Division of Rheumatology, Tufts Medical Center, Box 406, 800 Washington St, Boston, MA 02111, USA.
JAMA. 2013 Jan 9;309(2):155-62. doi: 10.1001/jama.2012.164487.
Knee osteoarthritis (OA), a disorder of cartilage and periarticular bone, is a public health problem without effective medical treatments. Some studies have suggested that vitamin D may protect against structural progression.
To determine whether vitamin D supplementation reduces symptom and structural progression of knee OA.
DESIGN, SETTING, AND PATIENTS: A 2-year randomized, placebo-controlled, double-blind, clinical trial involving 146 participants with symptomatic knee OA (mean age, 62.4 years [SD, 8.5]; 57 women [61%], 115 white race [79%]). Patients were enrolled at Tufts Medical Center in Boston between March 2006 and June 2009.
Participants were randomized to receive either placebo or oral cholecalciferol, 2000 IU/d, with dose escalation to elevate serum levels to more than 36 ng/mL.
Primary outcomes were knee pain severity (Western Ontario and McMaster Universities [WOMAC] pain scale, 0-20: 0, no pain; 20, extreme pain), and cartilage volume loss measured by magnetic resonance imaging. Secondary end points included physical function, knee function (WOMAC function scale, 0-68: 0, no difficulty; 68, extreme difficulty), cartilage thickness, bone marrow lesions, and radiographic joint space width.
Eighty-five percent of the participants completed the study. Serum 25-hydroxyvitamin D levels increased by a mean 16.1 ng/mL (95% CI, 13.7 to 18.6) in the treatment group and by a mean 2.1 mg/mL (95% CI, 0.5 to 3.7) (P < .001) in the placebo group. Baseline knee pain was slightly worse in the treatment group (mean, 6.9; 95% CI, 6.0 to 7.7) than in the placebo group (mean, 5.8; 95% CI, 5.0 to 6.6) (P = .08). Baseline knee function was significantly worse in the treatment group (mean, 22.7; 95% CI, 19.8 to 25.6) than in the placebo group (mean, 18.5; 95% CI, 15.8 to 21.2) (P = .04). Knee pain decreased in both groups by a mean -2.31 (95% CI, -3.24 to -1.38) in the treatment group and -1.46 (95% CI, -2.33 to -0.60) in the placebo group, with no significant differences at any time. The percentage of cartilage volume decreased by the same extent in both groups (mean, -4.30; 95% CI, -5.48 to -3.12 vs mean, -4.25; 95% CI, -6.12 to -2.39) (P = .96). There were no differences in any of the secondary clinical end points.
Vitamin D supplementation for 2 years at a dose sufficient to elevate 25-hydroxyvitamin D plasma levels to higher than 36 ng/mL, when compared with placebo, did not reduce knee pain or cartilage volume loss in patients with symptomatic knee OA.
clinicaltrials.gov Identifier: NCT00306774.
膝骨关节炎（OA）是一种软骨和关节周围骨的疾病，是一种没有有效医学治疗方法的公共健康问题。一些研究表明，维生素 D 可能具有预防结构进展的作用。
确定维生素 D 补充剂是否能减少膝关节 OA 的症状和结构进展。
设计、地点和患者：一项为期 2 年的随机、安慰剂对照、双盲、临床试验，涉及 146 名有症状的膝骨关节炎患者（平均年龄 62.4 岁[标准差 8.5]；57 名女性[61%]，115 名白种人[79%]）。患者于 2006 年 3 月至 2009 年 6 月在波士顿塔夫茨医疗中心招募。
参与者被随机分配接受安慰剂或口服胆钙化醇，2000IU/d，并逐步增加剂量以将血清水平升高至超过 36ng/ml。
主要结局指标为膝关节疼痛严重程度（西部安大略省和麦克马斯特大学[WOMAC]疼痛量表，0-20：0，无痛；20，极度疼痛）和磁共振成像测量的软骨体积损失。次要终点包括身体功能、膝关节功能（WOMAC 功能量表，0-68：0，无困难；68，极度困难）、软骨厚度、骨髓病变和放射关节间隙宽度。
85%的参与者完成了研究。治疗组血清 25-羟维生素 D 水平平均增加 16.1ng/ml（95%置信区间 13.7-18.6），安慰剂组平均增加 2.1mg/ml（95%置信区间 0.5-3.7）（P<.001）。治疗组的基线膝关节疼痛略高于安慰剂组（平均 6.9；95%置信区间 6.0-7.7）比安慰剂组（平均 5.8；95%置信区间 5.0-6.6）（P=.08）。治疗组的基线膝关节功能明显差于安慰剂组（平均 22.7；95%置信区间 19.8-25.6）比安慰剂组（平均 18.5；95%置信区间 15.8-21.2）（P=.04）。两组的膝关节疼痛均平均下降 2.31（95%置信区间 3.24-1.38），安慰剂组下降 1.46（95%置信区间 2.33-0.60），任何时候均无显著差异。两组的软骨体积减少程度相同（平均-4.30；95%置信区间-5.48-3.12 vs 平均-4.25；95%置信区间-6.12-2.39）（P=.96）。在任何次要临床终点均无差异。
与安慰剂相比，在 2 年内以足以将 25-羟维生素 D 血浆水平升高至 36ng/ml 以上的剂量补充维生素 D，并不能减少有症状的膝骨关节炎患者的膝关节疼痛或软骨体积损失。
clinicaltrials.gov 标识符：NCT00306774。
