Vitamin D deficiency has been reported in adult patients with autoimmune diseases including rheumatoid arthritis, however, the data in patients with juvenile idiopathic arthritis (JIA) are inconsistent. The aim of the study was to assess serum 25-hydroxyvitamin D (25(OH) D in children and adolescents with JIA, and to determine potential risk factors for vitamin D deficiency.
In this cross-sectional study, we evaluated 189 patients with JIA (113 girls, 76 boys) aged 317.7 years (mean 12.3±3.9), having been diagnosed with oligoarticular (49%), polyarticular (44%) or systemic (7%) manifestations of the disease. The therapies included glucocorticosteroid (GCS) and/or methotrexate (MTX) treatment. Clinical status, anthropometric measurements using standard methods, laboratory markers of inflammatory process (C-reactive protein level and ESR), serum 25(OH) D, calcium (Ca), phosphorus (PO4), and total alkaline phosphatase levels (ALP) were determined. Hypovitaminosis D was defined as serum 25(OH) D <20 ng/ml.
In the whole studied group, the mean 25(OH) D concentration was 16.26±9.4 ng/ml. Severely reduced 25(OH) D levels (<20 ng/ml) were found in 127 individuals with JIA (67%) and were independent of the clinical subtypes of JIA, nor were associated with age, sex or inflammatory markers. The 25(OH) D level was linked to higher serum Ca, ALP whereas it negatively correlated with BMI (r=−0.2; P=0.01). Obese JIA children showed significantly reduced 25(OH) D concentration in comparison to normal-weight peers. There was no relationship between steroid use and vitamin D status, although GCS treatment and the dose were associated with lower serum Ca ((r=−0.23), PO4 (r=−0.27) and decreased ALP ((r=−0.79; all P<0.01). Patients on MTX treatment also demonstrated lower Ca levels than those without MTX (2.51±0.09 vs 2.48±0.1; P=0.02), and a significant negative correlation was found between MTX weekly dose and 25(OH) D (r=−0.34). When children were divided in two groups according to the cut-off 25(OH) D level, the vitamin D deficiency (<20 ng/ml) was associated with MTX medication. The dose-dependent differences in 25(OH) D levels and serum Ca were observed between MTX users and non-users (26.96±4.6 vs 11.44±6.4 ng/ml; 2.52 vs 2.48 respectively; P<0.01), without ALP response.
Majority of children with JIA have reduced 25(OH) D. The high prevalence of clinically apparent vitamin D deficiency suggests a need to standardize vitamin D intake in this population. Methotrexate is a significant risk factor for suboptimal vitamin D status, therefore, patients on MTX therapy may require a correction of vitamin D supplementation to maintain optimal 25(OH) D levels. Long-term studies are needed to investigate whether the supplementation would alleviate the negative effect of MTX on vitamin D in JIA.
Disclosure: The authors declared no competing interests.
27 Jun 2015 - 30 Jun 2015