目的:Omega-3多不饱和脂肪酸(PUFAs)在调节炎症和脂质代谢中起关键作用。这项研究旨在确定SLE患者中omega-3缺乏的频率,并研究补充磷虾油浓缩物(KOC)是否可以补充omega-3水平并降低SLE疾病的活动性。
方法:多中心,随机化,双盲,我们在患有活动性SLE的成年患者中进行了安慰剂对照试验.符合条件的患者在前24周随机接受4克/天的KOC或安慰剂(植物油混合物),此后,患者可以选择进入开放标签扩展。主要终点是红细胞Omega-3指数从基线到第24周的改善。临床特征的变化,包括SLE疾病活动指数2000(SLEDAI-2K)疾病活动评分,也被监控。
结果:78名符合入选标准的患者被随机分为治疗组(每组39名)。整个SLE队列中的基线Omega-3指数平均为4.43%(±SD1.04%)。KOC治疗4周后,Omega-3指数迅速增加到7.17%±1.48%(n=38),24周后增加到8.05%±1.79%(n=25)(与基线相比,每个p<0.001),而接受安慰剂的患者与基线相比无显著变化.在接受KOC治疗的患者中,Omega-3指数的增加持续到第48周。患者在24周时从安慰剂转为KOC后,平均Omega-3指数显示快速且显着增加(从第24周(n=26)的4.63%±1.39%增加到第48周(n=12)的7.50%±1.75%;p<0.001)。尽管在整个研究人群中疾病活动没有变化,在24周的随机分组期间,KOC组的SLEDAI-2K评分在基线时具有高疾病活动度(SLEDAI-2K≥9)的患者中显著下降(p=0.04,p=0.02和p=0.01,与安慰剂相比,4、8和16周,分别;每组n=9)。科威特石油公司耐受性良好,没有重大的安全问题。
结论:KOC纠正了SLE患者的omega-3缺乏。补充KOC是安全的,并且在患有更活跃疾病的人中降低了疾病活动性。这些发现保证了在SLE的管理中使用KOC补充omega-3脂肪酸的进一步评估。
背景:NCT03626311。
OBJECTIVE: Omega-3 polyunsaturated fatty acids (PUFAs) play a critical role in regulating inflammation and lipid metabolism. This study sought to ascertain the frequency of omega-3 deficiency in patients with SLE and investigate whether supplementation with krill oil concentrate (KOC) could replenish omega-3 levels and decrease SLE disease activity.
METHODS: A multicentre, randomised, double-blind, placebo-controlled trial was conducted in adult patients with active SLE. Eligible patients were randomised to receive 4 g/day KOC or placebo (vegetable oil mixture) for the first 24 weeks, and thereafter patients could opt to enter an open-label extension. The primary end point was improvement of the red blood cell Omega-3 Index from baseline to week 24. Changes in clinical features, including SLE Disease Activity Index 2000 (SLEDAI-2K) disease activity scores, were also monitored.
RESULTS: Seventy-eight patients met eligibility criteria and were randomised to a treatment group (n=39 per group). The baseline Omega-3 Index in the total SLE cohort was a mean 4.43% (±SD 1.04%). After 4 weeks of KOC treatment, the Omega-3 Index rapidly increased to 7.17%±1.48% (n=38) and after 24 weeks to 8.05%±1.79% (n=25) (each p<0.001 vs baseline), whereas no significant change from baseline was noted in patients receiving placebo. Increases in the Omega-3 Index in KOC-treated patients persisted through week 48. After patients switched from placebo to KOC at 24 weeks, the mean Omega-3 Index showed a rapid and significant increase (from 4.63%±1.39% at week 24 (n=26) to 7.50%±1.75% at week 48 (n=12); p<0.001). Although there were no changes in disease activity in the study population overall, SLEDAI-2K scores decreased significantly in the KOC group during the 24-week randomised period among those who had high disease activity at baseline (SLEDAI-2K ≥9) (p=0.04, p=0.02 and p=0.01 vs placebo at 4, 8 and 16 weeks, respectively; n=9 per group). KOC was well-tolerated, with no significant safety concerns.
CONCLUSIONS: KOC corrected omega-3 deficiency in patients with SLE. Supplementation with KOC was safe and decreased disease activity in those with more active disease. These findings warrant further evaluation of omega-3 fatty acid supplementation with KOC in the management of SLE.
BACKGROUND: NCT03626311.