Evaluation of damage in giant cell arteritis

Abstract Objectives To evaluate damage and variables associated with damage in GCA. Methods Patients with GCA enrolled in a prospective, multicentre, longitudinal study were included. Per-protocol assessments were made with the Vasculitis Damage Index and the Large-Vessel Vasculitis Index of Damage....

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Veröffentlicht in:Rheumatology (Oxford, England) England), 2018-02, Vol.57 (2), p.322-328
Hauptverfasser: Kermani, Tanaz A, Sreih, Antoine G, Cuthbertson, David, Carette, Simon, Hoffman, Gary S, Khalidi, Nader A, Koening, Curry L, Langford, Carol A, McAlear, Carol A, Monach, Paul A, Moreland, Larry, Pagnoux, Christian, Seo, Philip, Warrington, Kenneth J, Ytterberg, Steven R, Merkel, Peter A
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container_end_page 328
container_issue 2
container_start_page 322
container_title Rheumatology (Oxford, England)
container_volume 57
creator Kermani, Tanaz A
Sreih, Antoine G
Cuthbertson, David
Carette, Simon
Hoffman, Gary S
Khalidi, Nader A
Koening, Curry L
Langford, Carol A
McAlear, Carol A
Monach, Paul A
Moreland, Larry
Pagnoux, Christian
Seo, Philip
Warrington, Kenneth J
Ytterberg, Steven R
Merkel, Peter A
description Abstract Objectives To evaluate damage and variables associated with damage in GCA. Methods Patients with GCA enrolled in a prospective, multicentre, longitudinal study were included. Per-protocol assessments were made with the Vasculitis Damage Index and the Large-Vessel Vasculitis Index of Damage. Results The study included 204 patients: 156 women (76%), mean age at diagnosis 71.3 years (s.d. 8.3), mean follow-up of 3.5 years (s.d. 1.9). One or more damage item was present in 54% at baseline and 79% at the last follow-up on the Vasculitis Damage Index, and 60% at baseline and 82% at the last follow-up on the Large-Vessel Vasculitis Index of Damage. The most frequently observed damage items were large-artery complications (29% cohort) and ocular (22%). Among 117 patients with new damage, most new items were ocular (63 patients), cardiac/vascular (48) and musculoskeletal (34). Of these, treatment-associated items were frequently observed, including cataracts (46 patients), osteoporosis (22) and weight gain (22). Disease-associated new damage included ischaemic optic neuropathy (3 patients), limb claudication (13), arterial occlusions (10) and damage requiring vascular intervention (10). In univariate analysis, the risk of damage increased 22% for every additional year of disease duration [odds ratio (OR) 1.22 (95% CI 1.04, 1.45)]. In 94 patients enrolled within ⩽90 days of diagnosis of GCA, the risk of new damage at the last follow-up decreased 30% for each additional relapse [OR 0.70 (95% CI 0.51, 0.97)]. Conclusions Large-artery complications and ocular manifestations are the most commonly occurring items of damage in GCA. Most new damage is associated with treatment. These findings emphasize the cumulative burden of disease in GCA.
doi_str_mv 10.1093/rheumatology/kex397
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Methods Patients with GCA enrolled in a prospective, multicentre, longitudinal study were included. Per-protocol assessments were made with the Vasculitis Damage Index and the Large-Vessel Vasculitis Index of Damage. Results The study included 204 patients: 156 women (76%), mean age at diagnosis 71.3 years (s.d. 8.3), mean follow-up of 3.5 years (s.d. 1.9). One or more damage item was present in 54% at baseline and 79% at the last follow-up on the Vasculitis Damage Index, and 60% at baseline and 82% at the last follow-up on the Large-Vessel Vasculitis Index of Damage. The most frequently observed damage items were large-artery complications (29% cohort) and ocular (22%). Among 117 patients with new damage, most new items were ocular (63 patients), cardiac/vascular (48) and musculoskeletal (34). Of these, treatment-associated items were frequently observed, including cataracts (46 patients), osteoporosis (22) and weight gain (22). Disease-associated new damage included ischaemic optic neuropathy (3 patients), limb claudication (13), arterial occlusions (10) and damage requiring vascular intervention (10). In univariate analysis, the risk of damage increased 22% for every additional year of disease duration [odds ratio (OR) 1.22 (95% CI 1.04, 1.45)]. In 94 patients enrolled within ⩽90 days of diagnosis of GCA, the risk of new damage at the last follow-up decreased 30% for each additional relapse [OR 0.70 (95% CI 0.51, 0.97)]. Conclusions Large-artery complications and ocular manifestations are the most commonly occurring items of damage in GCA. Most new damage is associated with treatment. These findings emphasize the cumulative burden of disease in GCA.