Anti-tumor necrosis factor-α therapy and changes of flow-mediated vasodilatation in psoriatic and rheumatoid arthritis patients.
Identifieur interne : 000345 ( PubMed/Corpus ); précédent : 000344; suivant : 000346Anti-tumor necrosis factor-α therapy and changes of flow-mediated vasodilatation in psoriatic and rheumatoid arthritis patients.
Auteurs : Gianluigi Mazzoccoli ; Incoronata Notarsanto ; Gennaro Davide De Pinto ; Mariangela Pia Dagostino ; Angelo De Cata ; Giuseppe D'Alessandro ; Roberto Tarquini ; Gianluigi VendemialeSource :
- Internal and emergency medicine ; 2010.
English descriptors
- KwdEn :
- Antibodies, Monoclonal (therapeutic use), Arthritis, Rheumatoid (drug therapy), Brachial Artery (physiology), Brachial Artery (ultrasonography), Etanercept, Female, Humans, Immunoglobulin G (therapeutic use), Immunosuppressive Agents (therapeutic use), Infliximab, Male, Middle Aged, Psoriasis (drug therapy), Receptors, Tumor Necrosis Factor (therapeutic use), Regional Blood Flow (drug effects), Regional Blood Flow (physiology), Tumor Necrosis Factor-alpha (antagonists & inhibitors), Vasodilation (drug effects).
- MESH :
- chemical , antagonists & inhibitors : Tumor Necrosis Factor-alpha.
- chemical , therapeutic use : Antibodies, Monoclonal, Immunoglobulin G, Immunosuppressive Agents, Receptors, Tumor Necrosis Factor.
- drug effects : Regional Blood Flow, Vasodilation.
- drug therapy : Arthritis, Rheumatoid, Psoriasis.
- physiology : Brachial Artery, Regional Blood Flow.
- ultrasonography : Brachial Artery.
- chemical : Etanercept, Female, Humans, Infliximab, Male, Middle Aged.
Abstract
For a long time, the endothelial covering of the vessels has been considered an inert surface. On the contrary, the endothelial cells are active and dynamic elements in the interaction between blood and tissues. The control of the vessel basal tone is obtained by the complex balance between the relaxing and contracting endothelial factors. Previous clinical studies show that patients suffering from rheumatoid arthritis and other autoimmune rheumatologic pathologies are at high risk of death being prematurely affected by atherosclerosis and cardiovascular diseases. Blocking tumor necrosis factor (TNF)-α by biological drugs improves the endothelial function. The aim of our study was to evaluate the effects of two anti-TNF-α drugs (infliximab and etanercept) on the endothelial function by evaluating the flow-mediated dilatation (FMD), which was measured in the brachial artery before and after treatment and after 8-12 weeks. We enrolled 36 patients (average age 52 ± 9.8 years, 12 men and 24 women), 25 of them were affected by rheumatoid arthritis (RA) and 11 were affected by psoriatic arthritis (PsA) and they were divided into three groups: 10 patients were treated with etanercept, 13 patients were treated with infliximab, 13 patients were treated with DMARDs. We measured the common carotid intimal-medial thickness (ccIMT) and the endothelial function was evaluated by FMD measurement in the brachial artery, before treatment, 1 h after the beginning of treatment and after 8-12 weeks. No statistically significant difference between the three groups was found for the ultrasonographic evaluation of the carotid IMT. On the contrary, the differences between FMD values before and after the treatment in the patients treated with etanercept (13.1 ± 0.01 vs. 18.8 ± 0.01%, p < 0.01) and in the patients treated with infliximab (11.8 ± 0.09 vs. 16.7 ± 0.09%, p < 0.01) were statistically significant. Long-term evaluation for infliximab and etanercept was performed by comparing the FMD values, respectively, 8 and 12 weeks after the first treatment. After 8 weeks, FMD value was similar to the value recorded at enrollment in the infliximab group (11.9 ± 0.03 vs. 13.54 ± 0.04%, p = 0.236) and the FMD values in the etanercept group after 12 weeks showed a not statistically significant reduction of vasodilatating effect (13.01 ± 0.03 vs. 15.67 ± 0.02%, p = 0.197). In conclusion, the use of biological drugs in patients affected by autoimmune arthritis can modify the endothelial function, as indicated by the induced FMD changes, but the long-term effect tends to be considerably reduced.
