Skip to main content
Top
Published in: Rheumatology International 8/2018

01-08-2018 | Biomarkers

Anti-cytokine therapy and plasma DNA in patients with rheumatoid arthritis

Authors: Lucia Lauková, Barbora Konečná, Barbora Vlková, Vanda Mlynáriková, Peter Celec, Emőke Šteňová

Published in: Rheumatology International | Issue 8/2018

Login to get access

Abstract

Background

Extracellular DNA (ecDNA) is increased in inflammation and it also induces inflammation. In patients with rheumatoid arthritis (RA), plasma ecDNA is higher than in healthy controls. Due to low specificity, it cannot be used for screening, but it might be useful for monitoring and prognosis of therapy success. The effect of treatment with biological disease-modifying antirheumatic drugs (bDMARDs) on plasma ecDNA in RA patients with regards to its subcellular origin has not been analyzed yet. The aim of this study was to describe the effects of bDMARDs on plasma ecDNA and its nuclear (nDNA) and mitochondrial (mtDNA) fractions in patients with RA.

Methods

Plasma samples of 32 patients with RA were collected before, as well as 3 and 6 months after starting the treatment with bDMARDs. Total plasma ecDNA was quantified fluorometrically. The subcellular origin of ecDNA was assessed using real time PCR. Treatment success was monitored using DAS28 and C-reactive protein (CRP).

Results

The clinical status of patients improved. Both DAS28 and CRP decreased by 52 and 73% after 3 months of treatment. Plasma ecDNA decreased significantly only after 6 months (by 26%). Real-time PCR showed that both, nDNA and mtDNA decreased by 63 and by 45% after 6 months.

Conclusion

Treatment with bDMARDs decreases plasma ecDNA of both nuclear and mitochondrial origin. Dynamics of ecDNA is slower than dynamics of standard clinical markers. Therefore, it is likely to be not useful for monitoring of the disease progress, at least for RA.
Literature
6.
go back to reference Singh JA, Hossain A, Tanjong Ghogomu E et al (2016) Biologics or tofacitinib for rheumatoid arthritis in incomplete responders to methotrexate or other traditional disease-modifying anti-rheumatic drugs: a systematic review and network meta-analysis. Cochrane Database Syst Rev 13:CD012183. https://doi.org/10.1002/14651858.CD012183 CrossRef Singh JA, Hossain A, Tanjong Ghogomu E et al (2016) Biologics or tofacitinib for rheumatoid arthritis in incomplete responders to methotrexate or other traditional disease-modifying anti-rheumatic drugs: a systematic review and network meta-analysis. Cochrane Database Syst Rev 13:CD012183. https://​doi.​org/​10.​1002/​14651858.​CD012183 CrossRef
Metadata
Title
Anti-cytokine therapy and plasma DNA in patients with rheumatoid arthritis
Authors
Lucia Lauková
Barbora Konečná
Barbora Vlková
Vanda Mlynáriková
Peter Celec
Emőke Šteňová
Publication date
01-08-2018
Publisher
Springer Berlin Heidelberg
Published in
Rheumatology International / Issue 8/2018
Print ISSN: 0172-8172
Electronic ISSN: 1437-160X
DOI
https://doi.org/10.1007/s00296-018-4055-8

Other articles of this Issue 8/2018

Rheumatology International 8/2018 Go to the issue
Obesity Clinical Trial Summary

At a glance: The STEP trials

A round-up of the STEP phase 3 clinical trials evaluating semaglutide for weight loss in people with overweight or obesity.

Developed by: Springer Medicine

Highlights from the ACC 2024 Congress

Year in Review: Pediatric cardiology

Watch Dr. Anne Marie Valente present the last year's highlights in pediatric and congenital heart disease in the official ACC.24 Year in Review session.

Year in Review: Pulmonary vascular disease

The last year's highlights in pulmonary vascular disease are presented by Dr. Jane Leopold in this official video from ACC.24.

Year in Review: Valvular heart disease

Watch Prof. William Zoghbi present the last year's highlights in valvular heart disease from the official ACC.24 Year in Review session.

Year in Review: Heart failure and cardiomyopathies

Watch this official video from ACC.24. Dr. Biykem Bozkurt discuss last year's major advances in heart failure and cardiomyopathies.