User login
DIFFUSE LUNG DISEASE AND LUNG TRANSPLANT NETWORK
Interstitial Lung Disease Section
Interstitial lung diseases (ILDs) are a diverse group of relentlessly progressive fibroinflammatory disorders. Pharmacotherapy includes antifibrotics and immunosuppressants as foundational strategies to mitigate loss of lung function. There has been a growing interest in telomere length and its response to immunosuppression in the ILD community.
Telomeres are repetitive nucleotide sequences that “cap” chromosomes and protect against chromosomal shortening during cell replication. Genetic and environmental factors can lead to premature shortening of telomeres. Once a critical length is reached, the cell enters senescence. Short telomere length has been linked to rapid progression, worse outcomes, and poor response to immunosuppressants in idiopathic pulmonary fibrosis (IPF).
Data in patients with non-IPF ILD (which is arguably more difficult to diagnose and manage) were lacking until a recent retrospective cohort study of patients from five centers across the US demonstrated that immunosuppressant exposure in patients with age-adjusted telomere length <10th percentile was associated with a reduced 2-year transplant-free survival in fibrotic hypersensitivity pneumonitis and unclassifiable ILD subgroups.1 This study was underpowered to detect associations in the connective tissue disease-ILD group. Interestingly, authors noted that immunosuppressant exposure was not associated with lung function decline in the short telomere group, suggesting that worse outcomes may be attributable to unmasking extrapulmonary manifestations of short telomeres, such as bone marrow failure and impaired adaptive immunity. Studies like these are essential to guide decision-making in the age of personalized medicine and underscore the necessity for prospective studies to validate these findings.
References
1. Zhang D, Adegunsoye A, Oldham JM, et al. Telomere length and immunosuppression in non-idiopathic pulmonary fibrosis interstitial lung disease. Eur Respir J. 2023;62(5):2300441.
DIFFUSE LUNG DISEASE AND LUNG TRANSPLANT NETWORK
Interstitial Lung Disease Section
Interstitial lung diseases (ILDs) are a diverse group of relentlessly progressive fibroinflammatory disorders. Pharmacotherapy includes antifibrotics and immunosuppressants as foundational strategies to mitigate loss of lung function. There has been a growing interest in telomere length and its response to immunosuppression in the ILD community.
Telomeres are repetitive nucleotide sequences that “cap” chromosomes and protect against chromosomal shortening during cell replication. Genetic and environmental factors can lead to premature shortening of telomeres. Once a critical length is reached, the cell enters senescence. Short telomere length has been linked to rapid progression, worse outcomes, and poor response to immunosuppressants in idiopathic pulmonary fibrosis (IPF).
Data in patients with non-IPF ILD (which is arguably more difficult to diagnose and manage) were lacking until a recent retrospective cohort study of patients from five centers across the US demonstrated that immunosuppressant exposure in patients with age-adjusted telomere length <10th percentile was associated with a reduced 2-year transplant-free survival in fibrotic hypersensitivity pneumonitis and unclassifiable ILD subgroups.1 This study was underpowered to detect associations in the connective tissue disease-ILD group. Interestingly, authors noted that immunosuppressant exposure was not associated with lung function decline in the short telomere group, suggesting that worse outcomes may be attributable to unmasking extrapulmonary manifestations of short telomeres, such as bone marrow failure and impaired adaptive immunity. Studies like these are essential to guide decision-making in the age of personalized medicine and underscore the necessity for prospective studies to validate these findings.
References
1. Zhang D, Adegunsoye A, Oldham JM, et al. Telomere length and immunosuppression in non-idiopathic pulmonary fibrosis interstitial lung disease. Eur Respir J. 2023;62(5):2300441.
DIFFUSE LUNG DISEASE AND LUNG TRANSPLANT NETWORK
Interstitial Lung Disease Section
Interstitial lung diseases (ILDs) are a diverse group of relentlessly progressive fibroinflammatory disorders. Pharmacotherapy includes antifibrotics and immunosuppressants as foundational strategies to mitigate loss of lung function. There has been a growing interest in telomere length and its response to immunosuppression in the ILD community.
