Reply to Ito.
Reply to Ito.
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回复伊藤。
DOI：
10.1093/cid/ciac951
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发表时间：
2023
期刊：
影响因子：
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通讯作者：
Kelly,CiaranP
中科院分区：
文献类型：
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作者：
Villafuerte-Gálvez,JavierA;Pollock,NiraR;Alonso,CarolynD;Chen,Xinhua;Xu,Hua;Wang,Lamei;White,Nicole;Banz,Alice;Miller,Mark;Daugherty,Kaitlyn;Gonzalez-Luna,AnneJ;Barrett,Caitlin;Sprague,Rebecca;Garey,KevinW;Kelly,CiaranP
编辑-伊藤博士就我们的非艰难梭菌感染性腹泻(NCD)对照组参与者的选择提出了问题[1，2]。正如作者所提到的，我们的研究发现艰难梭菌感染患者的粪便中IL-1β(IL-1β)浓度明显高于非艰难梭菌感染患者，提示IL-1β可能有助于鉴别艰难梭菌感染和非艰难梭菌感染患者。我们NCD组的患者是从一组住院的腹泻患者中鉴定出来的，这些患者的粪便经核酸扩增试验呈艰难梭菌阴性。所有样本都是作为常规临床护理的一部分获得的。作者正确地指出，我们的NCD群体是异质的。这一队列包括与许多不同情况相关的腹泻患者，可能包括感染性和非感染性腹泻，炎症性和非炎症性腹泻，以及渗透性和分泌性腹泻。唯一明确排除在NCD组之外的是已知的炎症性肠病病史。我们认为这种异质性是一种方法优势，因为它反映了现实世界中腹泻住院患者的队列。我们的对照组反映了临床实践中将考虑进行CDI检测的患者类型。我们承认，我们的发现可能不适用于所有的护理环境，例如卫生条件有限的地区的儿科患者或成人患者，这两个地区的炎症性感染性腹泻的比例可能比我们队列中的高。由其他病原体引起的急性感染性腹泻患者的粪便IL-1β升高是合理的，尽管我们还没有发现专门证实这一假说的文献。我们不认为粪便IL-1β可作为CDI的独立诊断试验。相反，我们设想将粪便IL-1β作为串联诊断策略的一部分，该策略将从超敏感的艰难梭菌毒素A和B检测或TcdB基因核酸扩增测试开始-这两种测试对微生物的存在都高度敏感和特异，但无法区分CDI和非结肠炎的定植。这种区分在很大程度上可以通过检测粪便中的炎性标志物，特别是IL-1β来实现。不能夸张地说，这些测试的目的不是为了替代，而只是为了补充基于患者临床表现的仔细的临床诊断考虑。
TO THE EDITOR—Dr. Ito raises questions about the selection of participants in our non-Clostridium difficile infection diarrhea (NCD) control group [1, 2]. As mentioned by the author, our study found significantly higher fecal concentrations of interleukin-1β (IL-1β) in C. difficile infection (CDI) patients when compared with subjects with NCD, suggesting that IL-1β may be useful in discriminating between patients with CDI and NCD. Patients in our NCD group were identified from a pool of hospitalized subjects who had diarrhea but whose stools were negative for C. difficile by nucleic acid amplification testing. All samples were obtained as part of routine clinical care. The author correctly points out that our NCD group is heterogeneous. This cohort encompassed subjects with diarrhea related to a number of different conditions, likely including infectious and noninfectious diarrhea, inflammatory and noninflammatory diarrhea, and osmotic and secretory diarrhea. The only definitive exclusion from the NCD group was a known history of inflammatory bowel disease. We see this heterogeneity as a methodological advantage because it is reflective of a real-world cohort of hospitalized patients with diarrhea. Our control group reflects the types of patients in whom CDI testing would be considered in clinical practice. We acknowledge that our findings may not be generalizable to every care setting, such as pediatric patients or adult patients in areas with limited sanitation, both of which may be expected to have a higher proportion of inflammatory infectious diarrhea than in our cohort. Elevation of fecal IL-1β with acute infectious diarrhea caused by other pathogens is plausible, though we have not found literature specifically substantiating this hypothesis. We do not believe that fecal IL-1β is a candidate for a stand-alone diagnostic test for CDI. Instead, we envision fecal IL-1β as part of a tandem diagnostic strategy that would begin with either an ultrasensitive C. difficile toxin A and B assay or a tcdB gene nucleic acid amplification testing—both tests are highly sensitive and specific for the presence of the organism but cannot differentiate CDI from colonization without colitis. This differentiation can be achieved, in large part, by measurement of inflammatory markers, particularly IL-1β, in the stool. It cannot be overstated that these tests do not aim to substitute for, but only to complement, careful clinical diagnostic considerations based on the patient’s clinical presentation.