{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T18:52:21Z","timestamp":1791139941435,"version":"4.1.0"},"reference-count":48,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2015,1,30]]},"abstract":"<jats:sec xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Potent anti\u2010inflammatory rheumatoid arthritis (RA) treatments are associated with reduced cardiovascular risk as well as increases in low\u2010density lipoprotein (\n                      <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content>\n                      ) cholesterol. This apparent paradox may be explained by favorable changes in other lipid measurements. The objective of this study was to determine the longitudinal association between changes in inflammation with advanced lipoprotein measurements and high\u2010density lipoprotein (\n                      <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>\n                      ) cholesterol efflux capacity.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods and Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      We conducted this study in a longitudinal\n                      <jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content>\n                      cohort from a large academic center, including subjects with high\u2010sensitivity C\u2010reactive protein (hs\u2010\n                      <jats:styled-content style=\"fixed-case\">CRP<\/jats:styled-content>\n                      ) reduction \u226510\u00a0mg\/L at 2 time points 1\u00a0year apart. Subjects receiving statins during the study period or preceding 6\u00a0months were excluded. We compared total cholesterol,\n                      <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content>\n                      cholesterol, HDL cholesterol, apolipoprotein B, and apolipoprotein A1 levels and\n                      <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>\n                      cholesterol efflux capacity at baseline and 1\u2010year follow\u2010up by using the paired\n                      <jats:italic>t<\/jats:italic>\n                      test. We also assessed the correlations between reductions in hs\u2010\n                      <jats:styled-content style=\"fixed-case\">CRP<\/jats:styled-content>\n                      with percentage change in lipid parameters. We studied 90\n                      <jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content>\n                      subjects (mean age 57\u00a0years, 89% female), all of whom were receiving disease\u2010modifying antirheumatic drugs. We observed a 7.2% increase in\n                      <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content>\n                      cholesterol levels (\n                      <jats:italic>P<\/jats:italic>\n                      =0.02) and improvement in efflux capacity by 5.7% (\n                      <jats:italic>P<\/jats:italic>\n                      =0.002) between baseline and follow\u2010up, with a median hs\u2010\n                      <jats:styled-content style=\"fixed-case\">CRP<\/jats:styled-content>\n                      reduction of 23.5\u00a0mg\/L. We observed significant correlations between reductions in hs\u2010\n                      <jats:styled-content style=\"fixed-case\">CRP<\/jats:styled-content>\n                      with increases in apolipoprotein A1 (\n                      <jats:italic>r<\/jats:italic>\n                      =0.27,\n                      <jats:italic>P<\/jats:italic>\n                      =0.01) and\n                      <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>\n                      cholesterol efflux capacity (\n                      <jats:italic>r<\/jats:italic>\n                      =0.24,\n                      <jats:italic>P<\/jats:italic>\n                      =0.02).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Among\n                      <jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content>\n                      subjects experiencing reductions in hs\u2010\n                      <jats:styled-content style=\"fixed-case\">CRP<\/jats:styled-content>\n                      , we observed increased\n                      <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content>\n                      cholesterol levels and concomitant improvements in\n                      <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>\n                      cholesterol efflux capacity. These findings provide further insight into lipid modulation and the beneficial effect of reduction in inflammation on lipids in vivo.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.114.001588","type":"journal-article","created":{"date-parts":[[2015,1,31]],"date-time":"2015-01-31T02:45:13Z","timestamp":1422672313000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":119,"title":["The Association Between Reduction in Inflammation and Changes in Lipoprotein Levels and HDL Cholesterol Efflux Capacity in Rheumatoid Arthritis"],"prefix":"10.1161","volume":"4","author":[{"given":"Katherine P.","family":"Liao","sequence":"first","affiliation":[{"name":"Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin P.","family":"Playford","sequence":"additional","affiliation":[{"name":"NIH Heart, Blood and Lung Institute, Bethesda, MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michelle","family":"Frits","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jonathan S.","family":"Coblyn","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christine","family":"Iannaccone","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael E.","family":"Weinblatt","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nancy S.","family":"Shadick","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nehal N.","family":"Mehta","sequence":"additional","affiliation":[{"name":"NIH Heart, Blood and Lung Institute, Bethesda, 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