Jankowski J, Hopwood D, Pringle R, Wormsley K G
Department of Medicine, Dundee University.
Am J Gastroenterol. 1993 Mar;88(3):402-8.
A 49-yr-old male was reviewed who had a 10-yr history of reflux esophagitis. He presented initially with frequent heartburn of moderate severity and, on subsequent endoscopy, was noted to have erosive esophagitis and, at that time, a high maximal gastric acid output. During the next 5 yr, his symptoms and acid output diminished. Eight years after presentation, he was noted to have developed a small area of Barrett's metaplasia, without dysplastic change. Ten years after the initial presentation he was completely asymptomatic, despite having extensive Barrett's metaplasia, now with high grade dysplasia. As a result, he was referred for esophagogastrectomy. At the time of surgery, he had alkaline reflux, with antacid gastric contents and, subsequently, hypochlorhydria was proven by a pentagastrin test. A second individual (male, 46 yr) who presented initially with reflux symptoms and gastric-type metaplasia, underwent gastric secretory studies that revealed a peak acid output of 16 mmol/L in 1986. During the period 1989 to 1991, his symptoms progressed despite H2 antagonist therapy. In this regard he was reinvestigated, and his peak acid output in 1991 was 0 mmol/L, and subsequent esophageal biopsies demonstrated intestinal metaplasia in four of six biopsies (two biopsies had high-grade dysplasia; the two others had gastric-type metaplasia). He has refused esophageal resection, and is being reviewed regularly at the endoscopy clinic. Flow cytometric analysis of the esophagus in both individuals revealed expression of epidermal growth factor receptor which was increased in the areas of high grade dysplasia, compared with Barrett's mucosa without dysplasia or normal cardiac mucosa. We conclude that alkaline reflux may accelerate the development of Barrett's esophagus (and intestinal type metaplasia) in patients with gastroesophageal reflux disease. The increased expressed of epidermal growth factor receptors in Barrett's mucosa with dysplasia compared with Barrett's mucosa without dysplasia may reflect the higher malignant potential of the former mucosa.
一名49岁男性接受复查，他有10年反流性食管炎病史。他最初表现为频繁的中度烧心症状，随后的内镜检查发现有糜烂性食管炎，当时胃酸最大分泌量较高。在接下来的5年里，他的症状和胃酸分泌量有所减轻。发病8年后，发现他出现了一小片Barrett化生区域，无发育异常改变。初次发病10年后，尽管有广泛的Barrett化生且现已出现高级别发育异常，但他完全没有症状。因此，他被转诊进行食管胃切除术。手术时，他存在碱性反流，胃内容物呈抗酸性，随后五肽胃泌素试验证实有胃酸缺乏。另一名个体（男性，46岁）最初表现为反流症状和胃型化生，进行了胃分泌研究，结果显示1986年胃酸峰值分泌量为16 mmol/L。在1989年至1991年期间，尽管接受了H2拮抗剂治疗，他的症状仍有进展。在这方面，他再次接受检查，1991年他的胃酸峰值分泌量为0 mmol/L，随后的食管活检显示6次活检中有4次出现肠化生（2次活检有高级别发育异常；另外2次有胃型化生）。他拒绝了食管切除术，目前在内镜诊所定期接受复查。对这两名个体的食管进行流式细胞术分析发现，与无发育异常的Barrett黏膜或正常贲门黏膜相比，高级别发育异常区域的表皮生长因子受体表达增加。我们得出结论，碱性反流可能会加速胃食管反流病患者Barrett食管（和肠化生）的发展。与无发育异常的Barrett黏膜相比，有发育异常的Barrett黏膜中表皮生长因子受体表达增加可能反映了前者黏膜更高的恶性潜能。
