Levels of DNASE1L3 Protein Are Potential Biomarker of Ankylosing Spondylitis, Study Suggests

Levels of DNASE1L3 Protein Are Potential Biomarker of Ankylosing Spondylitis, Study Suggests
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Analyzing the levels of a protein called DNASE1L3 may enable an accurate diagnosis of ankylosing spondylitis (AS), a study suggests.

Besides being able to distinguish between AS and generalized osteoarthritis, this potential biomarker may also differentiate between active and inactive AS disease.

The study, “Serum Deoxyribonuclease 1-like 3 is a potential biomarker for diagnosis of ankylosing spondylitis,” was published in the journal Clinica Chimica Acta.

AS is an inflammatory disorder that mainly affects the joints of the spine, causing chronic pain and lifelong physical disability. Current diagnosis relies on the use of magnetic resonance imaging (MRI). However, this imaging technique is less efficient at the early stages of the disease, when prompt and appropriate treatment is key for clinical remission.

Previous studies have found that the levels of DNASE1L3 are increased in the blood of people with autoimmune diseases. However, it was unknown whether they are also high in people with AS or with generalized osteoarthritis, a degenerative joint disease that resembles AS.

To address this, researchers in China analyzed whether assessing blood levels of DNASE1L3 may be a diagnostic biomarker of AS severity.

They analyzed blood samples from 60 patients with AS (mean age of 41.3 years), 60 others with generalized osteoarthritis (59.8 years), and 60 healthy people used as controls (44.1 years). Researchers measured levels of DNASE1L3, while also examining disease activity in AS using the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), where higher scores mean worse disease.

Results revealed that the median levels of DNASE1L3 were significantly higher in AS patients (297.2 ng/mL) than in both controls (38.79 ng/mL) and people with generalized osteoarthritis (35.91 ng/mL).

Participants with AS were then divided in two groups: inactive (BASDAI scores up to 4) and active disease (BASDAI scores higher than 4). This showed that the levels of DNASE1L3 correlated with disease activity, with higher levels detected in the active AS group (588.52 ng/mL) than in those with inactive disease (82.59 ng/mL).

In addition, higher amounts of DNASE1L3 were associated with those of inflammatory markers, namely C3 and C-reactive (CRP) protein.

A level of 89.67 ng/mL enables the distinction of AS from both healthy controls and those with generalized osteoarthritis. This value enables distinction from those with generalized osteoarthritis, with a sensitivity of 78.33% and a specificity of 81.67%, and from healthy controls with a sensitivity of 71.67% and a specificity of 78.33%. Sensitivity refers to the ability to correctly identify people with a given disorder, while specificity refers to the accuracy of the identification of unaffected individuals.

Also, DNASE1L3 outperformed other inflammatory markers as a diagnostic tool. Combined use with C3 and CRP did not lead to greater diagnostic accuracy.

These results suggest that the blood levels of DNASE1L3 could be used as a “biomarker with a positive diagnostic value in patients with AS, and which could be used as a differential diagnostic indicator for GOA [generalized osteoarthritis] and AS,” the researchers wrote.

Patricia holds her Ph.D. in Cell Biology from University Nova de Lisboa, and has served as an author on several research projects and fellowships, as well as major grant applications for European Agencies. She also served as a PhD student research assistant in the Laboratory of Doctor David A. Fidock, Department of Microbiology & Immunology, Columbia University, New York.
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José is a science news writer with a PhD in Neuroscience from Universidade of Porto, in Portugal. He has also studied Biochemistry at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario in London, Ontario, Canada. His work has ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.
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Patricia holds her Ph.D. in Cell Biology from University Nova de Lisboa, and has served as an author on several research projects and fellowships, as well as major grant applications for European Agencies. She also served as a PhD student research assistant in the Laboratory of Doctor David A. Fidock, Department of Microbiology & Immunology, Columbia University, New York.
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