Barrett's esophagus

from Wikipedia, the free encyclopedia
Classification according to ICD-10
K22.1 Barrett's ulcer
K22.7 Barrett's esophagus
ICD-10 online (WHO version 2019)

As Barrett's esophagus (after the British surgeon Norman Rupert Barrett described, in 1950 and 1957 respectively, the clinical picture, synonyms Barrett's metaplasia , Endobrachyösophagus of gr. Ἔνδον inside , βραχύς short , οἰσοφάγος esophagus ) is defined as a result of reflux disease , in which Chronic irritation caused by acidic stomach contents transforms the squamous epithelium of the lower esophagus into specialized columnar epithelium ( metaplasia ). This transformation is a preliminary stage of esophageal cancer , which is why it must be checked regularly. The development of an esophageal peptic ulcer on the metaplastic mucous membrane is known as Barrett's syndrome or Allison-Johnstone syndrome .

Endoscopic image of Barrett's esophagus

Epidemiology

Barrett's esophagus occurs in about 10% of people with reflux, which means a prevalence of 1-2% of the population in western states. Men are affected twice as often as women. Other risk factors for developing Barrett's esophagus include smoking, obesity, an axial hernia, and discomfort from reflux disease. The last three factors mentioned increase reflux or suggest damage to the esophageal mucosa. Colonization of the gastric mucosa by Helicobacter pylori lowers the risk of developing Barrett's esophagus, as it inhibits acid production and therefore the gastric juice attacks the mucous membrane of the esophagus less. A diet with fruits and vegetables also has a beneficial effect. The influence of alcohol on the development of Barrett's metaplasia is unclear.

Pathogenesis

In healthy people, the inside of the esophagus is completely lined by a multi-layered, uncornified squamous epithelium, which is designed to withstand the mechanical stress caused by food sliding past. In reflux disease , acidic stomach contents flow back into the esophagus from the stomach , causing squamous cell damage and chronic inflammation ( reflux esophagitis ). Usually the destroyed cells are replaced by squamous epithelium again. This no longer works for some people with reflux. Instead, a columnar epithelium forms , which produces mucus to protect against gastric acid, as is typical of the stomach and small intestine. This transformation from one type of tissue to another ( metaplasia ) characterizes Barrett's esophagus. It typically occurs at the lower end of the esophagus just before the transition into the stomach, because this is where the effect of the gastric contents flowing back is strongest. It is not clear where the columnar epithelium comes from; the chronic inflammation may activate transcription factors in the squamous epithelial cells, causing them to be converted directly into columnar epithelial cells. Or the columnar epithelium is formed by the various stem cells that sit in the mucous membrane or that migrate there. The transformation of the epithelial type is definitive and does not or only partially regress even with adequate treatment of the reflux. Although the columnar epithelium is more resistant to acid and pepsin exposure, it carries the risk of further degeneration (dysplasia, adenocarcinoma ). It also tends to ulcerate ( Barrett's ulcer ) and develop strictures (see section on complications ).

diagnosis

The diagnosis of Barrett's esophagus is made through a combination of endoscopic findings and microscopic examination of tissue samples. Barrett's esophagus itself does not cause any symptoms, but many patients receive an endoscopic examination of the esophagus and stomach because of their symptomatic reflux esophagitis , and the change is discovered.

Endoscopic criteria

A video endoscope is used to make the diagnosis ; Barrett's metaplasia is shown as reddish extensions in the esophageal mucous membrane from the stomach entrance towards the head. The changes that are directly visible during endoscopy are classified according to the Prague classification . Two dimensions are combined: 1. the length of the changes that extend over the entire circumference of the esophagus (circumferential metaplasia) is noted in centimeters together with the designation "C" and 2. the additional, mostly tongue-shaped extensions are also in Centimeters indicated with the designation "M" for maximum expansion. For example, a finding “C8M9” means a ring-shaped metaplasia of 8 cm and a maximum length of the metaplasia of 9 cm. The measurement is taken from the gastroesophageal junction. A distinction is made between the short-segment Barrett's esophagus (so-called short-segment Barrett's esophagus ) with a length of up to 3 cm and the long-segment Barrett's esophagus (so-called long-segment Barrett's esophagus ) with a length over 3 cm.

Histological criteria

For further diagnosis, extensive tissue samples ( biopsies ) are taken from the abnormal areas of the mucous membrane and examined microscopically in the pathology department . Here, on the one hand, it is determined whether there is a conversion of tissue to columnar epithelium. The detection of certain cells, the goblet cells , is also required here. These are typical of the epithelium of the small intestine ; only then can one speak of an intestinal (from Latin intestine , bowel) metaplasia.

