O'Riordan J M, Tucker O N, Byrne P J, McDonald G S A, Ravi N, Keeling P W N, Reynolds J V
University Department of Surgery, St James' Hospital, Dublin 8, Ireland.
Am J Gastroenterol. 2004 Feb;99(2):205-11. doi: 10.1111/j.1572-0241.2004.04057.x.
Barrett's esophagus results from chronic reflux of both acid and bile. Reflux of gastric and duodenal contents is facilitated through the denervated stomach following esophagectomy, but the development of Barrett's changes in this model and the relationship to gastric and esophageal physiology is poorly understood.
To document the development of new Barrett's changes, i.e., columnar metaplasia or specialized intestinal metaplasia (SIM) above the anastomosis, and relate this to the recovery of gastric acid production, acid and bile reflux, manometry, and symptoms.
Forty-eight patients at a median follow-up of 26 months (range = 12-67) postesophagectomy underwent endoscopy with biopsies taken 1-2 cm above the anastomosis. The indication for esophagectomy had been adenocarcinoma (n = 27), high-grade dysplasia (n = 2), and squamous cell cancer (n = 19). Physiology studies were performed in 27 patients and included manometry (n = 25), intraluminal gastric pH (n = 24), as well as simultaneous 24-hour esophageal pH (n = 27) and bile monitoring (n = 20).
Duodenogastric reflux increased over time, with differences between patients greater than and less than 3 years postesophagectomy for acid (p = 0.04) and bile (p = 0.02). Twenty-four patients (50%) developed columnar metaplasia and of these 13 had SIM. The prevalence of columnar metaplasia did not relate to the magnitude of acid or bile reflux, to preoperative neoadjuvant therapies, or to the original tumor histology. The duration of reflux was most significant, with increasing prevalence over time, with SIM in 13 patients at a median of 61 months postesophagectomy compared with 20 months in the 35 patients who were SIM-negative (p < 0.006). Supine reflux correlated with symptoms.
The development of Barrett's epithelium is frequent after esophagectomy, is time-related, reflecting chronic acid and bile exposure, and is not specific for adenocarcinoma or the presence of previous Barrett's epithelium. This model may represent a useful in vivo model of the pathogenesis of Barrett's metaplasia and tumorigenesis.
巴雷特食管由胃酸和胆汁的慢性反流引起。食管切除术后，去神经支配的胃促进了胃和十二指肠内容物的反流，但在该模型中巴雷特改变的发展及其与胃和食管生理的关系尚不清楚。
记录吻合口上方新的巴雷特改变（即柱状化生或特殊肠化生[SIM]）的发展情况，并将其与胃酸分泌的恢复、酸和胆汁反流、测压及症状相关联。
48例食管切除术后患者，中位随访时间为26个月（范围12 - 67个月），在吻合口上方1 - 2厘米处进行内镜检查并取活检。食管切除的指征为腺癌（27例）、高级别上皮内瘤变（2例）和鳞状细胞癌（19例）。27例患者进行了生理研究，包括测压（25例）、胃腔内pH值监测（24例）以及同步24小时食管pH值监测（27例）和胆汁监测（20例）。
十二指肠 - 胃反流随时间增加，食管切除术后大于和小于3年的患者在酸反流（p = 0.04）和胆汁反流（p = 0.02）方面存在差异。24例患者（50%）发生了柱状化生，其中13例有SIM。柱状化生的患病率与酸或胆汁反流的程度、术前新辅助治疗或原发肿瘤组织学无关。反流持续时间最为显著，患病率随时间增加，13例有SIM的患者在食管切除术后中位时间为61个月，而35例无SIM的患者为20个月（p < 0.006）。仰卧位反流与症状相关。
食管切除术后巴雷特上皮的发展很常见，与时间相关，反映了长期的酸和胆汁暴露，并非腺癌或既往存在巴雷特上皮所特有。该模型可能代表了巴雷特化生和肿瘤发生机制的一种有用的体内模型。