</description><identifier>ISSN: 1462-0324</identifier><identifier>EISSN: 1462-0332</identifier><identifier>DOI: 10.1093/rheumatology/kex397</identifier><identifier>PMID: 29112740</identifier><language>eng</language><publisher>England: Oxford University Press</publisher><subject>Aged ; Arteritis ; Autoimmune diseases ; Cardiovascular diseases ; Cataracts ; Clinical Science ; Diagnosis ; Eye Diseases - etiology ; Female ; Follow-Up Studies ; Giant Cell Arteritis - complications ; Giant Cell Arteritis - pathology ; Humans ; Intermittent Claudication - etiology ; Longitudinal Studies ; Male ; Middle Aged ; Odds Ratio ; Optic neuropathy ; Osteoporosis ; Prospective Studies ; Recurrence ; Risk Factors ; Severity of Illness Index ; Time Factors ; Vasculitis ; Vein &amp; artery diseases</subject><ispartof>Rheumatology (Oxford, England), 2018-02, Vol.57 (2), p.322-328</ispartof><rights>The Author 2017. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oup.com 2017</rights><rights>The Author 2017. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oup.com</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c538t-994d98f93b7d8d9bb4b0cfd82c136cd62e17469f65640911293e78ae4d156b0b3</citedby><cites>FETCH-LOGICAL-c538t-994d98f93b7d8d9bb4b0cfd82c136cd62e17469f65640911293e78ae4d156b0b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,1578,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29112740$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kermani, Tanaz A</creatorcontrib><creatorcontrib>Sreih, Antoine G</creatorcontrib><creatorcontrib>Cuthbertson, David</creatorcontrib><creatorcontrib>Carette, Simon</creatorcontrib><creatorcontrib>Hoffman, Gary S</creatorcontrib><creatorcontrib>Khalidi, Nader A</creatorcontrib><creatorcontrib>Koening, Curry L</creatorcontrib><creatorcontrib>Langford, Carol A</creatorcontrib><creatorcontrib>McAlear, Carol A</creatorcontrib><creatorcontrib>Monach, Paul A</creatorcontrib><creatorcontrib>Moreland, Larry</creatorcontrib><creatorcontrib>Pagnoux, Christian</creatorcontrib><creatorcontrib>Seo, Philip</creatorcontrib><creatorcontrib>Warrington, Kenneth J</creatorcontrib><creatorcontrib>Ytterberg, Steven R</creatorcontrib><creatorcontrib>Merkel, Peter A</creatorcontrib><creatorcontrib>Vasculitis Clinical Research Consortium</creatorcontrib><creatorcontrib>for the Vasculitis Clinical Research Consortium</creatorcontrib><title>Evaluation of damage in giant cell arteritis</title><title>Rheumatology (Oxford, England)</title><addtitle>Rheumatology (Oxford)</addtitle><description>Abstract Objectives To evaluate damage and variables associated with damage in GCA. Methods Patients with GCA enrolled in a prospective, multicentre, longitudinal study were included. Per-protocol assessments were made with the Vasculitis Damage Index and the Large-Vessel Vasculitis Index of Damage. Results The study included 204 patients: 156 women (76%), mean age at diagnosis 71.3 years (s.d. 8.3), mean follow-up of 3.5 years (s.d. 1.9). One or more damage item was present in 54% at baseline and 79% at the last follow-up on the Vasculitis Damage Index, and 60% at baseline and 82% at the last follow-up on the Large-Vessel Vasculitis Index of Damage. The most frequently observed damage items were large-artery complications (29% cohort) and ocular (22%). Among 117 patients with new damage, most new items were ocular (63 patients), cardiac/vascular (48) and musculoskeletal (34). Of these, treatment-associated items were frequently observed, including cataracts (46 patients), osteoporosis (22) and weight gain (22). Disease-associated new damage included ischaemic optic neuropathy (3 patients), limb claudication (13), arterial occlusions (10) and damage requiring vascular intervention (10). In univariate analysis, the risk of damage increased 22% for every additional year of disease duration [odds ratio (OR) 1.22 (95% CI 1.04, 1.45)]. In 94 patients enrolled within ⩽90 days of diagnosis of GCA, the risk of new damage at the last follow-up decreased 30% for each additional relapse [OR 0.70 (95% CI 0.51, 0.97)]. Conclusions Large-artery complications and ocular manifestations are the most commonly occurring items of damage in GCA. Most new damage is associated with treatment. These findings emphasize the cumulative burden of disease in GCA.