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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Gout and the risk of Alzheimer’s disease: a population-based, BMI-matched cohort study</title><author><name sortKey="Lu, Na" sort="Lu, Na" uniqKey="Lu N" first="Na" last="Lu">Na Lu</name><affiliation><nlm:aff id="A1">Clinical Epidemiology Unit, Boston University School of Medicine, Boston, Massachusetts, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A2">Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA</nlm:aff></affiliation></author><author><name sortKey="Dubreuil, Maureen" sort="Dubreuil, Maureen" uniqKey="Dubreuil M" first="Maureen" last="Dubreuil">Maureen Dubreuil</name><affiliation><nlm:aff id="A1">Clinical Epidemiology Unit, Boston University School of Medicine, Boston, Massachusetts, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A3">Section of Rheumatology, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, USA</nlm:aff></affiliation></author><author><name sortKey="Zhang, Yuqing" sort="Zhang, Yuqing" uniqKey="Zhang Y" first="Yuqing" last="Zhang">Yuqing Zhang</name><affiliation><nlm:aff id="A1">Clinical Epidemiology Unit, Boston University School of Medicine, Boston, Massachusetts, USA</nlm:aff></affiliation></author><author><name sortKey="Neogi, Tuhina" sort="Neogi, Tuhina" uniqKey="Neogi T" first="Tuhina" last="Neogi">Tuhina Neogi</name><affiliation><nlm:aff id="A1">Clinical Epidemiology Unit, Boston University School of Medicine, Boston, Massachusetts, USA</nlm:aff></affiliation></author><author><name sortKey="Rai, Sharan K" sort="Rai, Sharan K" uniqKey="Rai S" first="Sharan K" last="Rai">Sharan K. Rai</name><affiliation><nlm:aff id="A4">Arthritis Research Centre of Canada, University of British Columbia, Vancouver, British Columbia, Canada</nlm:aff></affiliation></author><author><name sortKey="Ascherio, Alberto" sort="Ascherio, Alberto" uniqKey="Ascherio A" first="Alberto" last="Ascherio">Alberto Ascherio</name><affiliation><nlm:aff id="A5">Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA</nlm:aff></affiliation></author><author><name sortKey="Hernan, Miguel A" sort="Hernan, Miguel A" uniqKey="Hernan M" first="Miguel A" last="Hernán">Miguel A. Hernán</name><affiliation><nlm:aff id="A5">Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA</nlm:aff></affiliation></author><author><name sortKey="Choi, Hyon K" sort="Choi, Hyon K" uniqKey="Choi H" first="Hyon K" last="Choi">Hyon K. Choi</name><affiliation><nlm:aff id="A2">Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">25739830</idno><idno type="pmc">4560667</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4560667</idno><idno type="RBID">PMC:4560667</idno><idno type="doi">10.1136/annrheumdis-2014-206917</idno><date when="2015">2015</date><idno type="wicri:Area/Pmc/Corpus">000709</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000709</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Gout and the risk of Alzheimer’s disease: a population-based, BMI-matched cohort study</title><author><name sortKey="Lu, Na" sort="Lu, Na" uniqKey="Lu N" first="Na" last="Lu">Na Lu</name><affiliation><nlm:aff id="A1">Clinical Epidemiology Unit, Boston University School of Medicine, Boston, Massachusetts, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A2">Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA</nlm:aff></affiliation></author><author><name sortKey="Dubreuil, Maureen" sort="Dubreuil, Maureen" uniqKey="Dubreuil M" first="Maureen" last="Dubreuil">Maureen Dubreuil</name><affiliation><nlm:aff id="A1">Clinical Epidemiology Unit, Boston University School of Medicine, Boston, Massachusetts, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A3">Section of Rheumatology, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, USA</nlm:aff></affiliation></author><author><name sortKey="Zhang, Yuqing" sort="Zhang, Yuqing" uniqKey="Zhang Y" first="Yuqing" last="Zhang">Yuqing Zhang</name><affiliation><nlm:aff id="A1">Clinical Epidemiology Unit, Boston University School of Medicine, Boston, Massachusetts, USA</nlm:aff></affiliation></author><author><name sortKey="Neogi, Tuhina" sort="Neogi, Tuhina" uniqKey="Neogi T" first="Tuhina" last="Neogi">Tuhina Neogi</name><affiliation><nlm:aff id="A1">Clinical Epidemiology Unit, Boston University School of Medicine, Boston, Massachusetts, USA</nlm:aff></affiliation></author><author><name sortKey="Rai, Sharan K" sort="Rai, Sharan K" uniqKey="Rai