| Theme |
Diagnosis and Treatment of Barrett's Esophagus : up-to-date |
| Title |
Barrett's Carcinogenesis and Reflux Esophagitis |
| Author |
Yugo Iwaya |
Department of Gastroenterology, Nagano Municipal Hospital / Department of Gastroenterology, Shinshu University School of Medicine |
| Author |
Takuma Okamura |
Department of Gastroenterology, Shinshu University School of Medicine |
| Author |
Shigenori Yamada |
Department of Gastroenterology, Shinshu University School of Medicine |
| Author |
Osamu Hasebe |
Department of Gastroenterology, Nagano Municipal Hospital |
| Author |
Jun Nakayama |
Department of Molecular Pathology, Shinshu University Graduate School of Medicine |
| [ Summary ] |
It is generally accepted that Barrett's adenocarcinoma develops from Barrett's esophagus as a result of chronic inflammation from reflux esophagitis. In this regard, both gastric acid and bile acid reflux are important to understand the Barrett's pathogenesis. Bile acid plays an important role in progression of Barrett's adenocarcinoma by increasing cell proliferation mediated by NF-κB activation and development of intestinal metaplasia mediated by CDX2. On the other hand, involvement of various cytokines associated with chronic inflammation is also important in the development of Barrett's esophagus and adenocarcinoma. Recently, a great deal of attention has been paid to Barrett's pathogenesis due to individual differences in immunological response. In addition, it has been shown that reduced αGlcNAc expression in Barrett's esophagus may play an important role in the development of Barrett's adenocarcinoma. Although observation of development of Barrett's adenocarcinoma during follow-ups for reflux esophagitis is very rare, Barrett's adenocarcinoma patients frequently have histories of reflux esophagitis in retrospective studies of endoscopic findings. In this review, we briefly summarize recent progress in treatment of Barrett's pathogenesis, primarily through focusing on reflux esophagitis. |