Metabolic syndrome and esophageal cancer risk: a systematic review and meta-analysis

被引:21
作者
Zhang, Jinjia [1 ]
Wu, Huadong [2 ]
Wang, Rongying [1 ]
机构
[1] Hebei Med Univ, Hosp 2, Dept Gen Practice, Heping Western Rd 215, Shijiazhuang 050000, Hebei, Peoples R China
[2] Hebei Med Univ, Hosp 2, Dept Gastrointestinal Surg, Shijiazhuang 050000, Hebei, Peoples R China
关键词
Metabolic syndrome; Esophageal cancer; Meta-analysis; BARRETTS-ESOPHAGUS; ADENOCARCINOMA; OBESITY; ASSOCIATION; HETEROGENEITY; PREVALENCE; CARCINOMA; LEPTIN;
D O I
10.1186/s13098-021-00627-6
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective Many clinical studies evaluating the relationship between metabolic syndrome and esophageal cancer yielded uncertain results. The purpose of this study is to systematically assess the relationship between metabolic syndrome and esophageal cancer. Methods We searched clinical studies on metabolic syndrome and esophageal cancer risk in PubMed, Embase, and the Cochrane Library. Meta-analysis was conducted by RevMan 5.3 softwares. Results A total of four cohort studies and two case-control studies met eligibility criteria and were included in the meta-analysis. Meta-analysis using a fixed-effect model indicated that MetS was related with a higher risk of EC (OR: 1.16, 95% CI 1.08-1.25). Subgroup analyses grouped by pathological types showed that MetS was related with a higher risk of EAC (OR: 1.19, 95% CI 1.10-1.28). Subgroup analyses grouped by metabolic conditions showed hyperglycemia (OR: 1.12, 95% CI 1.03-1.21),hypertension (OR: 1.23, 95% CI 1.04-1.46), obesity (OR: 1.40, 95% CI 1.22-1.60, P < 0.05) were related with a higher risk of EAC. Conclusions Overall, our meta-analysis provides high quality evidence that metabolic syndrome was related with a higher risk of EAC. Among the individual components of the metabolic syndrome, hyperglycemia, hypertension and obesity may be the key factors.
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页数:9
相关论文
共 49 条
[1]   Metabolic syndrome - a new world-wide definition. A consensus statement from the international diabetes federation [J].
Alberti, KGMM ;
Zimmet, P ;
Shaw, J .
DIABETIC MEDICINE, 2006, 23 (05) :469-480
[2]   The metabolic syndrome - a new worldwide definition [J].
Alberti, KGMM ;
Zimmet, P ;
Shaw, J .
LANCET, 2005, 366 (9491) :1059-1062
[3]   Predictive value in the analysis of RNASEL genotypes in relation to prostate cancer [J].
Alvarez-Cubero, M. J. ;
Entrala, C. ;
Fernandez-Rosado, F. ;
Martinez-Gonzalez, L. J. ;
Alvarez, J. C. ;
Suarez, A. ;
Lorente, J. A. ;
Cozar, J. M. .
PROSTATE CANCER AND PROSTATIC DISEASES, 2012, 15 (02) :144-149
[4]   The Link between the Metabolic Syndrome and Cancer [J].
Braun, Sandra ;
Bitton-Worms, Keren ;
LeRoith, Derek .
INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES, 2011, 7 (07) :1003-1015
[5]  
Bray F, 2018, CA-CANCER J CLIN, V68, P394, DOI [10.3322/caac.21492, 10.3322/caac.21609]
[6]   The pathobiology of diabetic complications - A unifying mechanism [J].
Brownlee, M .
DIABETES, 2005, 54 (06) :1615-1625
[7]   Hyperinsulinaemia and hyperglycaemia: possible risk factors of colorectal cancer among diabetic patients [J].
Chang, CK ;
Ulrich, CM .
DIABETOLOGIA, 2003, 46 (05) :595-607
[8]   O Alcohol consumption and liver cancer risk: a meta-analysis [J].
Chuang, Shu-Chun ;
Lee, Yuan-Chin Amy ;
Wu, Guo-Jie ;
Straif, Kurt ;
Hashibe, Mia .
CANCER CAUSES & CONTROL, 2015, 26 (09) :1205-1231
[9]   Abdominal obesity and the risk of esophageal and gastric cardia carcinomas [J].
Corley, Douglas A. ;
Kubo, Ai ;
Zhao, Wei .
CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION, 2008, 17 (02) :352-358
[10]   Adiponectin mediates antiproliferative and apoptotic responses in human MCF7 breast cancer cells [J].
Dieudonne, Marie-Noelle ;
Bussiere, Marianne ;
Dos Santos, Esther ;
Leneveu, Marie-Christine ;
Giudicelli, Yves ;
Pecquery, Rene .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2006, 345 (01) :271-279