The recent study, published in Arthritis Care & Research and conducted by a Michigan Medicine researcher, can help predict disease severity for a lung condition that is often fatal in scleroderma patients.
“Despite interstitial lung disease being the leading cause of death among scleroderma patients, there are very few markers that predict progression of the disease,” said John Varga, M.D., a corresponding author of the paper, chief of the Michigan Medicine Division of Rheumatology and associate director of the U-M Scleroderma Program.
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“CTRP9 is an entirely novel biomarker that has never been implicated in scleroderma. It will help physicians predict the course of the disease and identify those patients who would not need to be on aggressive treatment for their lung disease.”
The findings revealed that CTRP9, a novel adipokine, is associated with pulmonary function in scleroderma patients with interstitial lung disease. Scarring in the lungs can result from pulmonary conditions, making the optimal gas exchange more difficult.
For this study, researchers analysed data from 110 patients with interstitial lung disease and scleroderma, the latter of which affects more than 50,000 people in the United States. Over a four-year period, they measured CTRP9 serum levels and collected clinical and lung function data every 12 months.
Patients with higher levels of CTRP9 in their blood developed more severe lung disease, whereas low levels of the protein were associated with preserved function. The researchers also discovered a link between CTRP9 levels and monocytes, which are immune cells known to contribute to lung fibrosis.
While CTRP9 did not predict disease progression, researchers suggest one possible explanation: Interstitial lung disease frequently progresses rapidly after diagnosis, and because the subjects’ baseline disease duration was nine years, patients may have reached disease plateaus.
“The results from the new study add to the collection of biomarkers that could help for classification and treatment prediction for people living with scleroderma-associated lung disease,” Varga said.
“We look forward to future studies that validate and expand upon this work.”
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The study cited: DOI: 10.1002/acr.24749
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