Increased bilirubin levels in de novo Parkinson's disease
Background and purpose Oxidative stress is a central pathogenic mechanism of Parkinson's disease (PD), and the heme oxygenase (HO) bilirubin pathway is one of the main mammalian antioxidative defences. Indeed, there is growing evidence of HO−bilirubin upregulation from early phases of PD. Our a...
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| Veröffentlicht in: | European journal of neurology 2015-06, Vol.22 (6), p.954-959 |
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| container_title | European journal of neurology |
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| creator | Moccia, M. Picillo, M. Erro, R. Longo, K. Amboni, M. Santangelo, G. Palladino, R. Allocca, R. Caporale, O. Triassi, M. Pellecchia, M. T. Barone, P. Vitale, C. |
| description | Background and purpose
Oxidative stress is a central pathogenic mechanism of Parkinson's disease (PD), and the heme oxygenase (HO) bilirubin pathway is one of the main mammalian antioxidative defences. Indeed, there is growing evidence of HO−bilirubin upregulation from early phases of PD. Our aim was to investigate bilirubin as a possible biomarker of PD diagnosis and progression.
Methods
A cross‐sectional case−control study was performed to evaluate differences in bilirubin levels between newly diagnosed, drug‐naïve PD subjects and controls. Afterwards, PD subjects were included in a 2‐year longitudinal study to evaluate disease progression in relation to baseline bilirubin levels.
Results
Seventy‐five de novo PD subjects were selected and matched with 75 controls by propensity score. Analysis of variance showed higher bilirubin levels in PD patients compared with controls (P |
| doi_str_mv | 10.1111/ene.12688 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1891868949</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3666169101</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4908-3c575b1d11aedf8e64e769577365f8ffaf51b263708ad9ef39ea81790a8cafd33</originalsourceid><addsrcrecordid>eNqF0U1LHDEYB_BQKmrVQ79AGeih9TCaZ_J-lGV9AVkLrngMmZknkO3sjE0cq9_ebNfdg1DMJc_h9_wh_xDyFegJ5HOKPZ5AJbX-RPaBS10CY_A5z0xAKYDCHvmS0oJSWqmK7pK9SihOmdL7xFz1TUSXsC3q0IU41qEvOnzCLhV5arHoh6eh-OXi79Cnof-Rijak1cIh2fGuS3j0dh-Qu_PpfHJZXt9cXE3OrsuGG6pL1gglamgBHLZeo-SopBFKMSm89t55AXUlmaLatQY9M-g0KEOdbpxvGTsgP9e5D3H4M2J6tMuQGuw61-MwJgvagJbacPMxlUpKoNRApt_f0cUwxj4_ZKWE5mA4z-p4rZo4pBTR24cYli6-WKB2Vb3N1dt_1Wf77S1xrJfYbuWm6wxO1-Bv6PDl_0l2OptuIsv1RkiP-LzdyH9hpWJK2PvZhb09r2YTNheWs1fkHpnx</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1675841944</pqid></control><display><type>article</type><title>Increased bilirubin levels in de novo Parkinson's disease</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Moccia, M. ; Picillo, M. ; Erro, R. ; Longo, K. ; Amboni, M. ; Santangelo, G. ; Palladino, R. ; Allocca, R. ; Caporale, O. ; Triassi, M. ; Pellecchia, M. T. ; Barone, P. ; Vitale, C.</creator><creatorcontrib>Moccia, M. ; Picillo, M. ; Erro, R. ; Longo, K. ; Amboni, M. ; Santangelo, G. ; Palladino, R. ; Allocca, R. ; Caporale, O. ; Triassi, M. ; Pellecchia, M. T. ; Barone, P. ; Vitale, C.</creatorcontrib><description>Background and purpose
Oxidative stress is a central pathogenic mechanism of Parkinson's disease (PD), and the heme oxygenase (HO) bilirubin pathway is one of the main mammalian antioxidative defences. Indeed, there is growing evidence of HO−bilirubin upregulation from early phases of PD. Our aim was to investigate bilirubin as a possible biomarker of PD diagnosis and progression.