DOI: 10.1007/s11739-010-0458-6
PubMed: 20845087
Links to Exploration step
pubmed:20845087Le document en format XML
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Giovanni Rotondo (FG), Italy. g.mazzoccoli@tin.it</nlm:affiliation></affiliation></author><author><name sortKey="Notarsanto, Incoronata" sort="Notarsanto, Incoronata" uniqKey="Notarsanto I" first="Incoronata" last="Notarsanto">Incoronata Notarsanto</name></author><author><name sortKey="De Pinto, Gennaro Davide" sort="De Pinto, Gennaro Davide" uniqKey="De Pinto G" first="Gennaro Davide" last="De Pinto">Gennaro Davide De Pinto</name></author><author><name sortKey="Dagostino, Mariangela Pia" sort="Dagostino, Mariangela Pia" uniqKey="Dagostino M" first="Mariangela Pia" last="Dagostino">Mariangela Pia Dagostino</name></author><author><name sortKey="De Cata, Angelo" sort="De Cata, Angelo" uniqKey="De Cata A" first="Angelo" last="De Cata">Angelo De Cata</name></author><author><name sortKey="D Alessandro, Giuseppe" sort="D Alessandro, Giuseppe" uniqKey="D Alessandro G" first="Giuseppe" last="D'Alessandro">Giuseppe D'Alessandro</name></author><author><name sortKey="Tarquini, Roberto" sort="Tarquini, Roberto" uniqKey="Tarquini R" first="Roberto" last="Tarquini">Roberto Tarquini</name></author><author><name sortKey="Vendemiale, Gianluigi" sort="Vendemiale, Gianluigi" uniqKey="Vendemiale G" first="Gianluigi" last="Vendemiale">Gianluigi Vendemiale</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2010">2010</date><idno type="doi">10.1007/s11739-010-0458-6</idno><idno type="RBID">pubmed:20845087</idno><idno type="pmid">20845087</idno><idno type="wicri:Area/PubMed/Corpus">000345</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Anti-tumor necrosis factor-α therapy and changes of flow-mediated vasodilatation in psoriatic and rheumatoid arthritis patients.</title><author><name sortKey="Mazzoccoli, Gianluigi" sort="Mazzoccoli, Gianluigi" uniqKey="Mazzoccoli G" first="Gianluigi" last="Mazzoccoli">Gianluigi Mazzoccoli</name><affiliation><nlm:affiliation>Department of Internal Medicine, Scientific Institute and Regional General Hospital Casa Sollievo della Sofferenza, Opera di Padre Pio da Pietrelcina, Cappuccini Avenue, 71013 S. Giovanni Rotondo (FG), Italy. g.mazzoccoli@tin.it</nlm:affiliation></affiliation></author><author><name sortKey="Notarsanto, Incoronata" sort="Notarsanto, Incoronata" uniqKey="Notarsanto I" first="Incoronata" last="Notarsanto">Incoronata Notarsanto</name></author><author><name sortKey="De Pinto, Gennaro Davide" sort="De Pinto, Gennaro Davide" uniqKey="De Pinto G" first="Gennaro Davide" last="De Pinto">Gennaro Davide De Pinto</name></author><author><name sortKey="Dagostino, Mariangela Pia" sort="Dagostino, Mariangela Pia" uniqKey="Dagostino M" first="Mariangela Pia" last="Dagostino">Mariangela Pia Dagostino</name></author><author><name sortKey="De Cata, Angelo" sort="De Cata, Angelo" uniqKey="De Cata A" first="Angelo" last="De Cata">Angelo De Cata</name></author><author><name sortKey="D Alessandro, Giuseppe" sort="D Alessandro, Giuseppe" uniqKey="D Alessandro G" first="Giuseppe" last="D'Alessandro">Giuseppe D'Alessandro</name></author><author><name sortKey="Tarquini, Roberto" sort="Tarquini, Roberto" uniqKey="Tarquini R" first="Roberto" last="Tarquini">Roberto Tarquini</name></author><author><name sortKey="Vendemiale, Gianluigi" sort="Vendemiale, Gianluigi" uniqKey="Vendemiale G" first="Gianluigi" last="Vendemiale">Gianluigi Vendemiale</name></author></analytic><series><title level="j">Internal and emergency medicine</title><idno type="e-ISSN">1970-9366</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antibodies, Monoclonal (therapeutic use)</term><term>Arthritis, Rheumatoid (drug therapy)</term><term>Brachial Artery (physiology)</term><term>Brachial Artery (ultrasonography)</term><term>Etanercept</term><term>Female</term><term>Humans</term><term>Immunoglobulin G (therapeutic use)</term><term>Immunosuppressive Agents (therapeutic use)</term><term>Infliximab</term><term>Male</term><term>Middle Aged</term><term>Psoriasis (drug therapy)</term><term>Receptors, Tumor Necrosis Factor (therapeutic use)</term><term>Regional Blood Flow (drug effects)</term><term>Regional Blood Flow (physiology)</term><term>Tumor Necrosis Factor-alpha (antagonists & inhibitors)</term><term>Vasodilation (drug effects)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Tumor Necrosis Factor-alpha</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antibodies, Monoclonal</term><term>Immunoglobulin G</term><term>Immunosuppressive Agents</term><term>Receptors, Tumor Necrosis Factor</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Regional Blood Flow</term><term>Vasodilation</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Arthritis, Rheumatoid</term><term>Psoriasis</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Brachial Artery</term><term>Regional Blood Flow</term></keywords><keywords scheme="MESH" qualifier="ultrasonography" xml:lang="en"><term>Brachial Artery</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Etanercept</term><term>Female</term><term>Humans</term><term>Infliximab</term><term>Male</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">For