Barrett's esophagus

Barrett's esophagus
Other namesBarrett's oesophagus, Allison-Johnstone anomaly, columnar epithelium lined lower oesophagus (CELLO)
Endoscopic image of Barrett's esophagus, which is the area of dark reddish-brown mucosa at the base of the esophagus. (Biopsies showed intestinal metaplasia.)
SpecialtyGastroenterology
General surgery
SymptomsNausea

Barrett's esophagus is a condition in which there is an abnormal (metaplastic) change in the mucosal cells that line the lower part of the esophagus. The cells change from stratified squamous epithelium to simple columnar epithelium, interspersed with goblet cells that are normally only found in the small intestine and large intestine. This change is considered to be a premalignant condition because of its potential to transition into esophageal adenocarcinoma, an often-deadly cancer.[1][2]

The main cause of Barrett's esophagus is tissue adaptation to chronic acid exposure caused by reflux from the stomach.[3] Barrett's esophagus is diagnosed by endoscopy to visually observe the lower esophagus, followed by a biopsy of the affected area and microscopic examination of that tissue. The cells of Barrett's esophagus are classified into four categories: nondysplastic, low-grade dysplasia, high-grade dysplasia, and carcinoma. High-grade dysplasia and early stages of adenocarcinoma may be treated by endoscopic resection or radiofrequency ablation.[4] Later stages of adenocarcinoma may be treated with surgical resection or palliation. Those with nondysplastic or low-grade dysplasia are managed by yearly observation with endoscopy, or treatment with radiofrequency ablation. In patients with high-grade dysplasia, the risk of developing cancer is estimated to be at least 10% per year.[1]

The rate of esophageal adenocarcinoma has increased substantially in the Western world in recent years.[1] The condition is found in 5–15% of patients who seek medical care for heartburn (gastroesophageal reflux disease, or GERD), although a large subgroup of patients with Barrett's esophagus have no symptoms.

The condition is named after surgeon Norman Barrett (1903–1979), although the condition was originally described by Philip Rowland Allison in 1946.[5][6][7]

  1. ^ a b c Shaheen NJ, Richter JE (March 2009). "Barrett's oesophagus". Lancet. 373 (9666): 850–61. doi:10.1016/S0140-6736(09)60487-6. PMID 19269522. S2CID 13141959.
  2. ^ Koppert LB, Wijnhoven BP, van Dekken H, Tilanus HW, Dinjens WN (December 2005). "The molecular biology of esophageal adenocarcinoma". Journal of Surgical Oncology. 92 (3): 169–90. doi:10.1002/jso.20359. PMID 16299787. S2CID 42893278.
  3. ^ Stein HJ, Siewert JR (1993). "Barrett's esophagus: pathogenesis, epidemiology, functional abnormalities, malignant degeneration, and surgical management". Dysphagia. 8 (3): 276–88. doi:10.1007/BF01354551. PMID 8359051. S2CID 6715044.
  4. ^ Shaheen, Nicholas J.; Falk, Gary W.; Iyer, Prasad G.; Gerson, Lauren B.; American College of Gastroenterology (January 2016). "ACG Clinical Guideline: Diagnosis and Management of Barrett's Esophagus". The American Journal of Gastroenterology. 111 (1): 30–50, quiz 51. doi:10.1038/ajg.2015.322. ISSN 1572-0241. PMC 10245082. PMID 26526079. S2CID 2274838.
  5. ^ Allison PR (March 1948). "Peptic ulcer of the oesophagus". Thorax. 3 (1): 20–42. doi:10.1136/thx.3.1.20. PMC 1018255. PMID 18904843.
  6. ^ Cite error: The named reference Bani-Hani was invoked but never defined (see the help page).
  7. ^ Katz-Summercorn, Annalise C.; Frankell, Alexander M.; Fitzgerald, Rebecca C. (2016). "Chapter 4: Genetics and Biomarkers in Barrett's Esophagus and Esophageal Adenocarcinoma". In Pleskow, Douglas K.; Erim, Tolga (eds.). Barrett's Esophagus - Emerging Evidence for Improved Clinical Practice. pp. 37–60. doi:10.1016/B978-0-12-802511-6.00004-1. ISBN 9780128025116.
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