Risk Factors for Progression of Barrett's Esophagus to High Grade Dysplasia and Esophageal Adenocarcinoma.
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
17 03 2020
17 03 2020
Historique:
received:
05
07
2019
accepted:
01
03
2020
entrez:
19
3
2020
pubmed:
19
3
2020
medline:
18
11
2020
Statut:
epublish
Résumé
Barrett's esophagus (BE) is the only known precursor to esophageal adenocarcinoma (EAC). Methods of identifying BE patients at high risk for progression to high-grade dysplasia (HGD) or EAC are needed to improve outcomes and identify who will benefit most from intensive surveillance or ablative therapy. Clinical predictors of BE progression to HGD or EAC are poorly understood, with multiple contradictory studies. We performed a retrospective study which included 460 patients at Johns Hopkins Hospital who underwent at least 2 upper endoscopies 6 months apart showing biopsy-documented BE between 1992 and 2013. Patients with EAC or HGD at the initial endoscopy were excluded. Demographic, clinicopathological, and endoscopic data were collected. Univariate and multivariate Cox proportional hazards analyses with time to progression to HGD and EAC were performed. Among 460 patients included in the study, 132 BE patients developed HGD and 62 developed EAC. Significant EAC risk factors included age, abdominal obesity, caffeine intake, and the presence of HGD. Risk factors for HGD or EAC included age, caffeine intake, and low-grade dysplasia while colonic adenomas trended towards significance. Notably, a history of statin or SSRI usage reduced the risk of EAC or HGD by 49% or 61%, respectively. Our study validated several known and identified several novel risk factors, including a history of colonic adenomas or caffeine usage. Low-grade dysplasia was a risk factor for progression but various endoscopic characteristics were not, suggesting that screening strategies should focus on histology instead. We identified SSRIs as a new potentially chemoprotective medication.
Identifiants
pubmed: 32184470
doi: 10.1038/s41598-020-61874-7
pii: 10.1038/s41598-020-61874-7
pmc: PMC7078316
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
4899Subventions
Organisme : NCI NIH HHS
ID : P50 CA062924
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK118250
Pays : United States
Références
Spechler, S. J. Barrett esophagus and risk of esophageal cancer: a clinical review. JAMA 310, 627–636 (2013).
doi: 10.1001/jama.2013.226450
El-Serag, H. B. et al. Surveillance endoscopy is associated with improved outcomes of oesophageal adenocarcinoma detected in patients with Barrett’s oesophagus. Gut (2015).
Hvid-Jensen, F., Pedersen, L., Drewes, A. M., Sorensen, H. T. & Funch-Jensen, P. Incidence of adenocarcinoma among patients with Barrett’s esophagus. N. Engl. J. Med. 365, 1375–1383 (2011).
doi: 10.1056/NEJMoa1103042
Krishnamoorthi, R. et al. Rates and predictors of progression to esophageal carcinoma in a large population-based Barrett’s esophagus cohort. Gastrointest. Endosc. 84, 40–46 e47 (2016).
doi: 10.1016/j.gie.2015.12.036
Thrift, A. P., Kramer, J. R., Qureshi, Z., Richardson, P. A. & El-Serag, H. B. Age at onset of GERD symptoms predicts risk of Barrett’s esophagus. Am. J. Gastroenterol. 108, 915–922 (2013).
doi: 10.1038/ajg.2013.72
Tibshirani, R. Regression shrinkage and selection via the lasso. Journal of the Royal Statistical Society. Series B (Methodological), 267–288 (1996).
Grambsch, P. M. & Therneau, T. M. Proportional hazards tests and diagnostics based on weighted residuals. Biometrika 81, 515–526 (1994).
doi: 10.1093/biomet/81.3.515
Mathieu, L. N., Kanarek, N. F., Tsai, H. L., Rudin, C. M. & Brock, M. V. Age and sex differences in the incidence of esophageal adenocarcinoma: results from the Surveillance, Epidemiology, and End Results (SEER) Registry (1973-2008). Dis. Esophagus 27, 757–763 (2014).
doi: 10.1111/dote.12147
Cohen, S. & Booth, G. H. Jr. Gastric acid secretion and lower-esophageal-sphincter pressure in response to coffee and caffeine. N. Engl. J. Med. 293, 897–899 (1975).
