Arthr Res & Ther:来那度胺或成为治疗皮肤红斑狼疮的有效疗法
2013-05-06 T.Shen 生物谷
2012年12月8日 讯 /生物谷BIOON/ --尽管目前有一些疗法可以用于治疗皮肤红斑狼疮(CLE),但是有些人群对于对这些疗法没有响应或者失败,那么就需要科学家开发出新的疗法来应对此疾病。近日一项刊登在国际杂志Arthritis Research & Therapy上的研究报告指出,使用来那度胺(Lenalidomide)治疗CLE变得安全,其可以再两周时间内看到疗效。 来那度胺(
2012年12月8日 讯 /生物谷BIOON/ --尽管目前有一些疗法可以用于治疗皮肤红斑狼疮(CLE),但是有些人群对于对这些疗法没有响应或者失败,那么就需要科学家开发出新的疗法来应对此疾病。近日一项刊登在国际杂志Arthritis Research & Therapy上的研究报告指出,使用来那度胺(Lenalidomide)治疗CLE变得安全,其可以再两周时间内看到疗效。
来那度胺(Lenalidomide)被认为是潜在的,低毒、可选择性的一种治疗性药物,此前研究揭示了其治疗的一些可喜结果。为了检测其治疗皮肤红斑狼疮的效用,来自瓦尔德希伯伦大学医院的研究者对于15位年龄在7-30岁的CLE患者进行了II期临床试验。
经过临床治疗后,所有人病情都有了明显改善,86%的参与者完全有反应,其CLASI分值为0,,但是四分之三的由于进行来那度胺治疗病情得到改善的患者,在停药或者药物减少2至8星期内,其病情就会复发。
这项研究中给患者所带来的副作用较小,仅有2人报告表现出副作用,研究者Josep Ordi-Ros解释道,相比其它临床试验,这项研究所引发的较小的副作用是由于低剂量的来那度胺所引发的。在治疗后的15个月,我们并没有看到任何系统性红斑狼疮(SLE)的效应,这种新型疗法对于降低CLE所引发的反应比较有效,其和沙立度胺所治疗的效果一样,相比沙立度胺,来那度胺所引发的毒性较低一些。
这项研究虽然相对规模较小,可是其揭示了使用来那度胺在治疗皮肤红斑狼疮上所带来的疗效,这就为研究者开发新型疗法提供了希望。
与红斑狼疮相关的拓展阅读:
- AJHG:全基因组关联Meta分析搜寻系统性红斑狼疮易感基因
- Arthr Res & Ther:来那度胺或成为治疗皮肤红斑狼疮的有效疗法
- Lupus:血清肿瘤坏死因子-α水平与系统性红斑狼疮患者的生活质量和抑郁症状相关
- Blood:红斑狼疮治疗药不增加淋巴瘤风险
- 反应停联合羟氯喹治疗皮肤型红斑狼疮或更佳
- JAAD:反应停治疗皮肤型红斑狼疮需警惕卒中
- 补充维生素D有助治疗红斑狼疮
- 用抗疟药治疗皮肤型红斑狼疮需要耐心
- 专家视点—红斑狼疮患者妊娠的特殊挑战
- J Immunol:葡萄球菌可能是红斑狼疮的致病因素
- PLoS ONE:左建平等青蒿素衍生物治疗系统性红斑狼疮研究再获进展
- 孙凌云:系统性红斑狼疮(SLE)药物治疗研究进展
- 回顾系统性红斑狼疮的十年研究进展 更多信息请点击:有关红斑狼疮更多资讯
doi:10.1186/ar3818
PMC:
PMID:
Bias in effect size of systemic lupus erythematosus susceptibility loci across Europe: a case-control study.
Alonso-Perez E, Suarez-Gestal M, Calaza M, Sebastiani GD, Pullmann R, Papasteriades C, Kovacs A, Skopouli FN, Bijl M, Suarez A, Marchini M, Migliaresi S, Carreira P, Ordi-Ros J, Witte T, Ruzickova S, Santos MJ, Barizzone N, Blanco FJ, Lauwerys BR, Gomez-Reino JJ, Gonzalez A; European Consortium of SLE DNA Collections.
INTRODUCTION: We aimed to investigate whether the effect size of the systemic lupus erythematosus (SLE) risk alleles varies across European subpopulations. METHODS: European SLE patients (n = 1,742) and ethnically matched healthy controls (n = 2,101) were recruited at 17 centres from 10 different countries. Only individuals with self-reported ancestry from the country of origin were included. In addition, participants were genotyped for top ancestry informative markers and for 25 SLE associated SNPs. The results were used to compare effect sizes between the Central Eureopan and Southern European subgroups. RESULTS: Twenty of the 25 SNPs showed independent association with SLE, These SNPs showed a significant bias to larger effect sizes in the Southern subgroup, with 15/20 showing this trend (P = 0.019) and a larger mean odds ratio of the 20 SNPs (1.46 vs. 1.34, P = 0.02) as well as a larger difference in the number of risk alleles (2.06 vs. 1.63, P = 0.027) between SLE patients and controls than for Central Europeans. This bias was reflected in a very significant difference in the cumulative genetic risk score (4.31 vs. 3.48, P = 1.8 × 10-32). Effect size bias was accompanied by a lower number of SLE risk alleles in the Southern subjects, both patients and controls, the difference being more marked between the controls (P = 1.1 × 10-8) than between the Southern and Central European patients (P = 0.016). Seven of these SNPs showed significant allele frequency clines. CONCLUSION: Our findings showed a bias to larger effect sizes of SLE loci in the Southern Europeans relative to the Central Europeans together with clines of SLE risk allele frequencies. These results indicate the need to study risk allele clines and the implications of the polygenic model of inheritance in SLE.
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