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    <IdentifierDoi>10.3205/26rhk197</IdentifierDoi>
    <IdentifierUrn>urn:nbn:de:0183-26rhk1971</IdentifierUrn>
    <ArticleType>Meeting Abstract</ArticleType>
    <TitleGroup>
      <Title language="en">Arg16 &#946;<Subscript>2</Subscript>-adrenoceptor polymorphism: A genetic link to carotid intima-media-thickness in rheumatoid arthritis</Title>
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        <PersonNames>
          <Lastname>M&#246;bius</Lastname>
          <LastnameHeading>M&#246;bius</LastnameHeading>
          <Firstname>Amelie</Firstname>
          <Initials>A</Initials>
        </PersonNames>
        <Address>
          <Affiliation>Universit&#228;tsklinikum Leipzig (UKL) Klinik und Poliklinik f&#252;r Rheumatologie, Leipzig, Deutschland</Affiliation>
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        <Creatorrole corresponding="no" presenting="no">author</Creatorrole>
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      <Creator>
        <PersonNames>
          <Lastname>M&#252;hlberg</Lastname>
          <LastnameHeading>M&#252;hlberg</LastnameHeading>
          <Firstname>Katja</Firstname>
          <Initials>K</Initials>
        </PersonNames>
        <Address>
          <Affiliation>Universit&#228;tsklinikum Leipzig (UKL) Klinik und Poliklinik f&#252;r Angiologie, Leipzig, Deutschland</Affiliation>
        </Address>
        <Creatorrole corresponding="no" presenting="no">author</Creatorrole>
      </Creator>
      <Creator>
        <PersonNames>
          <Lastname>Seifert</Lastname>
          <LastnameHeading>Seifert</LastnameHeading>
          <Firstname>Olga</Firstname>
          <Initials>O</Initials>
        </PersonNames>
        <Address>
          <Affiliation>Universit&#228;tsklinikum Leipzig (UKL) Klinik und Poliklinik f&#252;r Rheumatologie, Leipzig, Deutschland</Affiliation>
        </Address>
        <Creatorrole corresponding="no" presenting="no">author</Creatorrole>
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      <Publisher>
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          <Corporatename>German Medical Science GMS Publishing House</Corporatename>
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        <Address>D&#252;sseldorf</Address>
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    <SubjectGroup>
      <SubjectheadingDDB>610</SubjectheadingDDB>
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      <DatePublished>20260909</DatePublished>
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    <Language>engl</Language>
    <License license-type="open-access" xlink:href="http://creativecommons.org/licenses/by/4.0/">
      <AltText language="en">This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License.</AltText>
      <AltText language="de">Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung).</AltText>
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      <Meeting>
        <MeetingId>M0656</MeetingId>
        <MeetingSequence>197</MeetingSequence>
        <MeetingCorporation>Deutsche Gesellschaft f&#252;r Rheumatologie</MeetingCorporation>
        <MeetingCorporation>Deutsche Gesellschaft f&#252;r Orthop&#228;dische Rheumatologie</MeetingCorporation>
        <MeetingCorporation>Gesellschaft f&#252;r Kinder- und Jugendrheumatologie</MeetingCorporation>
        <MeetingName>54. Kongress der Deutschen Gesellschaft f&#252;r Rheumatologie und Klinische Immunologie (DGRh), 36. Jahrestagung der Gesellschaft f&#252;r Kinder- und Jugendrheumatologie (GKJR), 40. Jahrestagung der Deutschen Gesellschaft f&#252;r Orthop&#228;dische Rheumatologie (DGORh)</MeetingName>
        <MeetingTitle>Deutscher Rheumatologiekongress 2026</MeetingTitle>
        <MeetingSession>Rheumatoide Arthritis</MeetingSession>
        <MeetingCity>Leipzig</MeetingCity>
        <MeetingDate>
          <DateFrom>20260909</DateFrom>
          <DateTo>20260912</DateTo>
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    <ArticleNo>RA.12</ArticleNo>
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      <MainHeadline>Text</MainHeadline><Pgraph><Mark1>Introduction: </Mark1>Increasing scientific evidence suggests that systemic inflammatory diseases play a central role in the development of arteriosclerosis <TextLink reference="1"></TextLink>. To better understand the pathogenesis, it is important to investigate which additional risk factors could contribute to atherosclerosis <TextLink reference="2"></TextLink>. In recent years, various candidate genes, genetic polymorphisms and susceptibility loci have been identified that are associated with atherosclerotic diseases <TextLink reference="3"></TextLink>. This study aimed to evaluate genetic and clinical predictors of carotid intima media thickness (cIMT) in patients with rheumatoid arthritis (RA).</Pgraph><Pgraph><Mark1>Methods: </Mark1>Out of a cohort of 133 RA patients, we studied typical arteriosclerosis risk factors (age, sex, body-mass-Index (BMI), lipid status, diabetes mellitus, and hypertension) as well as RA disease activity compared to 33 hand osteoarthritis (OA) patients. To evaluate arteriosclerosis, ultrasound examination of brain supplying arteries for determination of plaques was performed, as well as the assessment of cIMT. Genomic DNA of a subgroup of RA patients was extracted from EDTA blood leukocytes to analyse b2-adrenoceptor polymorphism (&#946;<Subscript>2</Subscript>AR-SNPs) at codon positions 16, 27 and 164 <TextLink reference="3"></TextLink>.</Pgraph><Pgraph><Mark1>Results: </Mark1>RA patients had a higher prevalence of plaques compare to the controls (34.6&#37; vs. 21.6&#37;). Moderate and high-grade stenosis was observed in 9&#37; RA patients versus 3&#37; OA patients. The mean cIMT was also higher in RA patients (0.992 &#177; 0.391 mm). Genetic analysis of a subgroup of RA patients revealed a moderate correlation between the Arg16 polymorphism of &#946;<Subscript>2</Subscript>AR and cIMT (Z &#61; &#8211;1.956, p &#61; 0.05). In multivariate regression analysis, age (&#946; &#61; 0.374, p &#61; 0.001) and disease activity (DAS28 &#62; 2,6; &#946; &#61; 0.311, p &#61; 0.007) were identified as independent predictors of increased cIMT in RA patients, while BMI, low-density lipoprotein, CRP, RF&#47;Anti-CCP, and radiological erosions showed no significant correlations.</Pgraph><Pgraph><Mark1>Conclusion: </Mark1>Both traditional atherosclerosis risk factors and RA disease activity may contribute to the development of atherosclerosis in RA patients. Additionally, the Arg16 polymorphism of the &#946;<Subscript>2</Subscript>AR was positively associated with cIMT functioning as surrogate of atherosclerotic changes in this patient group. Further studies are warranted to determine the role of genetic factors on arteriosclerosis.</Pgraph><Pgraph><Mark1>Disclosures: </Mark1>AM declares no conflicts of interest.</Pgraph></TextBlock>
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      <Reference refNo="1">
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