Methods
A cross‐sectional case−control study was performed to evaluate differences in bilirubin levels between newly diagnosed, drug‐naïve PD subjects and controls. Afterwards, PD subjects were included in a 2‐year longitudinal study to evaluate disease progression in relation to baseline bilirubin levels.
Results
Seventy‐five de novo PD subjects were selected and matched with 75 controls by propensity score. Analysis of variance showed higher bilirubin levels in PD patients compared with controls (P < 0.001). Linear regression analysis failed to show a relationship between bilirubin and Unified Parkinson's Disease Rating Scale (UPDRS) part III (P = 0.283) at baseline evaluation. At 2‐year follow‐up, indirect relationships between bilirubin levels and UPDRS part III (P = 0.028) and between bilirubin levels and levodopa‐equivalent daily dosage (P = 0.012) were found.
Conclusions
Parkinson's disease subjects showed higher levels of bilirubin compared with controls. Bilirubin increase might be due to HO overexpression as a compensatory response to oxidative stress occurring from early stages of PD.</description><identifier>ISSN: 1351-5101</identifier><identifier>EISSN: 1468-1331</identifier><identifier>DOI: 10.1111/ene.12688</identifier><identifier>PMID: 25740378</identifier><identifier>CODEN: EJNEFL</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Aged ; bilirubin ; Bilirubin - blood ; biomarker ; Biomarkers - blood ; Case-Control Studies ; Cross-Sectional Studies ; diagnosis ; Disease Progression ; Female ; heme ; Humans ; Longitudinal Studies ; Male ; Middle Aged ; motor ; Parkinson ; Parkinson Disease - blood ; progression</subject><ispartof>European journal of neurology, 2015-06, Vol.22 (6), p.954-959</ispartof><rights>2015 EAN</rights><rights>2015 EAN.</rights><rights>European Journal of Neurology © 2015 European Academy of Neurology</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4908-3c575b1d11aedf8e64e769577365f8ffaf51b263708ad9ef39ea81790a8cafd33</citedby><cites>FETCH-LOGICAL-c4908-3c575b1d11aedf8e64e769577365f8ffaf51b263708ad9ef39ea81790a8cafd33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fene.12688$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fene.12688$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25740378$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Moccia, M.</creatorcontrib><creatorcontrib>Picillo, M.</creatorcontrib><creatorcontrib>Erro, R.</creatorcontrib><creatorcontrib>Longo, K.</creatorcontrib><creatorcontrib>Amboni, M.</creatorcontrib><creatorcontrib>Santangelo, G.</creatorcontrib><creatorcontrib>Palladino, R.</creatorcontrib><creatorcontrib>Allocca, R.</creatorcontrib><creatorcontrib>Caporale, O.</creatorcontrib><creatorcontrib>Triassi, M.</creatorcontrib><creatorcontrib>Pellecchia, M. T.</creatorcontrib><creatorcontrib>Barone, P.</creatorcontrib><creatorcontrib>Vitale, C.</creatorcontrib><title>Increased bilirubin levels in de novo Parkinson's disease</title><title>European journal of neurology</title><addtitle>Eur J Neurol</addtitle><description>Background and purpose
Oxidative stress is a central pathogenic mechanism of Parkinson's disease (PD), and the heme oxygenase (HO) bilirubin pathway is one of the main mammalian antioxidative defences. Indeed, there is growing evidence of HO−bilirubin upregulation from early phases of PD. Our aim was to investigate bilirubin as a possible biomarker of PD diagnosis and progression.
Methods
A cross‐sectional case−control study was performed to evaluate differences in bilirubin levels between newly diagnosed, drug‐naïve PD subjects and controls. Afterwards, PD subjects were included in a 2‐year longitudinal study to evaluate disease progression in relation to baseline bilirubin levels.
