Objective Vitamin D has an important immunomodulatory effect, but there are no trials that directly address the boosting of serum levels of 25‐hydroxyvitamin D (25[OH]D) in juvenile‐onset systemic lupus erythematosus (SLE). The aim of this study was to evaluate the effect of vitamin D supplementation on disease activity and fatigue in juvenile‐onset SLE. Methods This study was a randomized, double‐blind, placebo‐controlled, 24‐week trial. Forty juvenile‐onset SLE patients were randomized (1:1) to receive oral cholecalciferol 50,000 IU/week (juvenile‐onset SLE‐VitD) or placebo (juvenile‐onset SLE‐PL). Medications remained stable throughout the study. Serum levels of 25(OH)D were measured using radioimmunoassay. Disease activity was assessed using the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) and the European Consensus Lupus Activity Measurement (ECLAM). Fatigue was assessed using the Kids Fatigue Severity Scale (K‐FSS). Results At baseline, groups were similar regarding age, body mass index, organ involvement, glucocorticoid dose, use of immunosuppressive drugs, SLEDAI, ECLAM, K‐FSS, and levels of 25(OH)D. After 24 weeks, the mean level of 25(OH)D was higher in the juvenile‐onset SLE‐VitD group than in the juvenile‐onset SLE‐PL group (P < 0.001). At the end of the intervention, a significant improvement in SLEDAI (P = 0.010) and in ECLAM (P = 0.006) was observed in the juvenile‐onset SLE‐VitD group compared to the juvenile‐onset SLE‐PL group. Regarding fatigue evaluation, a reduction of fatigue related to social life score was found in the juvenile‐onset SLE‐VitD group compared to the juvenile‐onset SLE‐PL group (P = 0.008). Cholecalciferol was well tolerated with no serious adverse events. Conclusion This study suggests that cholecalciferol supplementation for 24 weeks is effective in decreasing disease activity and improving fatigue in juvenile‐onset SLE patients.

The aim of this study was to analyze vitamin D levels and their association with bone mineral density and body composition in primary antiphospholipid syndrome. For this cross-sectional study 23 premenopausal women with primary antiphospholipid syndrome (Sapporo criteria) and 23 age- and race-matched healthy controls were enrolled. Demographic, anthropometric, clinical and laboratorial data were collected using clinical interview and chart review. Serum 25-hydroxyvitamin D levels, parathormone, calcium and 24-hour urinary calcium were evaluated in all subjects. Bone mineral density and body composition were studied by dual X-ray absorptiometry. The mean age of patients and controls was 33 years. Weight (75.61 [20.73] vs. 63.14 [7.34] kg, p = 0.009), body mass index (29.57 [7.17] vs. 25.35 [3.37] kg, p = 0.014) and caloric ingestion (2493 [1005.6] vs. 1990 [384.1] kcal/day, p = 0.03) were higher in PAPS than controls. All PAPS were under oral anticoagulant with INR within therapeutic range. Interestingly, biochemical bone parameters revealed lower levels of 25-hydroxyvitamin D [21.64 (11.26) vs. 28.59 (10.67) mg/dl, p = 0.039], serum calcium [9.04 (0.46) vs. 9.3 (0.46) mg/dl, p = 0.013] and 24-hour urinary calcium [106.55 (83.71) vs. 172.92 (119.05) mg/d, p = 0.027] in patients than in controls. Supporting these findings, parathormone levels were higher in primary antiphospholipid syndrome than in controls [64.82 (37.83) vs. 44.53 (19.62) pg/ml, p = 0.028]. The analysis of osteoporosis risk factors revealed that the two groups were comparable (p > 0.05). Lumbar spine, femoral neck, total femur and whole body bone mineral density were similar in both groups (p > 0.05). Higher fat mass [28.51 (12.93) vs. 20.01 (4.68) kg, p = 0.005] and higher percentage of fat [36.08 (7.37) vs. 31.23 (4.64)%, p = 0.010] were observed in PAPS in comparison with controls; although no difference was seen regarding lean mass. In summary, low vitamin D in primary antiphospholipid syndrome could be secondary to higher weight and fat mass herein observed most likely due to adipocyte sequestration. This weight gain may also justify the maintenance of bone mineral density even with altered biochemical bone parameters.

In conclusion, this study is the first demonstration of bone microstructure and strength deficits in JoSLE patients, particularly at the distal radius. Our results demonstrated that VF was associated with trabecular radius alteration and emphasized the potential detrimental effect of disease damage on this condition.

Objective Visceral adipose tissue (VAT) correlates with cardiovascular risk factors and has never been assessed in systemic lupus erythematosus (SLE). Our aim was to evaluate VAT in premenopausal SLE patients. Methods Sixty-three premenopausal SLE patients and 186 age-matched healthy women were included. Demographic, anthropometric, disease and treatment parameters were evaluated. VAT was measured by dual X-ray absorptiometry (DXA) with APEX 4.0 software. Results SLE patients had a disease duration of 5.25 ± 3.80 years, SLEDAI activity score of 4.35 ± 5.13, SLICC/ACR-DI of 0.70 ± 0.80, current prednisone dose of 11.60 ± 12.10 mg/day and cumulative glucocorticoid dose of 22.34 ± 12.94 g. Overweight/obese SLE patients and controls had similar VAT parameters ( p > 0.05). Among individuals with BMI <25 kg/m, SLE patients and controls had similar weight, fat mass and fat percentage ( p > 0.05) but patients had higher values of VAT parameters (VAT mass: 260.60 ± 117.23 vs. 194.77 ± 71.42 g, p = 0.001; VAT area: 54.05 ± 24.30 vs. 40.40 ± 14.82 cm, p = 0.001; VAT volume: 281.75 ± 126.81 vs. 210.61 ± 77.29 cm, p = 0.001) and trunk/limb fat mass ratio (0.78 ± 0.21 vs. 0.67 ± 0.12, p = 0.002) compared to controls. In SLE, VAT area correlated with weight ( r = 0.66, p < 0.001), non-HDL cholesterol ( r = 0.53, p < 0.001), LDL cholesterol ( r = 0.48, p < 0.001) and triglycerides ( r = 0.33, p = 0.008), but not with disease duration, SLEDAI, SLICC/ACR-DI or current glucocorticoid use ( p > 0.05). Conclusion This study provides original evidence that SLE is associated with increased VAT and altered adiposity distribution. The correlation with traditional risk factors for cardiovascular disease, independent of current glucocorticoid dose and disease activity, suggests the role of visceral fat as an additional tool for risk assessment in these young patients.

NCT01892748.