Haifer Craig, Lawrance Ian C, Center Jacqueline R, Clarke Michael W, Hart Prue H, Eisman John A, Lucas Robyn, Ghaly Simon
Department of Gastroenterology, St Vincent's Hospital, 390 Victoria St, Darlinghurst, NSW 2010, Australia.
St John of God Hospital, Centre for Inflammatory Bowel Disease, Subiaco, Australia.
Therap Adv Gastroenterol. 2019 Jul 26;12:1756284819865144. doi: 10.1177/1756284819865144. eCollection 2019.
Vitamin D deficiency is associated with active Crohn's disease (CD). However, it remains unclear if lower 25-hydroxyvitamin D [25(OH)D] concentration is the cause, or consequence, of intestinal inflammation. Existing literature has focused on circulating 25(OH)D rather than the active metabolite 1,25(OH)D, or its breakdown product, 24,25(OH)D. We aimed to characterise vitamin D metabolism in a cohort of patients with active and inactive CD.
Fifty-four patients with CD and not on corticosteroids or vitamin D supplements, were enrolled in a 6-month prospective cohort study. Sera were collected on enrolment and at 6 months and tested for 25(OH)D, 1,25(OH)D, 24,25(OH)D using liquid chromatography tandem mass spectroscopy as well as vitamin-D-binding protein.
There were no differences in 25(OH)D or 1,25(OH)D levels between participants with active inactive disease. Levels of 24,25(OH)D were significantly lower in those with active compared with inactive disease (mean 3.9 6.0 µmol/l; = 0.007) and therefore the ratio of 25(OH)D:24,25(OH)D was higher (mean 17.3 11.1; = 0.001). In those patients with active disease who achieved remission, there was a mean increase in 25(OH)D of 32.3 nmol/l (i.e. to a level in the sufficient range) and 24,25(OH)D of 2.1 µmol/l. These increases were not seen in patients with persistently active or inactive disease.
Levels of 24,25(OH)D, but not 25(OH)D, were lower in patients with active CD, and spontaneously increased with resolution of underlying inflammation. The utility of 24,25(OH)D as a biomarker of disease activity and vitamin D status in CD warrants further exploration.
维生素D缺乏与活动性克罗恩病(CD)相关。然而,尚不清楚较低的25-羟基维生素D[25(OH)D]浓度是肠道炎症的原因还是结果。现有文献主要关注循环中的25(OH)D,而非活性代谢物1,25(OH)D或其分解产物24,25(OH)D。我们旨在描述一组活动性和非活动性CD患者的维生素D代谢情况。
54例未使用皮质类固醇或维生素D补充剂的CD患者纳入一项为期6个月的前瞻性队列研究。在入组时和6个月时采集血清,采用液相色谱串联质谱法以及维生素D结合蛋白检测25(OH)D、1,25(OH)D、24,25(OH)D。
活动性和非活动性疾病患者的25(OH)D或1,25(OH)D水平无差异。与非活动性疾病患者相比,活动性疾病患者的24,25(OH)D水平显著降低(平均3.9对6.0µmol/l;P = 0.007),因此25(OH)D:24,25(OH)D的比值更高(平均17.3对11.1;P = 0.001)。在病情缓解的活动性疾病患者中,25(OH)D平均升高32.3nmol/l(即达到充足范围水平),24,25(OH)D平均升高2.1µmol/l。持续活动性或非活动性疾病患者未出现这些升高。
活动性CD患者的24,25(OH)D水平较低,而非25(OH)D水平,且随着潜在炎症的消退而自发升高。24,25(OH)D作为CD疾病活动和维生素D状态生物标志物的效用值得进一步探索。