Title: Diabetes and risk of esophageal and gastric adenocarcinomas.
Authors: Jiang, Xuejuan; Bernstein, Leslie; Tseng, Chiu-Chen; Wu, Anna H
Published In Int J Cancer, (2012 Sep 15)
Abstract: Diabetes has been consistently associated with an increased risk of liver, pancreas and endometrial cancer and has been implicated as a risk factor for esophageal and gastric cancers, although this association has been less well studied. We sought to determine the role of diabetes in the etiology of esophageal, gastric cardia and distal gastric adenocarcinomas (DGAs). This analysis included patients with esophageal adenocarcinoma (EA) (n = 209), gastric cardia adenocarcinoma (GCA) (n = 257) and DGA (n = 382), and 1,309 control participants from a population-based case-control study conducted in Los Angeles County. The study included non-Hispanic whites, African Americans, Hispanics and Asian Americans. The association of diabetes with the three tumor types was estimated using polytomous logistic regression. Odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were estimated. Nine percent of control participants and 13% of the case patients reported a history of diabetes. After adjustment for age, gender, race, birthplace, education, cigarette smoking status and body mass index, diabetes was associated with an increased risk of EA (OR, 1.48; 95% CI, 0.94-2.32; p = 0.089) and DGA (OR, 1.47; 95% CI, 1.01-2.15; p = 0.045), but was not associated with risk of GCA (OR, 0.96; 95% CI, 0.59-1.55; p = 0.87). However, the association between diabetes and risk of DGA was statistically significant only among patients for whom we interviewed their next of kin. Our study further investigated the association between diabetes and adenocarcinomas of the esophagus and distal stomach.
PubMed ID: 22161620
MeSH Terms: Adenocarcinoma/etiology*; Adult; Aged; Cardia; Case-Control Studies; Diabetes Complications/etiology*; Esophageal Neoplasms/etiology*; Female; Humans; Logistic Models; Male; Middle Aged; Odds Ratio; Risk; Stomach Neoplasms/etiology*