From the authors:
我们非常感谢González-García和C. torres-Duque的信,以回应我们的论文,比较了烟草烟雾中慢性阻塞性肺疾病(COPD)的不同表型相对生物质烟雾引起的COPD [1]。The information they provide from publications that we failed to cite strengthens the case for our conclusions and contributes to a better understanding of COPD sub-phenotypes.
一种phenotype, according to Agusti[[2], is the end result of the interaction between the genotype, the environment, and some degree of random variation that facilitates and/or limits these gene–environment interactions. The aim of phenotyping is to identify homogeneous groups of patients who have a different clinical course or who respond to specific therapeutic interventions. In COPD, this is an established strategy used to better understand subjects with the disease; the “pink puffer” and the “blue bloater” were the best known early phenotypes. Agusti[[2]表明,临床表型应至少预测一个临床相关结果,表明这需要纵向监测。
Our findings suggest that COPD associated with biomass exposure is a clinical phenotype with clear differences to COPD associated with tobacco smoking [[1,,,,3]。González-García和C. torres-duque的非常有趣的评论补充了与生物质暴露相关的COPD是与气道障碍有关的表型,而不是与肺气肿相关的表型。但是,尽管有大量的横断面证据[[4-7),生物质烟引起不同的表达式of COPD, there is a paucity of data on the clinical implications of this difference; for instance, is this phenotype related to a greater or lower mortality, or an accelerated or slower decline in forced expiratory volume in 1 s? As usual, much work remains to be done to discover the importance of these now well-established phenotypic differences.
Footnotes
Conflict of interest: Disclosures can be found alongside the online version of this article atwww.www.qdcxjkg.com
- received2014年2月12日。
- 公认February 18, 2014.
- ©ERS 2014