Are there groups of patients with non-dysplastic BO that require more frequent surveillance?

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Are there groups of patients with non-dysplastic BO that require more frequent surveillance?

Introduction

The aim of surveillance is to detect evidence of the progression of Barrett's Oesophagus (BO) to dysplasia and early cancer at a stage where an effective intervention will reduce morbidity and mortality. Overall, the surveillance protocol for patients with BO is based on observational studies on the conversion rate to oesophageal adenocarcinoma (OAC).[1] (See also “How frequently should patients with BO undergo endoscopy?"). A group of patients which may be targeted for more frequent surveillance may be defined as one which has evidence of a higher rate of progression to OAC. A number of studies have investigated risk factors for progression to OAC (see also What are the risk factors for progression from BO to neoplasia?), but these studies have been limited by features such as selection bias, low progression rates to OAC, high numbers of loss to follow up, retrospective reporting and the incomplete study of risk factors. However, a number of recommendations may still be made based on the available evidence. Note that these recommendations do not include patients with evidence of dysplasia, which is covered in a separate section (see also What is the appropriate management of low grade dysplasia in patients with BO?).

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What are the endoscopic and/or histological factors of non-dysplastic BO patients that may require more frequent surveillance?

Longer BO length has been consistently observed to have a higher rate of progression. Three meta-analysis have distinguished a higher incidence of progression to OAC in patients diagnosed with long (>3cm) versus short (<3cm) segment non-dysplastic BO [1][2][3]. A recent study confirmed these findings, reporting an increased risk of progression in patients with long BO length (hazard ratio 7, 95% CI 1.71 – 28.64).[4] In addition, three multi-centre studies consistently show on multi-variant analysis the increased relative risk of length (per centimetre) in the order of 1.1 – 1.21.[5][6][7]

Other observed features at endoscopy which may also be associated with a higher incidence of progression to OAC include the observation of ulcers, nodules and oesophageal strictures, with relative risk of 3.0 to 7.6 in these case series.[6][8] These features may be a marker of prevalent (i.e. pre-existing) dysplasia and/or OAC, thus confirming the need to biopsy all abnormal areas at endoscopy (see also What is the optimal tissue sampling at endoscopy for diagnosis of BO?).

Clear evidence for a sub-group of patients with a higher rate of progression to OAC is those with histological evidence of dysplasia.[9][10][11] The recommended management and surveillance for these patients is found in section What is the appropriate management of low grade dysplasia in patients with BO? and What are the goals of treatment of high grade dysplasia in patients with BO?.

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What are the patient factors of non-dysplastic BO patients that may require more frequent surveillance?

A number of patient factors which have been independently associated with increased risk of progression include age [12][9][11], male gender [11][13] and smoking.[14][12] Interestingly, those who have been on surveillance for BO for greater than 10 years have a higher cumulative incidence of OAC (9.2%, 95% CI 2.2 – 17.0).[5] Although the increased relative risk of each may be statistically significant, the rate of progression has yet to be determined and hence no recommendations have been suggested for a surveillance strategy. In addition, the combination of risk factors has not been studied and a risk algorithm for progression is yet to be developed and validated. However, it is likely that the combination of age, male gender and smoking may have the additive effect on progression to OAC.[15][16]

There are a number of other factors that have been suggested to be associated with the development of BO but yet to be fully studied as also contributing to an increased risk of progression to OAC. These include a strong family history of BO and/or OAC [17], racial/regional factors [18][19], dietary factors [20] and patients with poorly controlled gastro-oesophageal reflux disease.[4] However, it has observed that those who have regular use of proton-pump inhibitors have a significantly reduced relative risk of developing OAC (RR 0.29, 95% CI 0.12 – 0.79),[21] suggesting that the control of acid reflux has an important role in preventing the onset of OAC.

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What is the suggested surveillance protocol and management for a high risk group?

The suggested surveillance protocol should account for patient factors such as co-morbidities and patient preference. A multi-disciplinary meeting can aid the decision making processes for individual patients. Recommendations for patients may also take in to account current international guidelines. (See also How frequently should patients with BO undergo endoscopy?).

Patients with BO ≥3cm have a higher incidence of progression to OAC than those <3cm, and it is recommended that they continue surveillance indefinitely. British guidelines,[22] recommend surveillance endoscopy intervals of 2 to 3 yearly (as opposed to 3 to 5 yearly for those <3cm), whereas American guidelines do not make this distinction.[23] Those with BO for greater than 10 years may also have closer surveillance endoscopy intervals, although the time interval has not been outlined in other guidelines.

