The relationship between metabolic syndrome and increased risk of Barrett's esophagus: an updated systematic review and meta-analysis.
Barrett’s esophagus
Meta-analysis
Metabolic syndrome
Journal
BMC gastroenterology
ISSN: 1471-230X
Titre abrégé: BMC Gastroenterol
Pays: England
ID NLM: 100968547
Informations de publication
Date de publication:
06 May 2020
06 May 2020
Historique:
received:
27
08
2019
accepted:
05
04
2020
entrez:
8
5
2020
pubmed:
8
5
2020
medline:
20
2
2021
Statut:
epublish
Résumé
The relationship between metabolic syndrome (MetS) and Barrett's esophagus (BE) is still a challenging issue, and inconsistent results have been reported in different studies. Therefore, this study was conducted to determine the relationship between MetS and BE. In this study, we followed the MOOSE protocol and results were reported according to the PRISMA guidelines. All study steps were performed independently by two authors. If necessary, the dispute was resolved by consultation with a third author. The search strategy is designed to find published studies. Comprehensive search was done in the following databases until July 2019: Cochrane Library, PubMed/Medline, Web of Science, Science Direct, EMBASE, Scopus, CINAHL, EBSCO, and Google Scholar search engine. All analyses were performed using Comprehensive Meta-Analysis Software Ver.2, while p-value lower than 0.05 was considered significant. In 14 studies with a sample size of 108,416, MetS significantly increased the risk of BE (OR = 1.354; 95% CI: 1.145-1.600; P < 0.001; Heterogeneity: I MetS increases the risk of BE compared to control groups. The results of this study can help health practitioners by identifying a treatable risk factor for the most important risk factor for esophageal carcinoma (ie, BE). Future studies should examine whether treatment for MetS reduces the risk of BE.
Sections du résumé
BACKGROUND
BACKGROUND
The relationship between metabolic syndrome (MetS) and Barrett's esophagus (BE) is still a challenging issue, and inconsistent results have been reported in different studies. Therefore, this study was conducted to determine the relationship between MetS and BE.
METHODS
METHODS
In this study, we followed the MOOSE protocol and results were reported according to the PRISMA guidelines. All study steps were performed independently by two authors. If necessary, the dispute was resolved by consultation with a third author. The search strategy is designed to find published studies. Comprehensive search was done in the following databases until July 2019: Cochrane Library, PubMed/Medline, Web of Science, Science Direct, EMBASE, Scopus, CINAHL, EBSCO, and Google Scholar search engine. All analyses were performed using Comprehensive Meta-Analysis Software Ver.2, while p-value lower than 0.05 was considered significant.
RESULTS
RESULTS
In 14 studies with a sample size of 108,416, MetS significantly increased the risk of BE (OR = 1.354; 95% CI: 1.145-1.600; P < 0.001; Heterogeneity: I
CONCLUSION
CONCLUSIONS
MetS increases the risk of BE compared to control groups. The results of this study can help health practitioners by identifying a treatable risk factor for the most important risk factor for esophageal carcinoma (ie, BE). Future studies should examine whether treatment for MetS reduces the risk of BE.
Identifiants
pubmed: 32375671
doi: 10.1186/s12876-020-01267-2
pii: 10.1186/s12876-020-01267-2
pmc: PMC7412848
doi:
Types de publication
Journal Article
Meta-Analysis
Systematic Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
138Références
Neurogastroenterol Motil. 2011 Nov;23(11):989-94
pubmed: 21914043
Clin Gastroenterol Hepatol. 2013 Nov;11(11):1399-1412.e7
pubmed: 23707461
Cancer. 2017 Feb 15;123(4):657-665
pubmed: 27861759
J Gastroenterol Hepatol. 2007 Nov;22(11):1732-6
pubmed: 17914942
BMJ. 2015 Jan 02;350:g7647
pubmed: 25555855
Clin Gastroenterol Hepatol. 2018 Jul;16(7):1046-1055.e8
pubmed: 29199147
Am J Physiol Endocrinol Metab. 2003 Jun;284(6):E1065-71
pubmed: 12554597
JAMA. 2000 Apr 19;283(15):2008-12
pubmed: 10789670
Mayo Clin Proc. 2013 Feb;88(2):157-65
pubmed: 23374619
Gut. 2005 Aug;54(8):1062-6
pubmed: 15857935
Helicobacter. 2018 Aug;23(4):e12504
pubmed: 29938864
Clin Gastroenterol Hepatol. 2013 Aug;11(8):934-43
pubmed: 23466711
J Dig Dis. 2018 Dec;19(12):737-744
pubmed: 30375167
Gut. 2014 Jan;63(1):191-202
pubmed: 24092861
Biometrics. 1994 Dec;50(4):1088-101
pubmed: 7786990
Dig Dis Sci. 2016 Jan;61(1):238-46
pubmed: 26386857
Ann Surg. 2008 Jun;247(6):909-15
pubmed: 18520215
Dis Esophagus. 2010 Jul;23(5):386-91
pubmed: 20353443
Therap Adv Gastroenterol. 2019 Jun 03;12:1756284819853115
pubmed: 31210784
Dig Dis Sci. 2006 Mar;51(3):539-42
pubmed: 16614964
Metabolism. 2003 May;52(5):616-9
pubmed: 12759893
J Clin Gastroenterol. 2015 Apr;49(4):282-8
pubmed: 24671095
Therap Adv Gastroenterol. 2014 Nov;7(6):247-68
pubmed: 25364384
J Chin Med Assoc. 2017 Jan;80(1):15-18
pubmed: 27756532
Medicine (Baltimore). 2016 Aug;95(31):e4338
pubmed: 27495039
Cancer Epidemiol. 2016 Jun;42:9-14
pubmed: 26972225
Diabetes Metab Syndr. 2019 Mar - Apr;13(2):1481-1489
pubmed: 31336510
Am J Gastroenterol. 2008 Mar;103(3):788-97
pubmed: 18341497
Clin Cardiol. 2007 Dec;30(12):593-7
pubmed: 17607758
BMJ. 1997 Sep 13;315(7109):629-34
pubmed: 9310563
Atherosclerosis. 1999 Jan;142(1):207-10
pubmed: 9920523
Gastroenterology. 1997 May;112(5):1442-7
pubmed: 9136820
Clin Gastroenterol Hepatol. 2015 Nov;13(11):1907-18
pubmed: 26260107
Eur J Intern Med. 2002 Sep;13(6):369
pubmed: 12225781
Med Decis Making. 2005 Nov-Dec;25(6):646-54
pubmed: 16282215
Gastroenterol Clin North Am. 2015 Jun;44(2):203-31
pubmed: 26021191
Aliment Pharmacol Ther. 2015 Jun;41(11):1182-9
pubmed: 25801197
Obes Rev. 2002 Feb;3(1):9-15
pubmed: 12119661