Another point that needs to be clarified in the microscopic examination is the classification of tissue damage. More precisely, the question is whether a malignant tumor or a precursor of it ( dysplasia ) has already formed. This proliferation of damaged cells is collectively referred to as " neoplasia ". According to the Vienna classification, neoplasms are divided into tissue without dysplasia, tissue with possible dysplasia, tissue with well differentiated dysplasia (low grade dysplasia), tissue with poorly differentiated dysplasia (high grade dysplasia) and tissue with adenocarcinoma (non-invasive or possibly invasive). Further therapy is based on this classification.

definition

In the scientific community, opinions differ on how to precisely define Barrett's esophagus. There is disagreement about how long the metaplasia must be at least to be considered Barrett's esophagus in need of treatment. Some professional societies (including the Japanese Society for Gastroenterology and the Australian Cancer Society) do not require a minimum length, while others, such as the European and British professional societies, require a minimum length of 1 cm. The reason for the deviation is that very short metaplasias have a very low risk of degeneration. Also, very short sections are harder to judge. Another point of contention is the presence or absence of the goblet cells that indicate intestinal metaplasia. Column epithelium without goblet cells is typical of the gastric fundus and mouth. It is not clear that fundus-type columnar epithelium is a risk factor for esophageal cancer. Most professional societies therefore require proof of goblet cells in their guidelines, including the German Society for Gastroenterology, Digestive and Metabolic Diseases .

Complications

Strictures and ulcerations

A common complication (10 to 24%) is the formation of ulcers in the transformed epithelium. In fact, such an ulcer in the esophagus was the reason for the first description of the disease by the surgeon Norman Rupert Barrett in 1950. Such an ulcer can remain symptom-free, be apparent through bleeding or in the worst case through the wall of the esophagus into adjacent structures (such as the aorta or the Pericardium ) grow. A narrowing of the esophagus ( stricture ) develops in 15 to 40% of patients , mostly at the junction of the squamous and columnar epithelium.

Carcinogenesis

Barrett's esophagus is in need of treatment mainly because of the risk of developing esophageal adenocarcinoma , one of the two main forms of esophageal cancer . For patients with Barrett's metaplasia without signs of dysplasia, the annual risk of developing adenocarcinoma is 0.1-0.4%, which is a slightly increased risk. The likelihood increases significantly when there is dysplasia. The figures for this sometimes differ greatly from one another. Annual cancer rates between 1% and 5% to 9% have been reported for minor dysplasia. For high-grade dysplasias, a meta-analysis (a scientifically high-quality statistical evaluation of several studies) determined an annual risk of degeneration of 6.6%, although significantly higher rates of up to 28% were seen in therapy studies. Also, the risk of cancer depends on the length of the metaplasia (the longer the risk, the greater the risk), and men with Barrett's esophagus are twice as likely as women with Barrett's esophagus.

therapy

Surveillance and intervention

The aim of medical interventions is to prevent the development of esophageal adenocarcinomas, which have a poor prognosis. The most important measure is therefore the regular control of the findings and the removal of degenerate tissue, although the exact recommendations vary between the international specialist societies. The German guidelines recommend endoscopic control after one year and then every 3 to 4 years for Barrett's esophagus without dysplasia; other guidelines, such as those of the European Society for Gastrointestinal Endoscopy, make the control intervals long in these cases of Barrett's esophagus. If dysplasia is detected, there is the option (and recommendation) of endoscopic resection. With this method, the tumor is first sucked in during a normal endoscopic examination and then resected with a snare. In the case of malignant changes that grow deeper into the wall layers of the esophagus (into the submucosa), however, surgical therapy ( esophagectomy ) should be performed, since in this case there is a risk of lymph node metastasis . There is also the possibility of obliterating the Barrett's metaplasia . This is especially recommended as an accompanying therapy to the resection of dysplasias.

Medical therapy

There is no established drug therapy specific for Barrett's esophagus. Most patients are already on proton pump inhibitors (PPIs) to treat their reflux disease, which has a beneficial effect on acute inflammation of the esophagus, but does not appear to affect the further development of an existing Barrett's esophagus. However, there is evidence that PPIs in combination with asprin or other NSAIDs actually lower the risk of cancer. Something similar has been reported for statins . However, the data is not yet good enough for official recommendations to be made.

