Zhang Shi-Hao, Wang Yan, Wang Hejie, Zhong Menglan, Qi Xiaona, Xie Shao-Hua
School of Public Health, Fujian Medical University, Fuzhou, China.
Department of Nursing, Harbin Medical University Cancer Hospital, Harbin, China.
Cancer Epidemiol. 2025 Aug;97:102849. doi: 10.1016/j.canep.2025.102849. Epub 2025 May 17.
Previous epidemiological studies have provided inconsistent findings regarding the association between metabolic syndrome (MetS) and risk of esophageal cancer.
We conducted a comprehensive literature search for prospective studies in MEDLINE and EMBASE databases through April 2024. Random-effects meta-analysis was used to calculate pooled hazard ratios (HR) with 95 % confidence intervals (CI) for the associations between MetS and risk of esophageal cancer by histological type. Between-study heterogeneity was assessed by Cochran's Q test and I statistics.
Among 8097 identified studies, six studies were included. MetS was associated with an increased risk of esophageal adenocarcinoma (pooled HR=1.24; 95 %CI, 1.07-1.42; P=0.392, I=3.8 %, N = 6), but not esophageal squamous cell carcinoma (HR=0.89; 95 % CI, 0.58-1.36; P=0.040, I=68.9 %, N = 3). An increased risk of esophageal adenocarcinoma was indicated for hyperglycemia (HR= 1.14; 95 % CI, 1.01-1.29; P=0.693, I=0.0 %, N = 3) and obesity (HR=1.50; 95 % CI, 1.24-1.82; P=0.191, I=34.5 %, N = 5), rather than the other components of MetS, i.e. hypertension or levels of triglyceride or high-density lipoprotein. Hypertension was associated with seemingly increased risk of esophageal squamous cell carcinoma (HR=1.39; 95 % CI, 0.93-2.09; P=0.030, I=71.4 %, N = 3), while obesity was associated with a decreased risk (HR=0.65; 95 % CI, 0.38-1.12; P=0.009, I=78.7 %, N = 3); no associations were observed for the other components of MetS with esophageal squamous cell carcinoma.
MetS, particularly hyperglycemia and obesity, may increase the risk of esophageal adenocarcinoma. MetS, by and large, may not influence the risk of esophageal squamous cell carcinoma.
既往流行病学研究关于代谢综合征（MetS）与食管癌风险之间的关联得出了不一致的结果。
我们在MEDLINE和EMBASE数据库中对截至2024年4月的前瞻性研究进行了全面的文献检索。采用随机效应荟萃分析来计算合并风险比（HR）及95%置信区间（CI），以评估MetS与不同组织学类型食管癌风险之间的关联。通过Cochran's Q检验和I统计量评估研究间的异质性。
在8097项检索到的研究中，纳入了6项研究。MetS与食管腺癌风险增加相关（合并HR = 1.24；95%CI，1.07 - 1.42；P = 0.392，I = 3.8%，N = 6），但与食管鳞状细胞癌无关（HR = 0.89；95%CI，0.58 - 1.36；P = 0.040，I = 68.9%，N = 3）。高血糖（HR = 1.14；95%CI，1.01 - 1.29；P = 0.693，I = 0.0%，N = 3）和肥胖（HR = 1.50；95%CI，1.24 - 1.82；P = 0.191，I = 34.5%，N = 5）提示食管腺癌风险增加，但MetS的其他组分，即高血压、甘油三酯水平或高密度脂蛋白水平与食管腺癌风险增加无关。高血压似乎与食管鳞状细胞癌风险增加相关（HR = 1.39；95%CI，0.93 - 2.09；P = 0.030，I = 71.4%，N = 3），而肥胖与食管鳞状细胞癌风险降低相关（HR = 0.65；95%CI，0.38 - 1.12；P = 0.009，I = 78.7%，N = 3）；未观察到MetS的其他组分与食管鳞状细胞癌之间存在关联。
MetS，尤其是高血糖和肥胖，可能增加食管腺癌的风险。总体而言，MetS可能不会影响食管鳞状细胞癌的风险。
