Barrett esophagus etiology is still not fully understood. Although Barrett esophagus and gastroesophagus reflux relations between has been most scholars accepted, but Barrett esophagus mechanisms is still not clear. This is because in gastroesophagus reflux patients, only 10% for Barrett esophagus and development of 90% of the patients does not change.

What factors affecting the transformation between still a mystery. But no matter how to say, stomach – esophagus reflux is the most important and the most basic pathologic basis, besides duodenal – stomach – esophagus reflux and esophagus motor dysfunction of the esophagus with Barrett disease. There has long been one of the two theories, namely doctrine and obtain the congenital said.

1) Congenital theory from the perspective of human embryology, embryonic development to 34mm 3 ~ 4 months ago when (original), the predecessor of the esophagus (before) bowel mucosal coating columnar epithelium. Development – 130-160mm (18 ~ 20 weeks), squamous epithelium began to replace columnar epithelium, this change from the start and the esophagus gradually to the stomach and oral ends, and development of prenatal is complete.

This extension as any obstacles, may result in the lower esophagus after birth to still coating columnar epithelium and esophagus in residual columnar epithelial cells. Based on this theory, the theory of congenital that Barrett esophagus is caused by the body’s embryonic development process columnar epithelium without being squamous epithelium to replace the lower esophagus, thus caused by the embryonic columnar epithelium. Some clinical observation and support of congenital doctrine. An autopsy results prove that the baby in stillbirth esophagus was found columnar epithelium.

Borrie, etc, the pathogenesis of esophagus peak Barrett, is a two stage children series (0 ~ 10 years), the other is a ChengRenZu (40 years old), this article puts forward the etiology of children series is congenital. In addition, a pathologic study, reported in the theory that Barrett esophagus mentioned chronic inflammation and tissue fibrosis.

2) Obtain sexology said at present more and more, animal experiment and clinical research of evidence, Barrett esophagus is an acquired diseases, it and gastroesophagus reflux disease has close relationship. Long-term exposure to the lower esophagus, stomach acid solution and bile, cause inflammation and damage of esophagus mucosa, causing the columnar epithelium acid-proof alternative squamous epithelium.
Research proves, most patients with esophagus reflux Barrett existing esophagitis.

Clinical also found that some surgery, such as the esophagus, stomach muscularis incision surgical resection with esophagus anastomosis and gastroesophagus side after surgery anastomosis, etc all can happen Barrett esophagus. The mechanism is mainly due to the operation of the lower esophagus muscle damage caused by integrity, and bile acid reflux or dyskinesia oesophagus and stomach. In addition, there are also reported that chemotherapy drugs, esophagus squamous mucosa damage Barrett esophagus.

Animal model in the study of the etiology and pathogenesis Barrett esophagus mechanism played a very important role. In the late 1960s is a scholar tries to establish the model of the esophagus, Barrett animals but not succeed. Bremner and Gillen etc in previous animal models respectively based on the long-term, increase the conditions of high acid reflux, successfully built Barrett’s esophagus animal model, the results strongly support for Barrett said the esophagus. And some different animal model successively appeared.

3) Columnar epithelium source about Barrett esophagus columnar epithelium. Yet the source Currently there are several views: (1) the basal cells from squamous epithelium, (2) from cardiaoesophagus glands cell, (3) originates from gastric mucosa or stem cells.