Results
Seventy‐five de novo PD subjects were selected and matched with 75 controls by propensity score. Analysis of variance showed higher bilirubin levels in PD patients compared with controls (P < 0.001). Linear regression analysis failed to show a relationship between bilirubin and Unified Parkinson's Disease Rating Scale (UPDRS) part III (P = 0.283) at baseline evaluation. At 2‐year follow‐up, indirect relationships between bilirubin levels and UPDRS part III (P = 0.028) and between bilirubin levels and levodopa‐equivalent daily dosage (P = 0.012) were found.
Conclusions
Parkinson's disease subjects showed higher levels of bilirubin compared with controls. Bilirubin increase might be due to HO overexpression as a compensatory response to oxidative stress occurring from early stages of PD.</description><subject>Aged</subject><subject>bilirubin</subject><subject>Bilirubin - blood</subject><subject>biomarker</subject><subject>Biomarkers - blood</subject><subject>Case-Control Studies</subject><subject>Cross-Sectional Studies</subject><subject>diagnosis</subject><subject>Disease Progression</subject><subject>Female</subject><subject>heme</subject><subject>Humans</subject><subject>Longitudinal Studies</subject><subject>Male</subject><subject>Middle Aged</subject><subject>motor</subject><subject>Parkinson</subject><subject>Parkinson Disease - blood</subject><subject>progression</subject><issn>1351-5101</issn><issn>1468-1331</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0U1LHDEYB_BQKmrVQ79AGeih9TCaZ_J-lGV9AVkLrngMmZknkO3sjE0cq9_ebNfdg1DMJc_h9_wh_xDyFegJ5HOKPZ5AJbX-RPaBS10CY_A5z0xAKYDCHvmS0oJSWqmK7pK9SihOmdL7xFz1TUSXsC3q0IU41qEvOnzCLhV5arHoh6eh-OXi79Cnof-Rijak1cIh2fGuS3j0dh-Qu_PpfHJZXt9cXE3OrsuGG6pL1gglamgBHLZeo-SopBFKMSm89t55AXUlmaLatQY9M-g0KEOdbpxvGTsgP9e5D3H4M2J6tMuQGuw61-MwJgvagJbacPMxlUpKoNRApt_f0cUwxj4_ZKWE5mA4z-p4rZo4pBTR24cYli6-WKB2Vb3N1dt_1Wf77S1xrJfYbuWm6wxO1-Bv6PDl_0l2OptuIsv1RkiP-LzdyH9hpWJK2PvZhb09r2YTNheWs1fkHpnx</recordid><startdate>201506</startdate><enddate>201506</enddate><creator>Moccia, M.</creator><creator>Picillo, M.</creator><creator>Erro, R.</creator><creator>Longo, K.</creator><creator>Amboni, M.</creator><creator>Santangelo, G.</creator><creator>Palladino, R.</creator><creator>Allocca, R.</creator><creator>Caporale, O.</creator><creator>Triassi, M.</creator><creator>Pellecchia, M. T.</creator><creator>Barone, P.</creator><creator>Vitale, C.</creator><general>Blackwell Publishing Ltd</general><general>John Wiley & Sons, Inc</general><scope>BSCLL</scope><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>7TK</scope><scope>7U7</scope><scope>C1K</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201506</creationdate><title>Increased bilirubin levels in de novo Parkinson's disease</title><author>Moccia, M. ; Picillo, M. ; Erro, R. ; Longo, K. ; Amboni, M. ; Santangelo, G. ; Palladino, R. ; Allocca, R. ; Caporale, O. ; Triassi, M. ; Pellecchia, M. T. ; Barone, P. ; Vitale, C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4908-3c575b1d11aedf8e64e769577365f8ffaf51b263708ad9ef39ea81790a8cafd33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Aged</topic><topic>bilirubin</topic><topic>Bilirubin - blood</topic><topic>biomarker</topic><topic>Biomarkers - blood</topic><topic>Case-Control Studies</topic><topic>Cross-Sectional Studies</topic><topic>diagnosis</topic><topic>Disease Progression</topic><topic>Female</topic><topic>heme</topic><topic>Humans</topic><topic>Longitudinal Studies</topic><topic>Male</topic><topic>Middle Aged</topic><topic>motor</topic><topic>Parkinson</topic><topic>Parkinson Disease - blood</topic><topic>progression</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Moccia, M.