子：
6
作者：
Muench, Julia;Avanesov, Maxim;Patten, Monica
通讯作者：
Patten, Monica