a long time, the endothelial covering of the vessels has been considered an inert surface. On the contrary, the endothelial cells are active and dynamic elements in the interaction between blood and tissues. The control of the vessel basal tone is obtained by the complex balance between the relaxing and contracting endothelial factors. Previous clinical studies show that patients suffering from rheumatoid arthritis and other autoimmune rheumatologic pathologies are at high risk of death being prematurely affected by atherosclerosis and cardiovascular diseases. Blocking tumor necrosis factor (TNF)-α by biological drugs improves the endothelial function. The aim of our study was to evaluate the effects of two anti-TNF-α drugs (infliximab and etanercept) on the endothelial function by evaluating the flow-mediated dilatation (FMD), which was measured in the brachial artery before and after treatment and after 8-12 weeks. We enrolled 36 patients (average age 52 ± 9.8 years, 12 men and 24 women), 25 of them were affected by rheumatoid arthritis (RA) and 11 were affected by psoriatic arthritis (PsA) and they were divided into three groups: 10 patients were treated with etanercept, 13 patients were treated with infliximab, 13 patients were treated with DMARDs. We measured the common carotid intimal-medial thickness (ccIMT) and the endothelial function was evaluated by FMD measurement in the brachial artery, before treatment, 1 h after the beginning of treatment and after 8-12 weeks. No statistically significant difference between the three groups was found for the ultrasonographic evaluation of the carotid IMT. On the contrary, the differences between FMD values before and after the treatment in the patients treated with etanercept (13.1 ± 0.01 vs. 18.8 ± 0.01%, p < 0.01) and in the patients treated with infliximab (11.8 ± 0.09 vs. 16.7 ± 0.09%, p < 0.01) were statistically significant. Long-term evaluation for infliximab and etanercept was performed by comparing the FMD values, respectively, 8 and 12 weeks after the first treatment. After 8 weeks, FMD value was similar to the value recorded at enrollment in the infliximab group (11.9 ± 0.03 vs. 13.54 ± 0.04%, p = 0.236) and the FMD values in the etanercept group after 12 weeks showed a not statistically significant reduction of vasodilatating effect (13.01 ± 0.03 vs. 15.67 ± 0.02%, p = 0.197). In conclusion, the use of biological drugs in patients affected by autoimmune arthritis can modify the endothelial function, as indicated by the induced FMD changes, but the long-term effect tends to be considerably reduced.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">20845087</PMID><DateCreated><Year>2010</Year><Month>11</Month><Day>24</Day></DateCreated><DateCompleted><Year>2011</Year><Month>03</Month><Day>29</Day></DateCompleted><DateRevised><Year>2015</Year><Month>11</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1970-9366</ISSN><JournalIssue CitedMedium="Internet"><Volume>5</Volume><Issue>6</Issue><PubDate><Year>2010</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Internal and emergency medicine</Title><ISOAbbreviation>Intern Emerg Med</ISOAbbreviation></Journal><ArticleTitle>Anti-tumor necrosis factor-α therapy and changes of flow-mediated vasodilatation in psoriatic and rheumatoid arthritis patients.</ArticleTitle><Pagination><MedlinePgn>495-500</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s11739-010-0458-6</ELocationID><Abstract><AbstractText>For a long time, the endothelial covering of the vessels has been considered an inert surface. On the contrary, the endothelial cells are active and dynamic elements in the interaction between blood and tissues. The control of the vessel basal tone is obtained by the complex balance between the relaxing and contracting endothelial factors. Previous clinical studies show that patients suffering from rheumatoid arthritis and other autoimmune rheumatologic pathologies are at high risk of death being prematurely affected by atherosclerosis and cardiovascular diseases. Blocking tumor necrosis factor (TNF)-α by biological drugs improves the endothelial function. The aim of our study was to evaluate the effects of two anti-TNF-α drugs (infliximab and etanercept) on the endothelial function by evaluating the flow-mediated dilatation (FMD), which was measured in the brachial artery before and after treatment and after 8-12 weeks. We enrolled 36 patients (average age 52 ± 9.8 years, 12 men and 24 women), 25 of them were affected by rheumatoid arthritis (RA) and 11 were affected by psoriatic arthritis (PsA) and they were divided into three groups: 10 patients were treated with etanercept, 13 patients were treated with infliximab, 13 patients were treated with DMARDs. We measured the common carotid intimal-medial thickness (ccIMT) and the endothelial function was evaluated by FMD measurement in the brachial artery, before treatment, 1 h after the beginning of treatment and after 8-12 weeks. No statistically significant difference between the three groups was found for the ultrasonographic evaluation of the carotid IMT. On the contrary, the differences between FMD values before and after the