Lower UV exposure in early life may increase a child’s risk of juvenile idiopathic arthritis (JIA), Victorian research suggests.
In a retrospective study, researchers at the Murdoch Children’s Research Institute in Melbourne found an inverse relationship between cumulative sun exposure prior to diagnosis and risk of JIA.
The research, conducted in collaboration with clinicians in the Paediatric Rheumatology Unit of the Royal Children’s Hospital, also found an inverse relationship between maternal UV exposure during pregnancy and the offspring’s risk of JIA.
The findings of a dose-response relationship between UV exposure and risk of JIA suggested a possible role for vitamin D levels in the development of JIA, similar to the one seen for other autoinflammatory diseases such as MS, the researchers said.
‘[Our findings] provide the first body of evidence that circulating vitamin D prior to disease onset may contribute to JIA risk.
“If these associations are confirmed, they will point to an environmental factor amenable to intervention that has potential to reduce risk of developing this debilitating childhood disease,” they wrote in the journal Photochemistry and Photobiology.
In the study, the researchers obtained data by questionnaire from the families of 202 children with JIA participating in the ChiLdhood Arthritis Risk factor Identification sTudY (CLARITY). They compared the reported UV exposures in pregnancy and childhood with 202 matched controls.
An inverse association between total cumulative UV radiation exposure and JIA was observed, with a clear dose-response relationship, as a greater total UVR exposure showed an increasingly protective association with JIA (test for trend p=0.04).
The researchers noted that only pre-diagnosis UV exposure was measured in the study, which would help address the issue of whether low UV exposure was a cause or consequence of JIA through children with the disease having less exposure to sunlight after diagnosis.
They hypothesised that sun exposure might attenuate JIA risk through influence on circulating levels of vitamin D, which is believed to have anti-inflammatory and immunomodulatory effects.
“Of particular relevance to JIA, [vitamin D] signalling represses the transcription of Th1 cytokine genes, driving T helper responses towards a more regulatory Th2 phenotype, thus suppressing Th1-driven autoimmune responses. Feasibly then, lower 1,25(OH)2D3, through reduced UVR exposure, could reduce suppression of autoimmune responses in JIA,” they wrote.
However it was also possible that UV exposure had some effect on JIA risk independent of vitamin D, they added.
The next step will be to replicate the findings in studies that prospectively collect vitamin D and sun exposure measures, they said.