Mouyis M, Ostor A J K, Crisp A J, Ginawi A, Halsall D J, Shenker N, Poole K E S
Box 157, Department of Medicine, Division of Bone Research, University of Cambridge, Addenbrooke's Hospital, Cambridge, CB2 2QQ, UK.
Rheumatology (Oxford). 2008 Sep;47(9):1348-51. doi: 10.1093/rheumatology/ken203. Epub 2008 May 22.
A role for vitamin D in the pathogenesis of autoimmune and inflammatory diseases is emerging. We undertook an audit of 25-hydroxyvitamin D (25OHD) investigation and treatment in rheumatology outpatients.
Serum 25OHD requests were matched to electronic medical records from rheumatology and metabolic bone clinics (April 2006-March 2007). Data were analysed separately for two groups, 'Documented osteoporosis/osteopaenia' (Group 1) and 'General rheumatology outpatients' (Group 2, sub-divided by diagnosis). Hypovitaminosis D was defined by 25OHD levels <50 nmol/l. Values were compared with healthy adults to calculate geometric z-scores.
A total of 263 patients were included (Group 1, n = 122; Group 2, n = 141) with an overall median 25OHD of 44 nmol/l. The 25OHD level among general rheumatology patients (median 39 nmol/l, mean z score -1.2, was statistically significantly lower than among osteoporotic/osteopaenic patients (median 49 nmol/l, mean z score of -0.9, p < 0.05 for the difference). 25OHD was lower in inflammatory arthritis and chronic pain/fibromyalgia than in other groups. Prescribing was recorded in 100 in Group 1 (of whom 95% were prescribed calcium/800 IU cholecalciferol) and 83 in Group 2 (91% calcium/800 IU). Only 31% of the patients with 25OHD <50 nmol/l would have been identified using general guidelines for screening patients at 'high risk' of hypovitaminosis D.
Improved guidelines for managing hypovitaminosis D in rheumatology patients are needed. We found a high prevalence of hypovitaminosis D among secondary care patients in rheumatology and widespread supplementation with 800 IU cholecalciferol. Substantially reduced levels of serum 25OHD were identified among patients with inflammatory arthritis and chronic pain.
维生素D在自身免疫性疾病和炎性疾病发病机制中的作用正逐渐显现。我们对风湿病门诊患者的25-羟维生素D(25OHD)检测及治疗情况进行了一次审核。
将血清25OHD检测申请与风湿病和代谢性骨病门诊的电子病历进行匹配(2006年4月至2007年3月)。对“确诊骨质疏松症/骨质减少症”组(第1组)和“普通风湿病门诊患者”组(第2组,按诊断细分)分别进行数据分析。维生素D缺乏症定义为25OHD水平<50 nmol/L。将这些值与健康成年人进行比较以计算几何z分数。
共纳入263例患者(第1组,n = 122;第2组,n = 141),总体25OHD中位数为44 nmol/L。普通风湿病患者的25OHD水平(中位数39 nmol/L,平均z分数-1.2)在统计学上显著低于骨质疏松症/骨质减少症患者(中位数49 nmol/L,平均z分数-0.9,差异p < 0.05)。炎性关节炎和慢性疼痛/纤维肌痛患者的25OHD水平低于其他组。第1组有100例记录了处方用药(其中95%被处方了钙/800 IU胆钙化醇),第2组有83例(91%为钙/800 IU)。按照维生素D缺乏症“高危”患者筛查的一般指南,只有31%的25OHD<50 nmol/L的患者会被识别出来。
需要改进管理风湿病患者维生素D缺乏症的指南。我们发现二级护理的风湿病患者中维生素D缺乏症的患病率很高,并且广泛补充800 IU胆钙化醇。在炎性关节炎和慢性疼痛患者中发现血清25OHD水平大幅降低。