treatment in the patients treated with etanercept (13.1 ± 0.01 vs. 18.8 ± 0.01%, p < 0.01) and in the patients treated with infliximab (11.8 ± 0.09 vs. 16.7 ± 0.09%, p < 0.01) were statistically significant. Long-term evaluation for infliximab and etanercept was performed by comparing the FMD values, respectively, 8 and 12 weeks after the first treatment. After 8 weeks, FMD value was similar to the value recorded at enrollment in the infliximab group (11.9 ± 0.03 vs. 13.54 ± 0.04%, p = 0.236) and the FMD values in the etanercept group after 12 weeks showed a not statistically significant reduction of vasodilatating effect (13.01 ± 0.03 vs. 15.67 ± 0.02%, p = 0.197). In conclusion, the use of biological drugs in patients affected by autoimmune arthritis can modify the endothelial function, as indicated by the induced FMD changes, but the long-term effect tends to be considerably reduced.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mazzoccoli</LastName><ForeName>Gianluigi</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine, Scientific Institute and Regional General Hospital Casa Sollievo della Sofferenza, Opera di Padre Pio da Pietrelcina, Cappuccini Avenue, 71013 S. Giovanni Rotondo (FG), Italy. g.mazzoccoli@tin.it</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Notarsanto</LastName><ForeName>Incoronata</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>de Pinto</LastName><ForeName>Gennaro Davide</ForeName><Initials>GD</Initials></Author><Author ValidYN="Y"><LastName>Dagostino</LastName><ForeName>Mariangela Pia</ForeName><Initials>MP</Initials></Author><Author ValidYN="Y"><LastName>De Cata</LastName><ForeName>Angelo</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>D'Alessandro</LastName><ForeName>Giuseppe</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Tarquini</LastName><ForeName>Roberto</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Vendemiale</LastName><ForeName>Gianluigi</ForeName><Initials>G</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016430">Clinical Trial</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2010</Year><Month>09</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>Italy</Country><MedlineTA>Intern Emerg Med</MedlineTA><NlmUniqueID>101263418</NlmUniqueID><ISSNLinking>1828-0447</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000911">Antibodies, Monoclonal</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007074">Immunoglobulin G</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007166">Immunosuppressive Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018124">Receptors, Tumor Necrosis Factor</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014409">Tumor Necrosis Factor-alpha</NameOfSubstance></Chemical><Chemical><RegistryNumber>B72HH48FLU</RegistryNumber><NameOfSubstance UI="D000069285">Infliximab</NameOfSubstance></Chemical><Chemical><RegistryNumber>OP401G7OJC</RegistryNumber><NameOfSubstance UI="D000068800">Etanercept</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="ErratumIn"><RefSource>Intern Emerg Med. 2011 Feb;6(1):97</RefSource></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000911">Antibodies, Monoclonal</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001172">Arthritis, Rheumatoid</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000188">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001916">Brachial Artery</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000736">ultrasonography</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000068800">Etanercept</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007074">Immunoglobulin G</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007166">Immunosuppressive Agents</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000069285">Infliximab</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008875">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011565">Psoriasis</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000188">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D018124">Receptors, Tumor Necrosis Factor</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012039">Regional Blood Flow</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014409">Tumor Necrosis Factor-alpha</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000037">antagonists & inhibitors</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014664">Vasodilation</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000187">drug effects</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2010</Year><Month>7</Month><Day>4</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2010</Year><Month>8</Month><Day>31</Day></PubMedPubDate><PubMedPubDate PubStatus="aheadofprint"><Year>2010</Year><Month>9</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2010</Year><Month>9</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2010</Year><Month>9</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2011</Year><Month>3</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1007/s11739-010-0458-6</ArticleId><ArticleId IdType="pubmed">20845087</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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