Telomeres are repetitive nucleotide sequences that “cap” chromosomes and protect against chromosomal shortening during cell replication. Genetic and environmental factors can lead to premature shortening of telomeres. Once a critical length is reached, the cell enters senescence. Short telomere length has been linked to rapid progression, worse outcomes, and poor response to immunosuppressants in idiopathic pulmonary fibrosis (IPF).
Data in patients with non-IPF ILD (which is arguably more difficult to diagnose and manage) were lacking until a recent retrospective cohort study of patients from five centers across the US demonstrated that immunosuppressant exposure in patients with age-adjusted telomere length <10th percentile was associated with a reduced 2-year transplant-free survival in fibrotic hypersensitivity pneumonitis and unclassifiable ILD subgroups.1 This study was underpowered to detect associations in the connective tissue disease-ILD group. Interestingly, authors noted that immunosuppressant exposure was not associated with lung function decline in the short telomere group, suggesting that worse outcomes may be attributable to unmasking extrapulmonary manifestations of short telomeres, such as bone marrow failure and impaired adaptive immunity. Studies like these are essential to guide decision-making in the age of personalized medicine and underscore the necessity for prospective studies to validate these findings.
References
1. Zhang D, Adegunsoye A, Oldham JM, et al. Telomere length and immunosuppression in non-idiopathic pulmonary fibrosis interstitial lung disease. Eur Respir J. 2023;62(5):2300441.
<!--$RCSfile: InCopy_agile.xsl,v $ $Revision: 1.35 $-->
<!--$RCSfile: drupal.xsl,v $ $Revision: 1.7 $-->
<root generator="drupal.xsl" gversion="1.7"> <header> <fileName>168401_web2</fileName> <TBEID>0C050D76.SIG</TBEID> <TBUniqueIdentifier>MD_0C050D76</TBUniqueIdentifier> <newsOrJournal>News</newsOrJournal> <publisherName>Frontline Medical Communications</publisherName> <storyname/> <articleType>1</articleType> <TBLocation>mkalaycio-user</TBLocation> <QCDate/> <firstPublished>20240702T102035</firstPublished> <LastPublished>20240702T102035</LastPublished> <pubStatus qcode="stat:"/> <embargoDate/> <killDate/> <CMSDate>20240702T102035</CMSDate> <articleSource/> <facebookInfo/> <meetingNumber/> <byline/> <bylineText/> <bylineFull/> <bylineTitleText/> <USOrGlobal/> <wireDocType/> <newsDocType/> <journalDocType/> <linkLabel/> <pageRange/> <citation/> <quizID/> <indexIssueDate/> <itemClass qcode="ninat:text"/> <provider qcode="provider:imng"> <name>IMNG Medical Media</name> <rightsInfo> <copyrightHolder> <name>Frontline Medical News</name> </copyrightHolder> <copyrightNotice>Copyright (c) 2015 Frontline Medical News, a Frontline Medical Communications Inc. company. All rights reserved. This material may not be published, broadcast, copied, or otherwise reproduced or distributed without the prior written permission of Frontline Medical Communications Inc.</copyrightNotice> </rightsInfo> </provider> <abstract/> <metaDescription>Short telomere length and immunosuppression: Updates in nonidiopathic pulmonary fibrosis interstitial lung disease</metaDescription> <articlePDF/> <teaserImage>301977</teaserImage> <title/> <deck/> <disclaimer/> <AuthorList/> <articleURL/> <doi/> <pubMedID/> <publishXMLStatus/> <publishXMLVersion>1</publishXMLVersion> <useEISSN>0</useEISSN> <urgency/> <pubPubdateYear/> <pubPubdateMonth/> <pubPubdateDay/> <pubVolume/> <pubNumber/> <wireChannels/> <primaryCMSID/> <CMSIDs/> <keywords/> <seeAlsos/> <publications_g> <publicationData> <publicationCode>chph</publicationCode> <pubIssueName/> <pubArticleType/> <pubTopics/> <pubCategories/> <pubSections/> </publicationData> </publications_g> <publications> <term canonical="true">6</term> </publications> <sections> <term