doi: 10.1056/NEJM197510302931803
Zamora-Ros, R. et al. Tea and coffee consumption and risk of esophageal cancer: the European prospective investigation into cancer and nutrition study. Int. J. Cancer 135, 1470–1479 (2014).
doi: 10.1002/ijc.28789
Ren, J. S. et al. Tea, coffee, carbonated soft drinks and upper gastrointestinal tract cancer risk in a large United States prospective cohort study. Eur. J. Cancer 46, 1873–1881 (2010).
doi: 10.1016/j.ejca.2010.03.025
Sajja, K. C., El-Serag, H. B. & Thrift, A. P. Coffee or Tea, Hot or Cold, Are Not Associated With Risk of Barrett’s Esophagus. Clin. Gastroenterol. Hepatol. 14, 769–772 (2016).
doi: 10.1016/j.cgh.2015.12.007
Kumaravel, A. et al. Higher prevalence of colon polyps in patients with Barrett’s esophagus: a case-control study. Gastroenterol. Rep. 2, 281–287 (2014).
doi: 10.1093/gastro/gou050
Wilson, K. T., Fu, S., Ramanujam, K. S. & Meltzer, S. J. Increased expression of inducible nitric oxide synthase and cyclooxygenase-2 in Barrett’s esophagus and associated adenocarcinomas. Cancer Res. 58, 2929–2934 (1998).
Blount, P. L. et al. Clonal ordering of 17p and 5q allelic losses in Barrett dysplasia and adenocarcinoma. Proc. Natl Acad. Sci. USA 90, 3221–3225 (1993).
doi: 10.1073/pnas.90.8.3221
Rex, D. K. et al. Screening for Barrett’s esophagus in colonoscopy patients with and without heartburn. Gastroenterology 125, 1670–1677 (2003).
doi: 10.1053/j.gastro.2003.09.030
Sikkema, M. et al. Predictors for neoplastic progression in patients with Barrett’s Esophagus: a prospective cohort study. Am. J. Gastroenterol. 106, 1231–1238 (2011).
doi: 10.1038/ajg.2011.153
Weston, A. P. et al. Long-term follow-up of Barrett’s high-grade dysplasia. Am. J. Gastroenterol. 95, 1888–1893 (2000).
doi: 10.1111/j.1572-0241.2000.02234.x
Wani, S. et al. Risk factors for progression of low-grade dysplasia in patients with Barrett’s esophagus. Gastroenterology 141, 1179–1186, 1186 e1171 (2011).
Corley, D. A. et al. Impact of endoscopic surveillance on mortality from Barrett’s esophagus-associated esophageal adenocarcinomas. Gastroenterology 145, 312–319 e311 (2013).
doi: 10.1053/j.gastro.2013.05.004
Visrodia, K. et al. Magnitude of Missed Esophageal Adenocarcinoma After Barrett’s Esophagus Diagnosis: A Systematic Review and Meta-analysis. Gastroenterology 150, 599–607 e597; quiz e514–595 (2016).
Visrodia, K. et al. Systematic review with meta-analysis: prevalent vs. incident oesophageal adenocarcinoma and high-grade dysplasia in Barrett’s oesophagus. Aliment. Pharmacol. Ther. 44, 775–784 (2016).
doi: 10.1111/apt.13783
Kastelein, F., et al. Nonsteroidal anti-inflammatory drugs and statins have chemopreventative effects in patients with Barrett’s esophagus. Gastroenterology 141, 2000–2008; quiz e2013-2004 (2011).
Yue, C. T. & Liu, Y. L. Fluoxetine increases extracellular levels of 3-methoxy-4-hydroxyphenylglycol in cultured COLO320 DM cells. Cell Biochem. Funct. 23, 109–114 (2005).
doi: 10.1002/cbf.1193
Greer, K. B. et al. Insulin/Insulin-Like Growth Factor-1 Pathway in Barrett’s Carcinogenesis. Clin. Transl. Gastroenterol. 4, e31 (2013).
doi: 10.1038/ctg.2013.2
Trowbridge, R., Mittal, S. K., Sharma, P., Hunter, W. J. & Agrawal, D. K. Vitamin D receptor expression in the mucosal tissue at the gastroesophageal junction. Exp. Mol. Pathol. 93, 246–249 (2012).
doi: 10.1016/j.yexmp.2012.05.007