S" first="Sharan K" last="Rai">Sharan K. Rai</name><affiliation><nlm:aff id="A4">Arthritis Research Centre of Canada, University of British Columbia, Vancouver, British Columbia, Canada</nlm:aff></affiliation></author><author><name sortKey="Ascherio, Alberto" sort="Ascherio, Alberto" uniqKey="Ascherio A" first="Alberto" last="Ascherio">Alberto Ascherio</name><affiliation><nlm:aff id="A5">Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA</nlm:aff></affiliation></author><author><name sortKey="Hernan, Miguel A" sort="Hernan, Miguel A" uniqKey="Hernan M" first="Miguel A" last="Hernán">Miguel A. Hernán</name><affiliation><nlm:aff id="A5">Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA</nlm:aff></affiliation></author><author><name sortKey="Choi, Hyon K" sort="Choi, Hyon K" uniqKey="Choi H" first="Hyon K" last="Choi">Hyon K. Choi</name><affiliation><nlm:aff id="A2">Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA</nlm:aff></affiliation></author></analytic><series><title level="j">Annals of the rheumatic diseases</title><idno type="ISSN">0003-4967</idno><idno type="eISSN">1468-2060</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec id="S1"><title>Objective</title><p id="P1">While gout is associated with cardiovascular (CV)-metabolic comorbidities and their sequelae, the antioxidant effects of uric acid may have neuroprotective benefits. We evaluated the potential impact of incident gout on the risk of developing Alzheimer’s disease (AD) in a general population context.</p></sec><sec id="S2"><title>Methods</title><p id="P2">We conducted an age-matched, sex-matched, entry-time-matched and body mass index (BMI)-matched cohort study using data from The Health Improvement Network, an electronic medical record database representative of the UK general population, from 1 January 1995 to 31 December 2013. Up to five non-gout individuals were matched to each case of incident gout by age, sex, year of enrolment and BMI. We compared incidence rates of AD between the gout and comparison cohorts, excluding individuals with prevalent gout or dementia at baseline. Multivariate hazard ratios (HRs) were calculated, while adjusting for smoking, alcohol use, physician visits, social deprivation index, comorbidities and medication use. We repeated the same analysis among patients with incident osteoarthritis (OA) as a negative control exposure.</p></sec><sec id="S3"><title>Results</title><p id="P3">We identified 309 new cases of AD among 59 224 patients with gout (29% female, mean age 65 years) and 1942 cases among 238 805 in the comparison cohort over a 5-year median follow up (1.0 vs 1.5 per 1000 person-years, respectively). Univariate (age-matched, sex-matched, entry-time-matched and BMI-matched) and multivariate HRs for AD among patients with gout were 0.71 (95% CI 0.62 to 0.80) and 0.76 (95% CI 0.66 to 0.87), respectively. The inverse association persisted among subgroups stratified by sex, age group (<75 and ≥75 years), social deprivation index and history of CV disease. The association between incident OA and the risk of incident AD was null.</p></sec><sec id="S4"><title>Conclusions</title><p id="P4">These findings provide the first general population-based evidence that gout is inversely associated with the risk of developing AD, supporting the purported potential neuroprotective role of uric acid.</p></sec></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">0372355</journal-id><journal-id journal-id-type="pubmed-jr-id">640</journal-id><journal-id journal-id-type="nlm-ta">Ann Rheum Dis</journal-id><journal-id journal-id-type="iso-abbrev">Ann. Rheum. Dis.</journal-id><journal-title-group><journal-title>Annals of the rheumatic diseases</journal-title></journal-title-group><issn pub-type="ppub">0003-4967</issn><issn pub-type="epub">1468-2060</issn></journal-meta><article-meta><article-id pub-id-type="pmid">25739830</article-id><article-id pub-id-type="pmc">4560667</article-id><article-id pub-id-type="doi">10.1136/annrheumdis-2014-206917</article-id><article-id pub-id-type="manuscript">NIHMS692972</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Gout and the risk of Alzheimer’s disease: a population-based, BMI-matched cohort study</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Lu</surname><given-names>Na</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Dubreuil</surname><given-names>Maureen</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A3">3</xref></contrib><contrib