Gindea C, Birla R, Hoara P, Caragui A, Constantinoiu S
"Carol Davila" University of Medicine and Pharmacy, Bucharest; "Sf. Maria" Clinical Hospital, General and Esophageal Surgery Department, Bucharest, Romania.
J Med Life. 2014;7 Spec No. 3(Spec Iss 3):23-30.
The injury of the esophageal epithelium may be determined by the reflux of the gastric acid in the esophagus. Barrett's esophagus (BE) is characterized by the replacement of the normal squamous epithelium with the columnar epithelium, when the healing of the lesion occurs. According to some studies, the incidence of the esophageal adenocarcinoma in patients with BE is of about 0,5% per year. The term Barrett's esophagus is subjected to interpretation nowadays, so it lacks the clarity needed for the clinical and scientific communication on the subject of columnar metaplasia of the esophageal mucosa. The major pathogenetic factor in the development of BE is represented by the reflux disease. The cellular origin of BE is controversial and it represents an issue that needs to be resolved because it will have implications in the putative molecular mechanisms underlying the metaplastic process. The epigenetic or genetic changes, which alter protein expression, function, and/ or activity, in post-mitotic cells to drive transdifferentiation or in stem/ progenitor cells such that they are reprogrammed to differentiate into columnar rather than squamous cells, are driven by the inflammatory environment created by chronic reflux. In order to be able to develop better therapeutic strategies for the patients with this disease, an increasing interest in understanding the pathogenesis of BE at the cellular and molecular level presents these days.
食管上皮损伤可能由胃酸反流至食管所决定。巴雷特食管(BE)的特征是在病变愈合时,正常鳞状上皮被柱状上皮取代。根据一些研究,BE患者中食管腺癌的发病率约为每年0.5%。如今,“巴雷特食管”这一术语存在多种解释,因此在关于食管黏膜柱状化生这一主题的临床和科学交流中缺乏所需的清晰度。BE发生发展的主要致病因素是反流性疾病。BE的细胞起源存在争议,这是一个需要解决的问题,因为它将对化生过程潜在的分子机制产生影响。慢性反流所产生的炎症环境驱动了后生细胞中的表观遗传或基因变化,这些变化改变蛋白质表达、功能和/或活性,以驱动转分化,或在干细胞/祖细胞中使其重新编程,从而分化为柱状而非鳞状细胞。为了能够为患有这种疾病的患者制定更好的治疗策略,如今人们越来越关注在细胞和分子水平上理解BE的发病机制。