Barrett's esophagus Causes
Barrett's esophagus Causes is unknown. Stomach - esophageal reflux is the most basic pathological basis, in addition to the duodenum - stomach - esophageal reflux and esophageal motor dysfunction with the causes of Barrett's esophagus. There are two long-standing doctrine that is congenital and acquired theory.
1. Congenital theory. From the perspective of embryology, human embryo development to the time 3 ~ 34mm (4 months ago), the original foregut (esophagus) was covered by columnar epithelium mucosa. Development to 130 ~ 160mm (18 ~ 20 weeks), the squamous cell columnar epithelium began to substitute, this change started from the central esophagus and gradually at both ends of the mouth to the stomach and development, to be completed before birth. Subject to any such extension, such as obstruction, may lead to lower esophagus after birth and esophageal columnar epithelium lining the upper residual columnar epithelium cells. Based on this theory, the congenital theory that Barrett esophagus is due to the process of human embryo development is not columnar epithelium squamous epithelium due to entirely replace, the left lower esophageal columnar epithelium of the embryonic period. Barrett's esophagus have a peak incidence in two stages, a group of children (0 ~ 10 years old), and the other is the adult group (over 40 years of age), and therefore causes the child group is a congenital. In addition, a pathology report, Barrett esophagus was found in the doctrine referred to the day after the chronic inflammation and fibrosis.
2. Acquired theory. At present, an increasing number of animal experiments and clinical research evidence, Barrett esophagus is an acquired disease, it is closely related to gastroesophageal reflux disease. Lower esophageal long-term exposure to acidic solution, stomach enzymes and bile, resulting in esophageal mucosal inflammation and destruction, leading to acid-resistant alternative to the columnar epithelium squamous epithelium. Study confirmed that the majority of Barrett esophagus patients with reflux esophagitis. Clinical also found that after some surgery, such as esophageal muscularis incision, total gastrectomy plus jejunal esophageal anastomosis and side-to-side gastro-esophageal anastomosis may occur after surgery, such as Barrett esophagus. Mechanism of its occurrence was mainly due to surgery undermining the integrity of lower esophageal sphincter, resulting in gastric acid and bile reflux and delayed gastric emptying or esophageal. In addition, it has been reported by chemotherapy drugs can damage esophageal mucosa, cause Barrett esophagus.
Animal model of Barrett's esophagus in the etiology and pathogenesis of a very important role. 60's at the end of the 20th century, some scholars tried to establish an animal model of Barrett esophagus, but without success. Bremner and Gillen, such as in the previous basis of animal models, an increase of long-term high-acid reflux conditions, the successful establishment of animal model of Barrett's esophagus, the results strongly support the acquisition of Barrett esophagus theory. Since then, a number of different animal models has emerged.
3. Columnar epithelium sources. Barrett esophageal columnar epithelium on the source are several views: 1. from the basal cells of squamous epithelium; 2. gland cells from Mallory; 3. from the gastric mucosa or the original stem cells.