</description><subject>Aged</subject><subject>Arteritis</subject><subject>Autoimmune diseases</subject><subject>Cardiovascular diseases</subject><subject>Cataracts</subject><subject>Clinical Science</subject><subject>Diagnosis</subject><subject>Eye Diseases - etiology</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Giant Cell Arteritis - complications</subject><subject>Giant Cell Arteritis - pathology</subject><subject>Humans</subject><subject>Intermittent Claudication - etiology</subject><subject>Longitudinal Studies</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Odds Ratio</subject><subject>Optic neuropathy</subject><subject>Osteoporosis</subject><subject>Prospective Studies</subject><subject>Recurrence</subject><subject>Risk Factors</subject><subject>Severity of Illness Index</subject><subject>Time Factors</subject><subject>Vasculitis</subject><subject>Vein &amp; artery diseases</subject><issn>1462-0324</issn><issn>1462-0332</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkV1LwzAUhoMobk5_gSAFb7xwWz6aNLkRZMwPELzR65A2aZfZNjNph_v3dnSO6ZUX4QTOc17Oe14ALhGcICjI1C9MW6nGla7YTD_MFxHJERiimOExJAQf7_84HoCzEJYQQooIPwUDLBDCSQyH4Ha-VmWrGuvqyOWRVpUqTGTrqLCqbqLMlGWkfGO8bWw4Bye5KoO52NUReH-Yv82exi-vj8-z-5dxRglvxkLEWvBckDTRXIs0jVOY5ZrjDBGWaYYNSmImckZZDLebCGISrkysEWUpTMkI3PW6qzatjM5M3XhVypW3lfIb6ZSVvzu1XcjCrSXlFCJIO4GbnYB3n60Jjaxs2HpRtXFtkEgwxGn3UIde_0GXrvV1Z09iAhmllMOko0hPZd6F4E2-XwZBuU1DHqYh-zS6qatDH_uZn_N3wKQHXLv6l-I3GUCaeA</recordid><startdate>20180201</startdate><enddate>20180201</enddate><creator>Kermani, Tanaz A</creator><creator>Sreih, Antoine G</creator><creator>Cuthbertson, David</creator><creator>Carette, Simon</creator><creator>Hoffman, Gary S</creator><creator>Khalidi, Nader A</creator><creator>Koening, Curry L</creator><creator>Langford, Carol A</creator><creator>McAlear, Carol A</creator><creator>Monach, Paul A</creator><creator>Moreland, Larry</creator><creator>Pagnoux, Christian</creator><creator>Seo, Philip</creator><creator>Warrington, Kenneth J</creator><creator>Ytterberg, Steven R</creator><creator>Merkel, Peter A</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20180201</creationdate><title>Evaluation of damage in giant cell arteritis</title><author>Kermani, Tanaz A ; Sreih, Antoine G ; Cuthbertson, David ; Carette, Simon ; Hoffman, Gary S ; Khalidi, Nader A ; Koening, Curry L ; Langford, Carol A ; McAlear, Carol A ; Monach, Paul A ; Moreland, Larry ; Pagnoux, Christian ; Seo, Philip ; Warrington, Kenneth J ; Ytterberg, Steven R ; Merkel, Peter A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c538t-994d98f93b7d8d9bb4b0cfd82c136cd62e17469f65640911293e78ae4d156b0b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Aged</topic><topic>Arteritis</topic><topic>Autoimmune diseases</topic><topic>Cardiovascular diseases</topic><topic>Cataracts</topic><topic>Clinical Science</topic><topic>Diagnosis</topic><topic>Eye Diseases - etiology</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Giant Cell Arteritis - complications</topic><topic>Giant Cell Arteritis - pathology</topic><topic>Humans</topic><topic>Intermittent Claudication - etiology</topic><topic>Longitudinal Studies</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Odds Ratio</topic><topic>Optic neuropathy</topic><topic>Osteoporosis</topic><topic>Prospective Studies</topic><topic>Recurrence</topic><topic>Risk Factors</topic><topic>Severity of Illness Index</topic><topic>Time Factors</topic><topic>Vasculitis</topic><topic>Vein &amp; artery diseases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kermani, Tanaz A</creatorcontrib><creatorcontrib>Sreih, Antoine G</creatorcontrib><creatorcontrib>Cuthbertson, David</creatorcontrib><creatorcontrib>Carette, Simon</creatorcontrib><creatorcontrib>Hoffman, Gary S</creatorcontrib><creatorcontrib>Khalidi, Nader A</creatorcontrib><creatorcontrib>Koening, Curry L</creatorcontrib><creatorcontrib>Langford, Carol