Angiotensin Converting Enzyme Activity in Anti-TNF-Treated Rheumatoid Arthritis and Ankylosing Spondylitis Patients.

angiotensin converting enzyme ankylosing spondylitis anti-TNF therapy biologics rheumatoid arthritis vascular disease

Journal

Frontiers in medicine
ISSN: 2296-858X
Titre abrégé: Front Med (Lausanne)
Pays: Switzerland
ID NLM: 101648047

Informations de publication

Date de publication:
2021
Historique:
received: 29 09 2021
accepted: 10 12 2021
entrez: 14 2 2022
pubmed: 15 2 2022
medline: 15 2 2022
Statut: epublish

Résumé

Angiotensin-converting enzyme (ACE) and ACE2 have been implicated in the regulation of vascular physiology. Elevated synovial and decreased or normal ACE or ACE2 levels have been found in rheumatoid arthritis (RA). Very little is known about the effects of tumor necrosis factor α (TNF-α) inhibition on ACE or ACE2 homeostasis. In this study, we assessed the effects of one-year anti-TNF therapy on ACE and ACE2 production in RA and ankylosing spondylitis (AS) in association with other biomarkers. Forty patients including 24 RA patients treated with either etanercept (ETN) or certolizumab pegol (CZP) and 16 AS patients treated with ETN were included in a 12-month follow-up study. Serum ACE levels were determined by commercial ELISA, while serum ACE2 activity was assessed using a specific quenched fluorescent substrate. Ultrasonography was performed to determine flow-mediated vasodilation (FMD), common carotid intima-media thickness (ccIMT) and arterial pulse-wave velocity (PWV) in all patients. In addition, CRP, rheumatoid factor (RF) and ACPA were also measured. All assessments were performed at baseline and 6 and 12 months after treatment initiation. Anti-TNF therapy increased ACE levels in the full cohort, as well as in the RA and AS subsets. ACE2 activity increased in the full cohort, while the ACE/ACE2 ratio increased in the full cohort and in the RA subset ( Anti-TNF treatment may increase ACE and ACE2 in the sera of RA and AS patients. ACE and ACE2 may be associated with disease duration, markers of inflammation and vascular pathophysiology. The effects of TNF inhibition on ACE and ACE2 may reflect, in part, the effects of these biologics on the cardiovascular system.

Identifiants

pubmed: 35155468
doi: 10.3389/fmed.2021.785744
pmc: PMC8828652
doi:

Types de publication

Journal Article

Langues

eng

Pagination

785744

Informations de copyright

Copyright © 2022 Soós, Fagyas, Horváth, Végh, Pusztai, Czókolyová, Csongrádi, Hamar, Pethő, Bodnár, Kerekes, Hodosi, Szekanecz, Szamosi, Szántó, Szűcs, Papp and Szekanecz.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Auteurs

Boglárka Soós (B)

Division of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.

Miklós Fagyas (M)

Division of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.

Ágnes Horváth (Á)

Division of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.

Edit Végh (E)

Division of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.

Anita Pusztai (A)

Division of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.

Monika Czókolyová (M)

Division of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.

Alexandra Csongrádi (A)

Division of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.

Attila Hamar (A)

Division of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.

Zsófia Pethő (Z)

Division of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.

Nóra Bodnár (N)

Division of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.

György Kerekes (G)

Intensive Care Unit, Department of Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.

Katalin Hodosi (K)

Division of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.

Éva Szekanecz (É)

Department of Oncology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.

Szilvia Szamosi (S)

Division of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.

Sándor Szántó (S)

Division of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Department of Sports Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.

Gabriella Szűcs (G)

Division of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.

Zoltán Papp (Z)

Division of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.

Zoltán Szekanecz (Z)

Division of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.

Classifications MeSH