Patients with Ankylosing Spondylitis and Low Disease Activity because of Anti-TNF-Alpha Therapy Have Higher TRAIL Levels Than Controls: A Potential Compensatory Effect
Objective. TRAIL is a potential biomarker of cardiovascular (CV) disease. Ankylosing spondylitis (AS) is a chronic inflammatory disease associated with metabolic syndrome (MeS) and accelerated atherosclerosis. We assessed whether disease activity, systemic inflammation, and MeS features were associa...
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2014-01-01
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Series: | Mediators of Inflammation |
Online Access: | http://dx.doi.org/10.1155/2014/798060 |
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author | Fernanda Genre Raquel López-Mejías Javier Rueda-Gotor José A. Miranda-Filloy Begoña Ubilla Beatriz Carnero-López Natalia Palmou-Fontana Inés Gómez-Acebo Ricardo Blanco Trinitario Pina Rodrigo Ochoa Carlos González-Juanatey Javier Llorca Miguel A. González-Gay |
author_facet | Fernanda Genre Raquel López-Mejías Javier Rueda-Gotor José A. Miranda-Filloy Begoña Ubilla Beatriz Carnero-López Natalia Palmou-Fontana Inés Gómez-Acebo Ricardo Blanco Trinitario Pina Rodrigo Ochoa Carlos González-Juanatey Javier Llorca Miguel A. González-Gay |
author_sort | Fernanda Genre |
collection | DOAJ |
description | Objective. TRAIL is a potential biomarker of cardiovascular (CV) disease. Ankylosing spondylitis (AS) is a chronic inflammatory disease associated with metabolic syndrome (MeS) and accelerated atherosclerosis. We assessed whether disease activity, systemic inflammation, and MeS features were associated with circulating TRAIL levels in AS patients undergoing TNF-α antagonist infliximab therapy and if infliximab infusion modified TRAIL levels. Methods. We measured TRAIL serum levels in 30 nondiabetic AS patients without CV disease undergoing anti-TNF-α therapy, immediately before and after an infliximab infusion, and in 48 matched controls. Correlations of TRAIL levels with disease activity, systemic inflammation and MeS features, adipokines, and biomarkers of endothelial activation were evaluated. Changes in TRAIL levels following anti-TNF-α infusion were analyzed. Results. TRAIL levels were higher in AS patients than controls. TRAIL levels displayed an inverse correlation with total and LDL cholesterol. We observed an inverse correlation with QUICKI and a marginal association with HOMA-IR. We also found an inverse correlation with resistin and a marginal association with apelin and OPN. Anti-TNF-α infusion did not change TRAIL levels after 120′. Conclusion. Elevated TRAIL levels in AS patients may be the result of a compensatory mechanism to reduce CV risk in these patients. |
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institution | Kabale University |
issn | 0962-9351 1466-1861 |
language | English |
publishDate | 2014-01-01 |
publisher | Wiley |
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series | Mediators of Inflammation |
spelling | doaj-art-187813e9fb9c4bbe8543375adff56ecf2025-02-03T01:33:09ZengWileyMediators of Inflammation0962-93511466-18612014-01-01201410.1155/2014/798060798060Patients with Ankylosing Spondylitis and Low Disease Activity because of Anti-TNF-Alpha Therapy Have Higher TRAIL Levels Than Controls: A Potential Compensatory EffectFernanda Genre0Raquel López-Mejías1Javier Rueda-Gotor2José A. Miranda-Filloy3Begoña Ubilla4Beatriz Carnero-López5Natalia Palmou-Fontana6Inés Gómez-Acebo7Ricardo Blanco8Trinitario Pina9Rodrigo Ochoa10Carlos González-Juanatey11Javier Llorca12Miguel A. González-Gay13Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Rheumatology Division, IDIVAL, 39011 Santander, SpainEpidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Rheumatology Division, IDIVAL, 39011 Santander, SpainEpidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Rheumatology Division, IDIVAL, 39011 Santander, SpainRheumatology Division, Hospital Lucus Augusti, 27003 Lugo, SpainEpidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Rheumatology Division, IDIVAL, 39011 Santander, SpainOncology