A</creatorcontrib><creatorcontrib>McAlear, Carol A</creatorcontrib><creatorcontrib>Monach, Paul A</creatorcontrib><creatorcontrib>Moreland, Larry</creatorcontrib><creatorcontrib>Pagnoux, Christian</creatorcontrib><creatorcontrib>Seo, Philip</creatorcontrib><creatorcontrib>Warrington, Kenneth J</creatorcontrib><creatorcontrib>Ytterberg, Steven R</creatorcontrib><creatorcontrib>Merkel, Peter A</creatorcontrib><creatorcontrib>Vasculitis Clinical Research Consortium</creatorcontrib><creatorcontrib>for the Vasculitis Clinical Research Consortium</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Nursing &amp; Allied Health Premium</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Rheumatology (Oxford, England)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kermani, Tanaz A</au><au>Sreih, Antoine G</au><au>Cuthbertson, David</au><au>Carette, Simon</au><au>Hoffman, Gary S</au><au>Khalidi, Nader A</au><au>Koening, Curry L</au><au>Langford, Carol A</au><au>McAlear, Carol A</au><au>Monach, Paul A</au><au>Moreland, Larry</au><au>Pagnoux, Christian</au><au>Seo, Philip</au><au>Warrington, Kenneth J</au><au>Ytterberg, Steven R</au><au>Merkel, Peter A</au><aucorp>Vasculitis Clinical Research Consortium</aucorp><aucorp>for the Vasculitis Clinical Research Consortium</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Evaluation of damage in giant cell arteritis</atitle><jtitle>Rheumatology (Oxford, England)</jtitle><addtitle>Rheumatology (Oxford)</addtitle><date>2018-02-01</date><risdate>2018</risdate><volume>57</volume><issue>2</issue><spage>322</spage><epage>328</epage><pages>322-328</pages><issn>1462-0324</issn><eissn>1462-0332</eissn><abstract>Abstract Objectives To evaluate damage and variables associated with damage in GCA. Methods Patients with GCA enrolled in a prospective, multicentre, longitudinal study were included. Per-protocol assessments were made with the Vasculitis Damage Index and the Large-Vessel Vasculitis Index of Damage. Results The study included 204 patients: 156 women (76%), mean age at diagnosis 71.3 years (s.d. 8.3), mean follow-up of 3.5 years (s.d. 1.9). One or more damage item was present in 54% at baseline and 79% at the last follow-up on the Vasculitis Damage Index, and 60% at baseline and 82% at the last follow-up on the Large-Vessel Vasculitis Index of Damage. The most frequently observed damage items were large-artery complications (29% cohort) and ocular (22%). Among 117 patients with new damage, most new items were ocular (63 patients), cardiac/vascular (48) and musculoskeletal (34). Of these, treatment-associated items were frequently observed, including cataracts (46 patients), osteoporosis (22) and weight gain (22). Disease-associated new damage included ischaemic optic neuropathy (3 patients), limb claudication (13), arterial occlusions (10) and damage requiring vascular intervention (10). In univariate analysis, the risk of damage increased 22% for every additional year of disease duration [odds ratio (OR) 1.22 (95% CI 1.04, 1.45)]. In 94 patients enrolled within ⩽90 days of diagnosis of GCA, the risk of new damage at the last follow-up decreased 30% for each additional relapse [OR 0.70 (95% CI 0.51, 0.97)]. Conclusions Large-artery complications and ocular manifestations are the most commonly occurring items of damage in GCA. Most new damage is associated with treatment. These findings emphasize the cumulative burden of disease in GCA.</abstract><cop>England</cop><pub>Oxford University Press</pub><pmid>29112740</pmid><doi>10.1093/rheumatology/kex397</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record>
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source Oxford University Press Journals All Titles (1996-Current); MEDLINE; Alma/SFX Local Collection
subjects Aged
Arteritis
Autoimmune diseases
Cardiovascular diseases
Cataracts
Clinical Science
Diagnosis
Eye Diseases - etiology
Female
Follow-Up Studies
Giant Cell Arteritis - complications
Giant Cell Arteritis - pathology
Humans
Intermittent Claudication - etiology
Longitudinal Studies
Male
Middle Aged
Odds Ratio
Optic neuropathy
Osteoporosis
Prospective Studies
Recurrence
Risk Factors
Severity of Illness Index
Time Factors
Vasculitis
Vein & artery diseases
title Evaluation of damage in giant cell arteritis
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