Clayton Steven, Cauble Elliot, Kumar Ambuj, Patil Nirav, Ledford Dennis, Kolliputi Narasaiah, Lopes-Virella Maria F, Castell Donald, Richter Joel
Wake Forest Baptist Medical Center, Winston-Salem, NC, USA.
University of South Florida, Division of Gastroenterology, Florida, USA.
BMC Gastroenterol. 2019 Feb 11;19(1):28. doi: 10.1186/s12876-019-0937-9.
An elevation of serum inflammatory biomarkers in achalasia patients compared with controls recently was demonstrated. It has not been determined whether the elevation of inflammatory cytokines is unique to achalasia or occurs with other diseases involving the esophagus. The primary aim of our study was to compare the differences in plasma immunological profiles (TNF- α receptor, IL-6, IFN-γ, IL-12, IL-17, IL-22, and IL-23) of patients with achalasia, eosinophilic esophagitis (EoE), and gastroesophageal reflux disease (GERD). A secondary aim of this study was to classify these same plasma cytokine profiles in the three achalasia subtypes.
Plasma from 53 patients with achalasia, 22 with EoE, and 20 with GERD (symptoms plus esophagitis or + reflux study) were analyzed.
malignancy, autoimmune condition, immunodeficiency disorder, and treatment with steroids/immune modulating drugs. Cytokine levels were assayed via multiplex enzyme-linked immunosorbent assay (ELISA).
Our key finding revealed significant elevations in IL- 6 (p = 0.0158) in achalasia patients compared with EoE patients. Overall, plasma inflammatory biomarker patterns were not different in the three subtypes of achalasia.
There were no differences between the cytokine levels of any of the measured biomarkers between the achalasia and GERD groups suggesting that luminal stasis does increase biomarker levels for any of the cytokines examined in our study. While these results are an early first step towards clarifying some aspects of the pathogenesis of achalasia, they bring about many more questions that require further investigation and expansion. Further investigation with a larger cohort and a broader panel of biomarkers is needed.
最近有研究表明,与对照组相比,贲门失弛缓症患者血清炎症生物标志物水平升高。目前尚未确定炎症细胞因子的升高是贲门失弛缓症所特有的,还是在其他涉及食管的疾病中也会出现。我们研究的主要目的是比较贲门失弛缓症、嗜酸性食管炎(EoE)和胃食管反流病(GERD)患者血浆免疫谱(TNF-α受体、IL-6、IFN-γ、IL-12、IL-17、IL-22和IL-23)的差异。本研究的次要目的是对三种贲门失弛缓症亚型的相同血浆细胞因子谱进行分类。
分析了53例贲门失弛缓症患者、22例嗜酸性食管炎患者和20例胃食管反流病患者(有症状加食管炎或 + 反流研究)的血浆。
恶性肿瘤、自身免疫性疾病、免疫缺陷疾病以及使用类固醇/免疫调节药物治疗。通过多重酶联免疫吸附测定(ELISA)检测细胞因子水平。
我们的主要发现显示,与嗜酸性食管炎患者相比,贲门失弛缓症患者的IL-6显著升高(p = 0.0158)。总体而言,贲门失弛缓症的三种亚型的血浆炎症生物标志物模式没有差异。
贲门失弛缓症组和胃食管反流病组之间,任何测量的生物标志物的细胞因子水平均无差异,这表明管腔淤滞并不会增加我们研究中所检测的任何细胞因子的生物标志物水平。虽然这些结果是阐明贲门失弛缓症发病机制某些方面的早期第一步,但它们也带来了更多需要进一步研究和扩展的问题。需要对更大的队列和更广泛的生物标志物进行进一步研究。