Epidemiology of fecal mutagenicity.
Epidemiology of fecal mutagenicity.
复制标题
粪便致突变性的流行病学。
DOI：
10.1093/oxfordjournals.epirev.a036297
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发表时间：
1986
影响因子：
5.5
通讯作者：
M. Schiffman
中科院分区：
文献类型：
--
作者：
M. Schiffman
粪便致突变性存在独特的测量困难(63)；然而，粪便致突变性的人群研究是结直肠癌流行病学的常见方法学问题的典型。例如，相关研究已经将粪便的诱变性与结直肠癌的发病率以及可能增加结直肠癌风险的饮食习惯联系在一起。然而，生态学谬误的威胁对生化分析和其他流行病学数据一样强烈。粪便致突变性可能与高脂肪或低纤维摄入一起，仅仅代表了高危人群中仍未阐明的某些真实危险因素的相关性。另一方面，饮食试验可能会直接证实饮食对粪便诱变性(或另一个假定的“中间终点”)的影响，但不能直接解决诱变性与结直肠癌风险的关系。粪便致突变性的病例对照比较最初似乎提供了关于结直肠癌风险的更令人信服的证据，但实际上并不合适，因为疾病影响这种“暴露”的可能性是如此之大。具体地说，粪便的致突变性可能会受到诊断结直肠癌所需的临床测试的影响；它也可能受到恶性肿瘤本身的影响，或者间接受到可能伴随胃肠道疾病的饮食调整的影响。由此产生的偏见可能会混淆病例对照比较，就像回忆偏见会影响面试数据一样。因此，在试验用于比较病例和对照标本之前，对粪便致突变性和结直肠癌进行适当的病例对照研究必须考虑诊断工作对每个致突变试验的影响。此外，病例受试者应该在住院和康复期间进行跟踪，希望对一些治愈的患者来说，手术后的测量将排除疾病对暴露的任何影响。一项纳入这些额外努力的病例对照研究目前正在进行中。似乎有理由说，大多数纳入结直肠癌病例对照研究的生化分析将需要类似的修改。此外，即使排除了疾病或卫生保健对生化测量的影响，关于粪便致突变性或其他分析在病例对照研究中的作用的另一个问题仍将存在。在病例对照环境中使用生化测试类似于在病例对照访谈中询问有关当前吸烟或当前饮食的问题。目前的测量值仅反映了曝光变量在受试者一生中保持稳定的程度。
Fecal mutagenicity presents unique difficulties of measurement (63); nonetheless, population studies of fecal mutagenicity typify the common methodological problems of colorectal cancer epidemiology. For example, correlational studies have linked fecal mutagenicity both to colorectal cancer incidence and to dietary practices postulated to increase the risk of colorectal cancer. The threat of an ecologic fallacy, however, is just as strong for biochemical assays as for other epidemiologic data. Fecal mutagenicity may represent, along with high-fat or low-fiber intake, a mere correlate of some true risk factor still to be elucidated in high-risk populations. Dietary trials, on the other hand, may directly confirm the influence of diet on fecal mutagenicity (or another presumed "intermediate end point") but cannot directly address the relationship of mutagenicity to colorectal cancer risk. Case-control comparisons of fecal mutagenicity might initially seem to promise more compelling evidence regarding colorectal cancer risk, but they are actually unsuitable, since the possibility of disease affecting this "exposure" is so strong. Specifically, fecal mutagenicity might be affected by the clinical tests required to diagnose colorectal cancer; it might also be affected by the malignancy itself, or indirectly by the dietary modifications that can accompany gastrointestinal illness. The resultant biases threaten to confound a case-control comparison as much as recall bias can affect interview data. A proper case-control study of fecal mutagenicity and colorectal cancer must therefore consider the effect of diagnostic workup on each mutagenicity assay, before the test is used to compare case and control specimens. In addition, case subjects should be followed through hospitalization and recovery, in the hope that for some cured patients the measurements after surgery will exclude any effect of disease on exposure. A case-control study incorporating these extra efforts is now underway. It seems reasonable to state that most biochemical assays incorporated into case-control studies of colorectal cancer will require similar modifications. Moreover, even if an effect of disease or of health care on biochemical measurements is excluded, an additional concern regarding the role of fecal mutagenicity or other assays in case-control studies will remain. The use of biochemical tests in a case-control context is analogous to asking questions regarding current smoking or current diet in a case-control interview. The current measurements reflect past values only to the degree that the exposure variable remains stable during the subject's lifetime.(ABSTRACT TRUNCATED AT 400 WORDS)