JIA predisposes children to adult‐onset autoimmune diseases

02 Apr 2019
JIA predisposes children to adult‐onset autoimmune diseases

Juvenile idiopathic arthritis in children carries a heightened risk of developing autoimmune diseases—including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), ankylosing spondylitis (AS), psoriatic arthritis and Sjögren's syndrome—in adulthood, as reported in a recent study.

Researchers drew data from the National Taiwan Health Insurance Database and followed a cohort of 107,433 children (mean age at baseline, 6.5 years; 47.81 percent female) born between 1990 and 1997. In the cohort, 262 were JIA patients and 107,171 were assigned as controls. By the end of the study, the participants were at age 16–24 years.

The JIA group showed increased subsequent risk of developing autoimmune diseases compared with the control group. RA was the most common (incidence rate, 83.56 per 100,000 person‐months), followed by AS (58.39 per 100,000 person-months) and psoriatic diseases (33.26 per 100,000 person-months). The incidence rate of SLE was 16.61 per 100,000 person-months.

In Cox proportional regression models, children with JIA were about 37 times as likely as their non-JIA counterparts to develop any autoimmune disease in adulthood (adjusted hazard ratio [aHR], 37.00; 95 percent CI, 24.59–55.67; p<0.0001). When analysed separately, the aHRs were 207.37 (96.82–444.15) for RA, 40.97 (18.89–88.90) for AS, 19.02 (6.99–51.804) for psoriatic arthritis, 17.57 (5.52–55.92) for Sjögren's syndrome and 13.19 (3.22–54.00) for SLE.

Of note, the age at onset of JIA was associated with the risk of adult-onset autoimmune disease, with the greatest risks seen in the 3–5-year old age (aHR, 34.87; 4.85–250.62) and the 10–15-year age (aHR, 45.80; 29.69–70.64) groups.

In light of the findings, researchers pointed out that clinicians should advise examination of autoimmune status in adulthood for children diagnosed with JIA.

The relationship between JIA and adult-onset autoimmune diseases might be potentially explained by having similar genetic backgrounds with multiple susceptibility genes mostly associated with the T-cell receptor signalling pathway, researchers added. Further research is needed to ascertain the possible causes for such associations.

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