Clinical Chemistry
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Clinical Chemistry 53: 1609-1614, 2007; 10.1373/clinchem.2006.084509
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(Clinical Chemistry. 2007;53:1609-1614.)
© 2007 American Association for Clinical Chemistry, Inc.

Molecular Diagnostics and Genetics

Increased Concentrations of Antibody-Bound Circulatory Cell-Free DNA in Rheumatoid Arthritis

Xiao-Yan Zhong1, Ines von Mühlenen2, Ying Li1, Anjeung Kang1, Anurag Kumar Gupta1, Alan Tyndall2, Wolfgang Holzgreve1, Sinuhe Hahn1,a and Paul Hasler2,3,a

1 Laboratory for Prenatal Medicine, University Women’s Hospital, Department of Research, University Hospital Basel, Basel, Switzerland.
2 Departments of Rheumatology and Research, Felix Platter Spital and University Hospital Basel, Basel, Switzerland.
3 Rheumaklinik, Kantonsspital Aarau, Tellstrasse, Aarau, Switzerland.

aAddress correspondence to these authors at: Laboratory for Prenatal Medicine, University Women’s Hospital, Department of Research, Spitalstrasse 21, CH-4031 Basel, Switzerland. Fax 41 61 265 9399; e-mail shahn{at}uhbs.ch or Rheumaklinik, Kantonsspital Aarau, Tellstrasse, CH-5001 Aarau, Switzerland. Fax 4162 838 4630; e-mail paul.hasler{at}ksa.ch.

Background: Increased concentrations of cell-free DNA have been found in several disorders and have been interpreted as evidence of increased rates of cell death or turnover. Evidence from in vitro and animal experiments suggests that DNA may play a role in the pathogenesis of rheumatoid arthritis (RA).

Methods: We measured cell-free DNA in plasma and serum from patients with RA and healthy controls by use of quantitative PCR for glyceraldehyde-3-phosphate dehydrogenase (GAPDH) DNA. We used protein G SepharoseTM bead adsorption of plasma and elution to isolate antibody-bound DNA.

Results: In paired plasma and serum samples of 16 healthy controls the median GAPDH copies were 4500 genome equivalents (GE)/mL plasma (range 319–21 000) and in 26 RA patients 17 000 GE/mL plasma (2100–2 375 000, P = 0.0001). In the serum from normal controls the median GAPDH copies were 35 000 GE/mL (1700–239 000) and from RA patients 222 000 GE/mL (21 000–2 375 000, P = 0.004). A median of 81% of the cell-free DNA in RA was associated with antibody compared with 9% in healthy controls (P = 0.001). The concentrations of DNA did not vary with the type of therapy patients received.

Conclusions: These results provide new evidence for a role of cell-free DNA-antibody complexes in the etiology of RA, suggest new avenues for basic research, and may prove to be relevant to diagnosis and assessment of therapy.






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