</creatorcontrib><creatorcontrib>Picillo, M.</creatorcontrib><creatorcontrib>Erro, R.</creatorcontrib><creatorcontrib>Longo, K.</creatorcontrib><creatorcontrib>Amboni, M.</creatorcontrib><creatorcontrib>Santangelo, G.</creatorcontrib><creatorcontrib>Palladino, R.</creatorcontrib><creatorcontrib>Allocca, R.</creatorcontrib><creatorcontrib>Caporale, O.</creatorcontrib><creatorcontrib>Triassi, M.</creatorcontrib><creatorcontrib>Pellecchia, M. T.</creatorcontrib><creatorcontrib>Barone, P.</creatorcontrib><creatorcontrib>Vitale, C.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Moccia, M.</au><au>Picillo, M.</au><au>Erro, R.</au><au>Longo, K.</au><au>Amboni, M.</au><au>Santangelo, G.</au><au>Palladino, R.</au><au>Allocca, R.</au><au>Caporale, O.</au><au>Triassi, M.</au><au>Pellecchia, M. T.</au><au>Barone, P.</au><au>Vitale, C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased bilirubin levels in de novo Parkinson's disease</atitle><jtitle>European journal of neurology</jtitle><addtitle>Eur J Neurol</addtitle><date>2015-06</date><risdate>2015</risdate><volume>22</volume><issue>6</issue><spage>954</spage><epage>959</epage><pages>954-959</pages><issn>1351-5101</issn><eissn>1468-1331</eissn><coden>EJNEFL</coden><abstract>Background and purpose
Oxidative stress is a central pathogenic mechanism of Parkinson's disease (PD), and the heme oxygenase (HO) bilirubin pathway is one of the main mammalian antioxidative defences. Indeed, there is growing evidence of HO−bilirubin upregulation from early phases of PD. Our aim was to investigate bilirubin as a possible biomarker of PD diagnosis and progression.
Methods
A cross‐sectional case−control study was performed to evaluate differences in bilirubin levels between newly diagnosed, drug‐naïve PD subjects and controls. Afterwards, PD subjects were included in a 2‐year longitudinal study to evaluate disease progression in relation to baseline bilirubin levels.
Results
Seventy‐five de novo PD subjects were selected and matched with 75 controls by propensity score. Analysis of variance showed higher bilirubin levels in PD patients compared with controls (P < 0.001). Linear regression analysis failed to show a relationship between bilirubin and Unified Parkinson's Disease Rating Scale (UPDRS) part III (P = 0.283) at baseline evaluation. At 2‐year follow‐up, indirect relationships between bilirubin levels and UPDRS part III (P = 0.028) and between bilirubin levels and levodopa‐equivalent daily dosage (P = 0.012) were found.
Conclusions
Parkinson's disease subjects showed higher levels of bilirubin compared with controls. Bilirubin increase might be due to HO overexpression as a compensatory response to oxidative stress occurring from early stages of PD.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>25740378</pmid><doi>10.1111/ene.12688</doi><tpages>6</tpages></addata></record> |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Aged bilirubin Bilirubin - blood biomarker Biomarkers - blood Case-Control Studies Cross-Sectional Studies diagnosis Disease Progression Female heme Humans Longitudinal Studies Male Middle Aged motor Parkinson Parkinson Disease - blood progression |
| title | Increased bilirubin levels in de novo Parkinson's disease |
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