Leukocyte telomere length in relation to the risk of Barretts esophagus and esophageal adenocarcinoma

摘要

Chronic inflammation and oxidative damage caused by obesity, cigarette smoking, and chronic gastroesophageal reflux disease (GERD) are major risk factors associated with Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC). EAC has been increasing the past few decades, and early discovery and treatment are crucial for survival. Telomere shortening due to cell division and oxidative damage may reflect the impact of chronic inflammation and could possibly be used as predictor for disease development. We examined the prevalence of shorter leukocyte telomere length (LTL) among individuals with GERD, BE, or EAC using a pooled analysis of studies from the Barrett's and Esophageal Adenocarcinoma Consortium (BEACON). Telomere length was measured in leukocyte DNA samples by Q‐PCR. Participants included 1173 patients (386 with GERD, 384 with EAC, 403 with BE) and 736 population‐based controls. The association of LTL (in tertiles) along the continuum of disease progression from GERD to style="fixed-case">BE to style="fixed-case">EAC was calculated using study‐specific odds ratios ( style="fixed-case">ORs) and 95% confidence intervals ( style="fixed-case">CIs) from logistic regression models adjusted for potential confounders. Shorter style="fixed-case">LTL were less prevalent among style="fixed-case">GERD patients ( style="fixed-case">OR 0.57; 95% style="fixed-case">CI: 0.35–0.93), compared to population‐based controls. No statistically significant increased prevalence of short/long style="fixed-case">LTL among individuals with style="fixed-case">BE or style="fixed-case">EAC was observed. In contrast to some earlier reports, our findings add to the evidence that leukocyte telomere length is not a biomarker of risk related to the etiology of style="fixed-case">EAC. The findings do not suggest a relationship between style="fixed-case">LTL and style="fixed-case">BE or style="fixed-case">EAC.