期刊文献+

二肽基肽酶-4抑制剂致大疱性类天疱疮国内外文献分析 被引量:2

Bullous pemphigoid induced by dipeptidyl peptidase-4 inhibitors:an analysis of domestic and foreign literature
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摘要 目的:分析二肽基肽酶-4抑制剂致大疱性类天疱疮的发生规律及特点,为安全用药提供参考。方法:检索中国学术期刊全文数据库、维普中文科技期刊数据库、万方数据库和Pubmed数据库收载的二肽基肽酶-4抑制剂致大疱性类天疱疮文献并进行分析。结果:21例不良反应中,男性11例,女性10例,年龄60岁及以上患者20例(95.2%)。21例患者中,服用维格列汀者15例,服用西格列汀者3例,服用利拉列汀者3例。用药至发生大疱性类天疱疮的时间为1~37个月,平均时间8个月。结论:临床医师应了解二肽基肽酶-4抑制剂致大疱性类天疱疮的规律和特点,加强用药监测,以便及时发现和处理大疱性类天疱疮。 Objective: To analyze the general patterns and characteristics of bullous pemphigoid( BP)induced by dipeptidyl peptidase-4( DPP-4) inhibitors and to provide references for the clinical medication.Methods: BP of DPP-4 inhibitors reported in domestic and foreign academic journals via China National Knowledge Infrastructure( CNKI),Wanfang databases,VIP and Pubmed were collected and analyzed statistically. Results:Totally 21 cases of BP induced by DPP-4 inhibitors were collected,including 11 men and 10 women. Patients over the age of 60 years showed the higher incidence( n = 20,95. 2%). 21 cases of BP induced by DPP-4 inhibitors included vildagliptin( n = 15),sitagliptin( n = 3) and linagliptine( n = 3). The average time was 8 months( range 1 ~ 37 months). Conclusion: Clinicians should be aware of the rules and characteristics of BP induced by DPP-4 inhibitors,and strengthen monitoring to detect and deal with DPP-4 inhibitors induced BP in time.
作者 程军
出处 《中国新药杂志》 CAS CSCD 北大核心 2017年第18期2237-2240,共4页 Chinese Journal of New Drugs
关键词 二肽基肽酶-4抑制剂 大疱性类天疱疮 文献分析 dipeptidyl peptidase-4 inhibitors bullous pemphigoid(BP) literature analysis
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  • 1Bolognia JL, Jorizzo JL, Schaffer JV. Dermatology[M]. 3rd Ed. USA: Elsevier, 2012: Chapter 28.
  • 2Van den Bergh F, Giudiee GJ. BP180 (type XVII collagen) and its role in cutaneous biology and disease[J]. Adv Dermatol, 2003, 19: 37-71.
  • 3Seppanen A, Suuronen T, Hofmann SC, et al. Distribution of collagen XVII in the human brain[J]. Brain Res, 2007, 1158: 50-56.
  • 4Van den Bergh F, Fu CL, Olague Marchan M, et al. The NC16A domain of collagen XVII plays a role in triple helix assembly and stability[J]. Biochem Biophys Res Commun, 2006, 350(4): 1032-1037.
  • 5Mihai S, Sitaru C. Immunopathology and molecular diagnosis of autoimmune bullous diseases [J]. J Cell Mol Med, 2007, 11(3): 462-481.
  • 6Tasanen K, Tunggal L, Chometon G, et al. Keratinocytes from patients lacking collagen XVII display a migratory phenotype[J]. Am J Pathol, 2004, 164(6): 2027-2038.
  • 7Qiao H, Shibaki A, Long HA, et al. Collagen XVII participates in keratinocyte adhesion to collagen IV, and in p38MAPK-dependent migration and cell signaling [J]. J Invest Dermatol, 2009, 129(9): 2288-2295.
  • 8Van den Bergh F, Eliason SL, Giudice GJ. Type XVII collagen (BP180) can function as a cell-matrix adhesion molecule via binding to laminin 332[J]. Matrix Biol, 2011, 30(2): 100-108.
  • 9Baldo M, Bhogal B, Groves RW, et al. Childhood vulval lichen sclerosus: autoimmunity to the basement membrane zone protein BP180 and its relationship to autoimmunity[J]. Clin Exp Dermatol, 2010, 35(5): 543-545.
  • 10Baldo M, Bailey A, Bhogal B, et al. T cells reactive with the NC16A domain of BP180 are present in vulval lichen sclerosus and lichen planus [J]. J Eur Acad Dermatol Venereol, 2010, 24(2): 186-190.

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