Web links

Commons : Barrett's esophagus  - collection of images, videos and audio files

Literature and Sources

  • Dietel, Dudenhausen, Suttorp (ed.): Harrison's internal medicine. Volume 2, McGraw-Hill, ABW Wissenschaftsverlag 2003.
  • NJ Shaheen, MA Crosby, EM Bozymski, RS Sandler: Is there publication bias in the reporting of cancer risk in Barrett's esophagus? In: Gastroenterology . (2000); 119 (2), pp. 333-338.
  • BHA von Rahden, HJ Stein: Barrett's Esophagus and Barrett's Carcinoma. In: Curr GERD Rep. (2007); 1, pp. 125-132.
  • O. Pech, A. May, T. Rabenstein, C. Ell: Endoscopic resection of early oesophageal cancer. In: Gut 56 (2007), p. 1625.
  • O. Pech, A. Behrens, A. May, L. Nachbar, L. Gossner, T. Rabenstein, H. Manner, E. Guenter, J. Huijsmans, M. Vieth, M. Stolte, C. Ell: Long- term results and risk factor analysis for recurrence after curative endoscopic therapy in 349 patients with high-grade intraepithelial neoplasia and mucosal adenocarcinoma in Barrett's esophagus. In: Good. (2008); 57 (9): 1200-1206.
  • C. Ell, A. May, O. Pech, L. Gossner, E. Guenter, A. Behrens, L. Nachbar, J. Huijsmans, M. Vieth, M. Stolte: Curative endoscopic resection of early esophageal adenocarcinomas (Barrett's cancer ). In: Gastrointest Endosc . (2007); 65, pp. 3-10.
  • O. Pech, L. Gossner, A. May, T. Rabenstein, M. Vieth, M. Stolte, M. Berres, C. Ell: Long-term results of photodynamic therapy with 5-aminolevulinic acid for superficial Barrett's cancer and high -grade intraepithelial neoplasia. In: Gastrointest Endosc. (2005); 62, pp. 24-30.
  • JD Birkmeyer, AE Siewers, EV Finlayson, TA Stukel, FL Lucas, I. Batista, HG Welch, DE Wennberg: Hospital volume and surgical mortality in the United States. In: N Engl J Med . (2002); 346 (15), pp. 1128-1137.
  • JD Birkmeyer, TA Stukel, AE Siewers, PP Goodney, DE Wennberg, FL Lucas: Surgeon volume and operative mortality in the United States. In: N Engl J Med. (2003); 349 (22), pp. 2117-2127.

Individual evidence

  1. ^ NR Barrett: The lower esophagus lined by columnar epithelium. In: Surgery 1957; 41, pp. 881-894. PMID 13442856 .
  2. ↑ MB Cook et al: A systematic review and meta-analysis of the sex ratio for Barrett's esophagus, erosive reflux disease, and nonerosive reflux disease. In: Am J Epidemiol. 2005 Dec 1; 162 (11), pp. 1050-1061. PMID 16221805 .
  3. ↑ a b c d e f g h i j k l Yonne Peters, Ali Al-Kaabi, Nicholas J. Shaheen, Amitabh Chak, Andrew Blum: Barrett esophagus . In: Nature Reviews Disease Primers . tape 5 , no. 1 , December 2019, ISSN  2056-676X , p. 35 , doi : 10.1038 / s41572-019-0086-z ( nature.com [accessed August 21, 2020]).
  4. ↑ a b c d e Stuart J. Spechler, Rhonda F. Souza: Barrett's Esophagus . In: New England Journal of Medicine . tape 371 , no. 9 , August 28, 2014, ISSN  0028-4793 , p. 836-845 , doi : 10.1056 / NEJMra1314704 ( nejm.org [accessed August 22, 2020]).
  5. ↑ Peter J. Kahrilas, Ikuo Hirano: Diseases of the esophagus . In: Harrison's internal medicine , 19th edition in German. ABW Wissenschaftsverlag, Berlin 2016, p. 2344.
  6. ↑ DGVS: S2k guidelines for reflux disease, as of 05/2014 , p. 89. Last accessed on August 22, 2020.
  7. Jump up ↑ Philippe G Guillem, Henri L Porte, Alain Saudemont, Pierre A Quandalle, Alain J Wurtz: Perforation of Barrett's ulcer: a challenge in esophageal surgery . In: The Annals of Thoracic Surgery . tape 69 , no. 6 , June 2000, p. 1707–1710 , doi : 10.1016 / S0003-4975 (00) 01310-2 ( elsevier.com [accessed August 23, 2020]).
  8. ^ Rao Milind: Natural history of Barrett's esophagus . In: World Journal of Gastroenterology . tape 18 , no. 27 , 2012, ISSN  1007-9327 , p. 3483 , doi : 10.3748 / wjg.v18.i27.3483 , PMID 22826612 , PMC 3400849 (free full text) - ( wjgnet.com [accessed August 23, 2020]).
  9. ↑ a b Anil K. Rustgi, Hashem B. El-Serag: Esophageal Carcinoma . In: New England Journal of Medicine . tape 371 , no. 26 , December 25, 2014, ISSN  0028-4793 , p. 2499–2509 , doi : 10.1056 / NEJMra1314530 ( nejm.org [accessed August 23, 2020]).
  10. ↑ DGVS: S2k guidelines for reflux disease, as of 05/2014 , p. 100. Last accessed on 23 August 2020.
  11. Jump up ↑ Bas Weusten, Raf Bisschops, Emanuel Coron, Mário Dinis-Ribeiro, Jean-Marc Dumonceau: Endoscopic management of Barrett's esophagus: European Society of Gastrointestinal Endoscopy (ESGE) Position Statement . In: Endoscopy . tape 49 , no. 02 , January 25, 2017, ISSN  0013-726X , p. 191–198 , doi : 10.1055 / s-0042-122140 ( thieme-connect.de [accessed on 23 August 2020]).