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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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 |
format | Article |
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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><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 & 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 & 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 & 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 & Calcified Tissue Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & 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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