There is currently no evidence for an intensive surveillance protocol for one or more other risk factors e.g. male, older age, smoking, uncontrolled GORD. Modifications such smoking cessation, weight loss in obese patients and acid suppression therapy may be encouraged but there is currently no data on their outcomes.

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Evidence summary and recommendations

Evidence summary Level References
Patients with a longer length of BO (particularly ≥3cm) are a higher risk group for progression to OAC. III-2 [1], [2], [7], [4], [3], [6], [5]
Patients with risk profiles such as, older age, male and smokers may also be at higher risk of progression to OAC. II, III-2 [9], [11], [12], [13], [14]
Evidence-based recommendationQuestion mark transparent.png Grade
Patients with Barrett's Oesophagus length equal to or greater than 3cm may have intensive surveillance, possibly every two to three years following the Seattle protocol.
C
The given value was not understood.


Evidence-based recommendationQuestion mark transparent.png Grade
Patients with one or more modifiable risk factors for progression to oesophageal adenocarcinoma (such as smoking) should be encouraged to make lifestyle changes.
D


Practice pointQuestion mark transparent.png

Patients with Barrett's Oesophagus length equal to or greater than 3cm may have more frequent surveillance than those less than 3cm.

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Issues requiring more clinical research study

  • Are there other risks factors that may modify progression rates that are not yet studied? Eg family history, medications
  • Is there an algorithm that may be used to quantify the risk of progression to BO?
  • Does modification of known risk factors improve patient outcomes?
  • Are there other means to risk stratify patients requiring intensive surveillance, eg the use of biomarkers?

