窄谱中波紫外线联合阿维A治疗中重度银屑病疗效观察被引量：2

导出

摘要目的探讨窄谱中波紫外线联合阿维A治疗中重度银屑病的临床疗效。方法选择38例中重度银屑病患者,随机分为对照组和实验组各19例,对照组给予窄谱中波紫外线(NB-UVB)照射治疗,实验组采用NB-UVB联合阿维A同时治疗,观察比较两组患者的临床疗效以及银屑病皮损面积和严重程度(PASI)、皮肤病生活质量指数(DLQI)。结果实验组的临床疗效明显优于对照组,且实验组患者的PASI和DLQI指标明显低于对照组,两组比较差异具有统计学意义(P<0.05)。结论窄谱中波紫外线联合阿维A治疗中重度银屑病疗效显著,具有较高的临床价值,值得推广应用。

作者冯维勇

机构地区广东省云浮市慢性病防治中心

出处《中国现代药物应用》 2014年第2期118-119,共2页 Chinese Journal of Modern Drug Application

关键词窄谱中波紫外线阿维A 中重度银屑病疗效观察

分类号 R758.63 [医药卫生—皮肤病学与性病学]

引文网络
相关文献

参考文献3

1宋国刚.NB-UVB联合阿维A治疗寻常性银屑病40例[J].中国中西医结合皮肤性病学杂志,2012,11(1):56-56. 被引量：4
2Marks R, Barton SP, Shuttleworth D,et al. Assessment of disease progress in psoriasis. Arch Dermatol, 1989,125 (2) :235-240.
3孔一真,甄莉.寻常型银屑病患者皮损中HBD-2、IL-1β和NF-κBp65表达的研究[J].中国医药导报,2011,8(1):27-28. 被引量：8

二级参考文献14

1顾有守.中、重度银屑病的联合疗法[J].临床皮肤科杂志,2005,34(3):196-198. 被引量：47
2田夫军,赵天恩.NB-UVB和PUVA在银屑病治疗中的应用现状[J].中国麻风皮肤病杂志,2006,22(6):484-486. 被引量：4
3Welhkamp K,Sechwichtenberg L,Schroder JM,et al.Pseudomonas aeruginosa and IL-1 beta-mediated induction of human beta-defensin-2 in keratinocytes is controlled by Nf-kappaB and AP-1[J].J Inwest Dermatol,2006,126:121-127.
4Wehkamp J,Harder J,Wehkamp K,et al.NF-kappa B-and AP-1-mediated induction of human beta defensin-2 in intestinal epithelial ceils by Escherichia coil Nissle 1917:a novel effect of a probiotie bacterium[J].Infect Immun,2004,72(10):5750-5758.
5Tsutsumi-Ishii Y,Nagaoka I.NF-kappa B-mediated transcriptional regulation of human beta-defensin-2 gene following lipopolysaccharide stimulation[J].J Leukoc Biol,2002,71(1):154-162.
6Tsutsumi Y,Nagaoka I.Modulation of human beta-de-fensin-2 transcription in pulmonary epithelial cells by lipopolysaceharide-stimulated mononuclear phagocytes viaproinflammatory cytokine production[J].J Immunol,2003,170(8):4226.
7Jang BC,Ki JL,Paik JH,et al.Up-regulation of human β-defensin 2 by interleukin-1β in A549 cells:involvement of PI3K,PKC,p38 MAPK,JNK,and NF-KB[J].Biochem Biophys Res Commun,2004,320(8):1026-1033.
8Dyror E,Yndestad A,Ueland T,et al.Antiinflammatory effects of tetradecylthioacetie acid involve both peroxisome proliferator-activated receptor alpha-dependent and independent pathways[J].J Arterioscler Thromb Vasc Biol,2005,25(7):1364-1369.
9Wittmann M,Purwar R,Hartmann C,et al.Human keratinocytes respend to interleukin-18:implication for the course of chronic inflammatory skin diseases[J].J Invest Dermatol,2005,124(6):1225-1233.
10Krueger JG,Bowcock A.Psoriasis pathophysiology:current concepts of pathogenesis[J].Ann Rheum Dis,2005,64(1):30-36.