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Dissecting the Environmental Underpinnings of Primary Biliary Cirrhosis.

机译：剖析原发性胆汁性肝硬化的环境基础。

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摘要

Background: Primary biliary cirrhosis is a cholestatic liver disease characterized by immune-mediated destruction of bile ducts. Its pathogenesis is largely unknown, yet likely a result of complex interactions between environment and genetic predisposition. Aim: To identify environmental risk factors associated with disease development and clinical outcomes using detailed patient questionnaires and biochemical response to Ursodeoxycholic Acid. Methods: Questionnaire data were prospectively collected from subsets of the Mayo Clinic Primary Biliary Cirrhosis Genetic Epidemiology Registry. Biochemical response was assessed via the Toronto criteria within 2 years of treatment start. Case and control responses were compared using logistic regression, adjusting for recruitment age, sex, and education level. Categorical data were analyzed using chi-square tests and continuous data were analyzed using Wilcoxon rank sum tests. Survival was estimated starting at 2 years following initiation of UDCA treatment when subjects were classified as responders or non-responders. Results: History and duration of smoking, second-hand smoke exposure, autoimmune disease, and having a first- (but not a second-) degree relative with PBC are associated with increased PBC risk. Further dissection of coffee exposure revealed decreased coffee consumption among patients with PSC, but not PBC. Finally, the application of the Toronto criteria performed well to assess biochemical response to Ursodeoxycholic Acid among PBC in the MCPGE Registry. Conclusion: Environmental risks and treatment response to therapy may represent an approach to dichotomize PBC and further refine our understanding of disease underpinnings using an integrative approach.
机译：背景：原发性胆汁性肝硬化是一种以免疫介导的胆管破坏为特征的胆汁淤积性肝病。其发病机理很大程度上未知，但很可能是环境与遗传易感性之间复杂相互作用的结果。目的：通过详细的患者问卷调查和对熊去氧胆酸的生化反应，确定与疾病发展和临床结果相关的环境危险因素。方法：前瞻性地从Mayo诊所原发性胆汁性肝硬化遗传流行病学注册表的子集中收集问卷数据。在治疗开始后的两年内，通过多伦多标准评估了生化反应。使用逻辑回归比较病例和对照的反应，调整招聘年龄，性别和教育水平。使用卡方检验分析分类数据，并使用Wilcoxon秩和检验分析连续数据。当受试者被分类为有反应者或无反应者时，估计从开始UDCA治疗后2年开始生存。结果：吸烟史，持续时间，二手烟暴露，自身免疫性疾病以及相对于PBC具有一等（但不是二等）学位与PBC风险增加相关。进一步剖析咖啡暴露可发现PSC患者（而非PBC）的咖啡消耗减少。最后，多伦多标准的应用在评估MCPGE注册中心中PBC中对熊去氧胆酸的生化反应方面表现良好。结论：环境风险和治疗对治疗的反应可能代表了一种将PBC二分法，并通过综合方法进一步完善了我们对疾病基础的理解。

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  • 作者

    Lammert, Craig.;

  • 作者单位

    College of Medicine - Mayo Clinic.;

  • 授予单位 College of Medicine - Mayo Clinic.;
  • 学科 Medicine.;Environmental health.
  • 学位 M.S.
  • 年度 2015
  • 页码 91 p.
  • 总页数 91
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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