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References

  1. 1.0 1.1 1.2 Desai TK, Krishnan K, Samala N, Singh J, Cluley J, Perla S, et al. The incidence of oesophageal adenocarcinoma in non-dysplastic Barrett's oesophagus: a meta-analysis. Gut 2012 Jul;61(7):970-6 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/21997553.
  2. 2.0 2.1 Yousef F, Cardwell C, Cantwell MM, Galway K, Johnston BT, Murray L. The incidence of esophageal cancer and high-grade dysplasia in Barrett's esophagus: a systematic review and meta-analysis. Am J Epidemiol 2008 Aug 1;168(3):237-49 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/18550563.
  3. 3.0 3.1 Thomas T, Abrams KR, De Caestecker JS, Robinson RJ. Meta analysis: Cancer risk in Barrett's oesophagus. Aliment Pharmacol Ther 2007 Dec;26(11-12):1465-77 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/17900269.
  4. 4.0 4.1 4.2 Coleman HG, Bhat SK, Murray LJ, McManus DT, O'Neill OM, Gavin AT, et al. Symptoms and Endoscopic Features at Barrett's Esophagus Diagnosis: Implications for Neoplastic Progression Risk. Am J Gastroenterol 2014 Mar 4 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/24589668.
  5. 5.0 5.1 5.2 Sikkema M, Looman CW, Steyerberg EW, Kerkhof M, Kastelein F, van Dekken H, et al. Predictors for neoplastic progression in patients with Barrett's Esophagus: a prospective cohort study. Am J Gastroenterol 2011 Jul;106(7):1231-8 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/21577245.
  6. 6.0 6.1 6.2 Rugge M, Zaninotto G, Parente P, Zanatta L, Cavallin F, Germanà B, et al. Barrett's esophagus and adenocarcinoma risk: the experience of the North-Eastern Italian Registry (EBRA). Ann Surg 2012 Nov;256(5):788-94; discussion 794-5. doi: 10.1097/SLA.0b013e3182737a7e. Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/23095623.
  7. 7.0 7.1 Anaparthy R, Gaddam S, Kanakadandi V, Alsop BR, Gupta N, Higbee AD, et al. Association Between Length of Barrett's Esophagus and Risk of High-Grade Dysplasia or Adenocarcinoma in Patients Without Dysplasia. Clin Gastroenterol Hepatol 2013 May 21 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/23707463.
  8. Hillman LC, Chiragakis L, Clarke AC, Kaushik SP, Kaye GL. Barrett's esophagus: Macroscopic markers and the prediction of dysplasia and adenocarcinoma. J Gastroenterol Hepatol 2003 May;18(5):526-33 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/12702044.
  9. 9.0 9.1 9.2 Verbeek RE, van Oijen MG, ten Kate FJ, Vleggaar FP, Schipper ME, Casparie MK, et al. Surveillance and follow-up strategies in patients with high-grade dysplasia in Barrett's esophagus: a Dutch population-based study. Am J Gastroenterol 2012 Apr 1;107(4):534-42 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/22270082.
  10. Hvid-Jensen F, Pedersen L, Drewes AM, Sørensen HT, Funch-Jensen P. Incidence of adenocarcinoma among patients with Barrett's esophagus. N Engl J Med 2011 Oct 13;365(15):1375-83 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/21995385.
  11. 11.0 11.1 11.2 11.3 Bhat S, Coleman HG, Yousef F, Johnston BT, McManus DT, Gavin AT, et al. Risk of malignant progression in Barrett's esophagus patients: results from a large population-based study. J Natl Cancer Inst 2011 Jul 6;103(13):1049-57 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/21680910.
  12. 12.0 12.1 12.2 Gatenby PA, Caygill CP, Ramus JR, Charlett A, Watson A. Barrett's columnar-lined oesophagus: demographic and lifestyle associations and adenocarcinoma risk. Dig Dis Sci 2008 May;53(5):1175-85 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/17939050.
  13. 13.0 13.1 de Jonge PJ, van Blankenstein M, Looman CW, Casparie MK, Meijer GA, Kuipers EJ. Risk of malignant progression in patients with Barrett's oesophagus: a Dutch nationwide cohort study. Gut 2010 Aug;59(8):1030-6 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/20639249.
  14. 14.0 14.1 Coleman HG, Bhat S, Johnston BT, McManus D, Gavin AT, Murray LJ. Tobacco smoking increases the risk of high-grade dysplasia and cancer among patients with Barrett's esophagus. Gastroenterology 2012 Feb;142(2):233-40 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/22062359.
  15. Hardikar S, Onstad L, Blount PL, Odze RD, Reid BJ, Vaughan TL. The role of tobacco, alcohol, and obesity in neoplastic progression to esophageal adenocarcinoma: a prospective study of Barrett's esophagus. PLoS One 2013;8(1):e52192 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/23300966.
  16. Oberg S, Wenner J, Johansson J, Walther B, Willén R. Barrett esophagus: risk factors for progression to dysplasia and adenocarcinoma. Ann Surg 2005 Jul;242(1):49-54 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/15973101.
  17. Chak A, Chen Y, Vengoechea J, Canto MI, Elston R, Falk GW, et al. Variation in age at cancer diagnosis in familial versus nonfamilial Barrett's esophagus. Cancer Epidemiol Biomarkers Prev 2012 Feb;21(2):376-83 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/22178570.
  18. Corley DA, Kubo A, Levin TR, Block G, Habel L, Rumore G, et al. Race, ethnicity, sex and temporal differences in Barrett's oesophagus diagnosis: a large community-based study, 1994-2006. Gut 2009 Feb;58(2):182-8 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/18978173.
  19. Ford AC, Forman D, Reynolds PD, Cooper BT, Moayyedi P. Ethnicity, gender, and socioeconomic status as risk factors for esophagitis and Barrett's esophagus. Am J Epidemiol 2005 Sep 1;162(5):454-60 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/16076833.
  20. Dong LM, Kristal AR, Peters U, Schenk JM, Sanchez CA, Rabinovitch PS, et al. Dietary supplement use and risk of neoplastic progression in esophageal adenocarcinoma: a prospective study. Nutr Cancer 2008;60(1):39-48 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/18444134.
  21. Singh S, Garg SK, Singh PP, Iyer PG, El-Serag HB. Acid-suppressive medications and risk of oesophageal adenocarcinoma in patients with Barrett's oesophagus: a systematic review and meta-analysis. Gut 2013 Nov 12 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/24221456.
  22. Fitzgerald RC, di Pietro M, Ragunath K, Ang Y, Kang JY, Watson P, et al. British Society of Gastroenterology guidelines on the diagnosis and management of Barrett's oesophagus. Gut 2014 Jan;63(1):7-42 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/24165758.
  23. Wang KK, Sampliner RE, Practice Parameters Committee of the American College of Gastroenterology. Updated guidelines 2008 for the diagnosis, surveillance and therapy of Barrett's esophagus. Am J Gastroenterol 2008 Mar;103(3):788-97 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/18341497.

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Appendices


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