*Department of Pediatrics, Emory University School of Medicine, Atlanta, Georgia; †Division of Gastroenterology, Hepatology and Nutrition, Children's Healthcare of Atlanta, Atlanta, Georgia; ‡Nutrition and Health Sciences Program, Laney Graduate School, Emory University, Atlanta, Georgia; §Department of Medicine, Emory University School of Medicine; and ‖Atlanta VA Medical Center, Atlanta, Georgia.
Inflamm Bowel Dis. 2017 Sep;23(9):1650-1658. doi: 10.1097/MIB.0000000000001178.
Anemia, iron deficiency, and hypovitaminosis D are well-known comorbidities in inflammatory bowel disease (IBD). Epidemiologic studies have linked vitamin D deficiency with increased risk of anemia, and in vitro studies suggest that vitamin D may improve iron recycling through downregulatory effects on hepcidin and proinflammatory cytokines.
We aimed to investigate the association of vitamin D status with inflammation, iron biomarkers, and anemia in pediatric IBD. Cross-sectional data were obtained from N = 69 patients with IBD aged 5 to <19 years. Iron biomarkers (ferritin, soluble transferrin receptor), and 25-hydroxyvitamin D (25(OH)D), inflammatory biomarkers (C-reactive protein and α-1-acid glycoprotein), hepcidin, and hemoglobin were collected. Iron biomarkers were regression corrected for inflammation. Multivariable logistic/linear models were used to examine the associations of 25(OH)D with inflammation, iron status, hepcidin, and anemia.
Approximately 50% of subjects were inflamed (C-reactive protein >5 mg/L or α-1-acid glycoprotein >1 g/L). Iron deficiency prevalence (inflammation-corrected ferritin <15 μg/L or soluble transferrin receptor >8.3 mg/L) was 67%; anemia was 36%, and vitamin D insufficiency (25(OH)D <30 ng/mL) was 77%. In linear regression models, vitamin D insufficiency was associated with increased hepcidin levels (β [SE] = 0.6 [0.2], P = 0.01) and reduced hemoglobin (β [SE] = -0.9 [0.5], P = 0.046), controlling for age, sex, race, insurance status, body mass index for age, inflammation, disease diagnosis (ulcerative colitis versus Crohn's disease), and disease duration, compared with 25(OH)D ≥30 ng/mL.
Our results suggest that concentrations of 25(OH)D ≥30 ng/mL are associated with lower hepcidin and higher hemoglobin levels. Further research is needed to clarify the association of vitamin D with inflammation, iron status, and anemia in pediatric IBD.
贫血、缺铁和维生素 D 缺乏是炎症性肠病（IBD）的常见合并症。流行病学研究表明，维生素 D 缺乏与贫血风险增加有关，体外研究表明，维生素 D 可能通过下调铁调素和促炎细胞因子来改善铁的再循环。
我们旨在研究维生素 D 状态与儿科 IBD 中的炎症、铁生物标志物和贫血之间的关系。从年龄在 5 至<19 岁的 69 名 IBD 患者中获得横断面数据。收集了铁生物标志物（铁蛋白、可溶性转铁蛋白受体）和 25-羟维生素 D（25(OH)D）、炎症生物标志物（C 反应蛋白和α-1-酸性糖蛋白）、铁调素和血红蛋白。铁生物标志物经炎症校正后进行回归。使用多元逻辑/线性模型检查 25(OH)D 与炎症、铁状态、铁调素和贫血的关系。
大约 50%的患者存在炎症（C 反应蛋白>5mg/L 或α-1-酸性糖蛋白>1g/L）。缺铁患病率（经炎症校正的铁蛋白<15μg/L 或可溶性转铁蛋白受体>8.3mg/L）为 67%；贫血患病率为 36%，维生素 D 不足（25(OH)D<30ng/mL）为 77%。在线性回归模型中，与 25(OH)D≥30ng/mL 相比，维生素 D 不足与铁调素水平升高（β[SE] = 0.6[0.2]，P = 0.01）和血红蛋白降低相关（β[SE] = -0.9[0.5]，P = 0.046），校正年龄、性别、种族、保险状况、年龄体重指数、炎症、疾病诊断（溃疡性结肠炎与克罗恩病）和疾病持续时间。
我们的结果表明，25(OH)D 浓度≥30ng/mL 与较低的铁调素和较高的血红蛋白水平相关。需要进一步研究以阐明维生素 D 与儿科 IBD 中的炎症、铁状态和贫血之间的关系。