Division, Hospital Del Bierzo, Ponferrada, 24411 León, SpainRheumatology Division, Hospital General de Almansa, 02640 Albacete, SpainDepartment of Epidemiology and Computational Biology, School of Medicine, University of Cantabria, IDIVAL, and CIBER Epidemiología y Salud Pública (CIBERESP), 39011 Santander, SpainEpidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Rheumatology Division, IDIVAL, 39011 Santander, SpainEpidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Rheumatology Division, IDIVAL, 39011 Santander, SpainEpidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Rheumatology Division, IDIVAL, 39011 Santander, SpainCardiology Division, Hospital Lucus Augusti, 27003 Lugo, SpainDepartment of Epidemiology and Computational Biology, School of Medicine, University of Cantabria, IDIVAL, and CIBER Epidemiología y Salud Pública (CIBERESP), 39011 Santander, SpainEpidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Rheumatology Division, IDIVAL, 39011 Santander, SpainObjective. TRAIL is a potential biomarker of cardiovascular (CV) disease. Ankylosing spondylitis (AS) is a chronic inflammatory disease associated with metabolic syndrome (MeS) and accelerated atherosclerosis. We assessed whether disease activity, systemic inflammation, and MeS features were associated with circulating TRAIL levels in AS patients undergoing TNF-α antagonist infliximab therapy and if infliximab infusion modified TRAIL levels. Methods. We measured TRAIL serum levels in 30 nondiabetic AS patients without CV disease undergoing anti-TNF-α therapy, immediately before and after an infliximab infusion, and in 48 matched controls. Correlations of TRAIL levels with disease activity, systemic inflammation and MeS features, adipokines, and biomarkers of endothelial activation were evaluated. Changes in TRAIL levels following anti-TNF-α infusion were analyzed. Results. TRAIL levels were higher in AS patients than controls. TRAIL levels displayed an inverse correlation with total and LDL cholesterol. We observed an inverse correlation with QUICKI and a marginal association with HOMA-IR. We also found an inverse correlation with resistin and a marginal association with apelin and OPN. Anti-TNF-α infusion did not change TRAIL levels after 120′. Conclusion. Elevated TRAIL levels in AS patients may be the result of a compensatory mechanism to reduce CV risk in these patients.http://dx.doi.org/10.1155/2014/798060 |
spellingShingle | Fernanda Genre Raquel López-Mejías Javier Rueda-Gotor José A. Miranda-Filloy Begoña Ubilla Beatriz Carnero-López Natalia Palmou-Fontana Inés Gómez-Acebo Ricardo Blanco Trinitario Pina Rodrigo Ochoa Carlos González-Juanatey Javier Llorca Miguel A. González-Gay Patients with Ankylosing Spondylitis and Low Disease Activity because of Anti-TNF-Alpha Therapy Have Higher TRAIL Levels Than Controls: A Potential Compensatory Effect Mediators of Inflammation |
title | Patients with Ankylosing Spondylitis and Low Disease Activity because of Anti-TNF-Alpha Therapy Have Higher TRAIL Levels Than Controls: A Potential Compensatory Effect |
title_full | Patients with Ankylosing Spondylitis and Low Disease Activity because of Anti-TNF-Alpha Therapy Have Higher TRAIL Levels Than Controls: A Potential Compensatory Effect |
title_fullStr | Patients with Ankylosing Spondylitis and Low Disease Activity because of Anti-TNF-Alpha Therapy Have Higher TRAIL Levels Than Controls: A Potential Compensatory Effect |
title_full_unstemmed | Patients with Ankylosing Spondylitis and Low Disease Activity because of Anti-TNF-Alpha Therapy Have Higher TRAIL Levels Than Controls: A Potential Compensatory Effect |
title_short | Patients with Ankylosing Spondylitis and Low Disease Activity because of Anti-TNF-Alpha Therapy Have Higher TRAIL Levels Than Controls: A Potential Compensatory Effect |
title_sort | patients with ankylosing spondylitis and low disease activity because of anti tnf alpha therapy have higher trail levels than controls a potential compensatory effect |
url | http://dx.doi.org/10.1155/2014/798060 |
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