Juvenile idiopathic arthritis (JIA) affects the wellbeing of thousands of children worldwide, but scientists may have found a way to better classify, predict outcome of, and treat JIA. Thanks to a discovery of gene expression differences, your child’s doctor may be able to spare him or her from stronger, riskier treatments, if your child has a milder form of JIA, and target more aggressive treatment to children whose wellness is at risk of more severe arthritis.
According to Robert A. Colbert, MD, PhD, chief of the NIAMS Paediatric Translational Research Branch, the way doctors currently diagnose JIA is imprecise and based on the presence on six weeks worth of joint inflammation. Then, a few factors, such as the number of joints involved, and the presence of a fever and rash, help doctors to classify children into one of a handful of subtypes of JIA, making it easier to predict a patient’s most likely outcome and guide appropriate treatments. However, Colbert says, ‘recent research suggests there is more variability in JIA than the four or five major subtypes we currently recognize.’
For the study, which was published in Arthritis & Rheumatism, researchers led by Michael Barnes, PhD, of Cincinnati Children’s Hospital Medical Centre, used gene expression technology to look for differences in the children’s blood samples that corresponded with the different forms of JIA.
Colbert was another leader of this research programme, and he reported, ‘We analyzed gene expression patterns in blood cells and found that we could indeed distinguish the major subtypes of JIA. Many of the genes whose expression is altered function in the immune system. This means that not only is there immune activation, but it differs depending on the subtype of JIA that is present.’
He continued, ‘In paediatric rheumatology, we are at the early stages of improving our classification system for JIA. We expect that complementary studies designed to uncover the genetic differences that contribute to susceptibility will confirm the presence of several JIA subtypes, and add important information about what causes this group of diseases.’
He added that these findings could hopefully lead to the development of individually tailored treatments that maximise the benefits, while minimizing the risks: ‘We look forward to the day when we can use a combination of genetic and gene expression tests in the clinic to help us better diagnose and treat childhood arthritis.’
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