canonical="true">39299</term> <term>52072</term> </sections> <topics> <term canonical="true">27442</term> </topics> <links> <link> <itemClass qcode="ninat:picture"/> <altRep contenttype="image/jpeg">images/24012a5f.jpg</altRep> <description role="drol:caption">Dr. Mamta Chhabria</description> <description role="drol:credit">CHEST</description> </link> <link> <itemClass qcode="ninat:picture"/> <altRep contenttype="image/jpeg">images/24012a60.jpg</altRep> <description role="drol:caption">Dr. Ryan D. Boente</description> <description role="drol:credit">CHEST</description> </link> </links> </header> <itemSet> <newsItem> <itemMeta> <itemRole>Main</itemRole> <itemClass>text</itemClass> <title/> <deck/> </itemMeta> <itemContent> <p> <strong>Short telomere length and immunosuppression: Updates in nonidiopathic pulmonary fibrosis interstitial lung disease</strong> </p> <h2>DIFFUSE LUNG DISEASE AND LUNG TRANSPLANT NETWORK</h2> <h3>Interstitial Lung Disease Section</h3> <p>By Mamta Chhabria, MD, Fellow-in-Training<br/><br/>Ryan D. Boente, MD, Member-at-Large<br/><br/></p> <p>Interstitial lung diseases (ILDs) are a diverse group of relentlessly progressive fibroinflammatory disorders. Pharmacotherapy includes antifibrotics and immunosuppressants as foundational strategies to mitigate loss of lung function. There has been a growing interest in telomere length and its response to immunosuppression in the ILD community.[[{"fid":"301977","view_mode":"medstat_image_flush_left","fields":{"format":"medstat_image_flush_left","field_file_image_alt_text[und][0][value]":"Dr. Mamta Chhabria","field_file_image_credit[und][0][value]":"CHEST","field_file_image_caption[und][0][value]":"Dr. Mamta Chhabria"},"type":"media","attributes":{"class":"media-element file-medstat_image_flush_left"}}]]</p> <p>Telomeres are repetitive nucleotide sequences that “cap” chromosomes and protect against chromosomal shortening during cell replication. Genetic and environmental factors can lead to premature shortening of telomeres. Once a critical length is reached, the cell enters senescence. Short telomere length has been linked to rapid progression, worse outcomes, and poor response to immunosuppressants in idiopathic pulmonary fibrosis (IPF). [[{"fid":"301978","view_mode":"medstat_image_flush_right","fields":{"format":"medstat_image_flush_right","field_file_image_alt_text[und][0][value]":"Dr. Ryan D. Boente","field_file_image_credit[und][0][value]":"CHEST","field_file_image_caption[und][0][value]":"Dr. Ryan D. Boente"},"type":"media","attributes":{"class":"media-element file-medstat_image_flush_right"}}]] <br/><br/>Data in patients with non-IPF ILD (which is arguably more difficult to diagnose and manage) were lacking until a recent retrospective cohort study of patients from five centers across the US demonstrated that immunosuppressant exposure in patients with age-adjusted telomere length <10th percentile was associated with a reduced 2-year transplant-free survival in fibrotic hypersensitivity pneumonitis and unclassifiable ILD subgroups.<sup>1</sup> This study was underpowered to detect associations in the connective tissue disease-ILD group. Interestingly, authors noted that immunosuppressant exposure was not associated with lung function decline in the short telomere group, suggesting that worse outcomes may be attributable to unmasking extrapulmonary manifestations of short telomeres, such as bone marrow failure and impaired adaptive immunity. Studies like these are essential to guide decision-making in the age of personalized medicine and underscore the necessity for prospective studies to validate these findings.<br/><br/><b>References</b><br/><br/>1. Zhang D, Adegunsoye A, Oldham JM, et al. Telomere length and immunosuppression in non-idiopathic pulmonary fibrosis interstitial lung disease. <em>Eur Respir J</em>. 2023;62(5):2300441.</p> </itemContent> </newsItem> </itemSet></root>