contrib-type="author"><name><surname>Zhang</surname><given-names>Yuqing</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Neogi</surname><given-names>Tuhina</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Rai</surname><given-names>Sharan K</given-names></name><xref ref-type="aff" rid="A4">4</xref></contrib><contrib contrib-type="author"><name><surname>Ascherio</surname><given-names>Alberto</given-names></name><xref ref-type="aff" rid="A5">5</xref></contrib><contrib contrib-type="author"><name><surname>Hernán</surname><given-names>Miguel A</given-names></name><xref ref-type="aff" rid="A5">5</xref></contrib><contrib contrib-type="author"><name><surname>Choi</surname><given-names>Hyon K</given-names></name><xref ref-type="aff" rid="A2">2</xref></contrib></contrib-group><aff id="A1"><label>1</label>Clinical Epidemiology Unit, Boston University School of Medicine, Boston, Massachusetts, USA</aff><aff id="A2"><label>2</label>Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA</aff><aff id="A3"><label>3</label>Section of Rheumatology, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, USA</aff><aff id="A4"><label>4</label>Arthritis Research Centre of Canada, University of British Columbia, Vancouver, British Columbia, Canada</aff><aff id="A5"><label>5</label>Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA</aff><author-notes><corresp id="FN1"><bold>Correspondence to</bold> Hyon K Choi, Division of Rheumatology, Allergy, and Immunology, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, Bulfinch 165, Boston, MA 02114, USA; <email>choi.hyon@mgh.harvard.edu</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>26</day><month>5</month><year>2015</year></pub-date><pub-date pub-type="epub"><day>04</day><month>3</month><year>2015</year></pub-date><pub-date pub-type="ppub"><month>3</month><year>2016</year></pub-date><pub-date pub-type="pmc-release"><day>01</day><month>3</month><year>2017</year></pub-date><volume>75</volume><issue>3</issue><fpage>547</fpage><lpage>551</lpage><pmc-comment>elocation-id from pubmed: 10.1136/annrheumdis-2014-206917</pmc-comment>
<abstract><sec id="S1"><title>Objective</title><p id="P1">While gout is associated with cardiovascular (CV)-metabolic comorbidities and their sequelae, the antioxidant effects of uric acid may have neuroprotective benefits. We evaluated the potential impact of incident gout on the risk of developing Alzheimer’s disease (AD) in a general population context.</p></sec><sec id="S2"><title>Methods</title><p id="P2">We conducted an age-matched, sex-matched, entry-time-matched and body mass index (BMI)-matched cohort study using data from The Health Improvement Network, an electronic medical record database representative of the UK general population, from 1 January 1995 to 31 December 2013. Up to five non-gout individuals were matched to each case of incident gout by age, sex, year of enrolment and BMI. We compared incidence rates of AD between the gout and comparison cohorts, excluding individuals with prevalent gout or dementia at baseline. Multivariate hazard ratios (HRs) were calculated, while adjusting for smoking, alcohol use, physician visits, social deprivation index, comorbidities and medication use. We repeated the same analysis among patients with incident osteoarthritis (OA) as a negative control exposure.</p></sec><sec id="S3"><title>Results</title><p id="P3">We identified 309 new cases of AD among 59 224 patients with gout (29% female, mean age 65 years) and 1942 cases among 238 805 in the comparison cohort over a 5-year median follow up (1.0 vs 1.5 per 1000 person-years, respectively). Univariate (age-matched, sex-matched, entry-time-matched and BMI-matched) and multivariate HRs for AD among patients with gout were 0.71 (95% CI 0.62 to 0.80) and 0.76 (95% CI 0.66 to 0.87), respectively. The inverse association persisted among subgroups stratified by sex, age group (<75 and ≥75 years), social deprivation index and history of CV disease. The association between incident OA and the risk of incident AD was null.</p></sec><sec id="S4"><title>Conclusions</title><p id="P4">These findings provide the first general population-based evidence that gout is inversely associated with the risk of developing AD, supporting the purported potential neuroprotective role of uric acid.</p></sec></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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