A recent study offers a genomic characterization of remission in juvenile rheumatoid arthritis patients, outlining the process behind remission and providing insight into why children often experience recurrences despite it.
According to the study, 35% to 50% of children with juvenile rheumatoid arthritis achieve remission while being treated with the standard treatments.
Yet, James N. Jarvis, MD, lead author, clinical professor of pediatrics in the University at Buffalo School of Medicine and Biomedical Sciences, points out that while the children appear to be normal and symptom free, the immune system remains agitated. “Our study provides some insight into why so many children in remission experience disease flares even when their disease has been stable for weeks or months, and why 50% of children who try to come off medication experience disease flares within 2 to 6 months,” Jarvis says.
During the study, researchers reportedly compared gene expression profiles from two independent cohorts of 14 patients each, all in remission from juvenile rheumatoid arthritis, to those of 15 healthy controls. Patients were treated with two different medication regimes and followed every 2 to 3 months for at least a year.
Researchers say the new study reinforces preliminary research conducted by Jarvis, indicating that remission experienced by patients with juvenile rheumatoid arthritis on medication is a distinct biological state. This biological state results from pro-inflammatory responses, countered by anti-inflammatory responses caused by gene expression changes induced by medication.
Jarvis notes that a key study result suggests that remission in these patients is linked to HNF4a, a transcription factor that binds to DNA and serves as an “on” or “off” switch for gene expression. The study found that more than 200 genes in white blood cells were expressed differently in children taking a blended treatment of methotrexate and etanercept when compared to health controls. Researchers explain that some of those differently expressed genes have been shown to bind to HNF4a.
Jarvis designates the study as, “a first step toward the goal of identifying biomarkers that will ultimately allow clinicians to personalize treatment by predicting which patients will respond best to which therapies.”
Source: University at Buffalo