Clinical phenotype associations with various types of anti-dsDNA antibodies in patients with recent onset of rheumatic symptoms. Results from a multicentre observational study.
Despite anti-dsDNA antibodies constitute a wide range of specificities, they are considered as the hallmark for systemic lupus erythematosus (SLE).


OBJECTIVE
To identify clinical phenotypes associated with anti-dsDNA antibodies, independently of any clinical diagnoses.


METHODS
Patients with recent onset of any rheumatic symptoms were screened for antinuclear antibodies (ANA). All ANA-positive and matching ANA-negative patients were examined, and their clinical phenotypes were registered, using a systematic chart formulated after consensus between the participating centres. All patients were tested for different anti-dsDNA antibody specificities with assays habitually used in each participating laboratory. Crithidia Luciliae Immuno Fluorescence Test (CLIFT) was performed three times (with two different commercial kits); solid and solution phase ELISA were performed four times. Associations between clinical phenotypes and results of anti-dsDNA assays were evaluated by linear regression analysis (LRA) and principal component analysis (PCA).


RESULTS
Totally, 292 ANA-positive and 292 matching ANA-negative patients were included in the study. A full dataset for statistical analysis was obtained in 547 patients. Anti-dsDNA antibodies were most frequently detected by ELISA. LRA showed that overall positivity of anti-dsDNA antibodies was associated with proteinuria and pleuritis. Alopecia was significantly associated only with CLIFT-positivity. Besides confirming the same findings, PCA showed that combined positivity of CLIFT and ELISA was also associated with lymphopenia.


CONCLUSIONS
Our results show that different anti-dsDNA antibody specificities are associated with nephropathy, pleuritis, alopecia and lymphopenia, regardless of the diagnosis. It may challenge the importance of anti-dsDNA antibodies as a diagnostic hallmark for SLE.
Section of Rheumatology, Department of Clinical Sciences , Lund University , Lund , Sweden.
Michele
M
Compagno
Department of Biochemistry , Institute of Medical Biology , University of Tromsø , Tromsø , Norway.
Ole P
OP
Rekvig
Section of Rheumatology, Department of Clinical Sciences , Lund University , Lund , Sweden.
Anders A
AA
Bengtsson
Section of Rheumatology, Department of Clinical Sciences , Lund University , Lund , Sweden.
Gunnar
G
Sturfelt
Statens Serum Institut , Copenhagen , Denmark.
Niels H H
NH
Heegaard
Section of Rheumatology, Department of Clinical Sciences , Lund University , Lund , Sweden.
Andreas
A
Jönsen
Department of Rheumatology , Rigshospitalet , Copenhagen University Hospital , Copenhagen , Denmark.
Rasmus Sleimann
RS
Jacobsen
Bone and Joint Research Group, Department of Clinical Medicine, Faculty of Health Science , University of Tromsø , Tromsø , Norway.
Gro Ø
GØ
Eilertsen
Department of Biochemistry , Institute of Medical Biology , University of Tromsø , Tromsø , Norway.
Christopher G
CG
Fenton
Department of Laboratory Medicine, Section of Microbiology, Immunology and Glycobiology , Lund University , Lund , Sweden.
Lennart
L
Truedsson
Bone and Joint Research Group, Department of Clinical Medicine, Faculty of Health Science , University of Tromsø , Tromsø , Norway ; Division of Medicine, Rheumatology Section , Royal Darwin Hospital , Darwin, Northern Territory , Australia.
Johannes C
JC
Nossent
Department of Rheumatology , Rigshospitalet , Copenhagen University Hospital , Copenhagen , Denmark.
Søren
S
Jacobsen
Autoantibodies; Autoimmune Diseases; Autoimmunity; Lupus Nephritis; Systemic Lupus Erythematosus