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Anti-tumor necrosis factor-α therapy and changes of flow-mediated vasodilatation in psoriatic and rheumatoid arthritis patients.

Identifieur interne : 000D79 ( Main/Exploration ); précédent : 000D78; suivant : 000D80

Anti-tumor necrosis factor-α therapy and changes of flow-mediated vasodilatation in psoriatic and rheumatoid arthritis patients.

Auteurs : Gianluigi Mazzoccoli [Italie] ; Incoronata Notarsanto ; Gennaro Davide De Pinto ; Mariangela Pia Dagostino ; Angelo De Cata ; Giuseppe D'Alessandro ; Roberto Tarquini ; Gianluigi Vendemiale

Source :

RBID : pubmed:20845087

English descriptors

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


Affiliations:


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Le document en format XML

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<name sortKey="Mazzoccoli, Gianluigi" sort="Mazzoccoli, Gianluigi" uniqKey="Mazzoccoli G" first="Gianluigi" last="Mazzoccoli">Gianluigi Mazzoccoli</name>
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<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>
<country xml:lang="fr">Italie</country>
<wicri:regionArea>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)</wicri:regionArea>
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<name sortKey="De Cata, Angelo" sort="De Cata, Angelo" uniqKey="De Cata A" first="Angelo" last="De Cata">Angelo De Cata</name>
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<name sortKey="Vendemiale, Gianluigi" sort="Vendemiale, Gianluigi" uniqKey="Vendemiale G" first="Gianluigi" last="Vendemiale">Gianluigi Vendemiale</name>
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<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>
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<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>
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<name sortKey="Dagostino, Mariangela Pia" sort="Dagostino, Mariangela Pia" uniqKey="Dagostino M" first="Mariangela Pia" last="Dagostino">Mariangela Pia Dagostino</name>
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<name sortKey="De Cata, Angelo" sort="De Cata, Angelo" uniqKey="De Cata A" first="Angelo" last="De Cata">Angelo De Cata</name>
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<name sortKey="D Alessandro, Giuseppe" sort="D Alessandro, Giuseppe" uniqKey="D Alessandro G" first="Giuseppe" last="D'Alessandro">Giuseppe D'Alessandro</name>
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<name sortKey="Tarquini, Roberto" sort="Tarquini, Roberto" uniqKey="Tarquini R" first="Roberto" last="Tarquini">Roberto Tarquini</name>
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<name sortKey="Vendemiale, Gianluigi" sort="Vendemiale, Gianluigi" uniqKey="Vendemiale G" first="Gianluigi" last="Vendemiale">Gianluigi Vendemiale</name>
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<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>
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<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>
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<term>Regional Blood Flow</term>
<term>Vasodilation</term>
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<term>Arthritis, Rheumatoid</term>
<term>Psoriasis</term>
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<term>Brachial Artery</term>
<term>Regional Blood Flow</term>
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<keywords scheme="MESH" qualifier="ultrasonography" xml:lang="en">
<term>Brachial Artery</term>
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<keywords scheme="MESH" type="chemical" xml:lang="en">
<term>Etanercept</term>
<term>Female</term>
<term>Humans</term>
<term>Infliximab</term>
<term>Male</term>
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<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>
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<noCountry>
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