Background and aims Sessile serrated adenomas (SSAs) are recognised as precursors to microsatellite unstable adenocarcinomas. This study attempts to estimate the progression rate of SSAs based upon the epidemiology of a large cohort as well as identify relationships to other colorectal polyps. Methods Pathological reports generated at Caris Diagnostics from 290 810 colonoscopic specimens on 179 111 patients were analysed using computerised algorithms.

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In genomic analyses of BE tissues from patients with or without later progression to HGD or EAC, we found significantly higher numbers of TP53 mutations in BE from patients with subsequent progression. These mutations were frequently detected before the onset of dysplasia or substantial changes in copy number.

Background & Aims Eosinophilic esophagitis (EoE) is of increasing prevalence and thought to result from allergic processes. Helicobacter pylori has been inversely associated with allergic diseases, but there is no known relationship between H. pylori, EoE and esophageal eosinophilia. We investigated the association between esophageal eosinophilia and H. pylori infection. Methods We performed a cross-sectional study of data, collected from a United States pathology database, on 165,017 patients in the US who received esophageal and gastric biopsies from 2008 and 2010. Patients with and without H. pylori on gastric biopsy were compared and odds of esophageal eosinophilia were determined. Results From the data analyzed, 56,301 (34.1%) had normal esophageal biopsies, 5,767 (3.5%) had esophageal eosinophilia, and 11,170 (4.8%) had H. pylori infection. Esophageal eosinophilia was inversely associated with H. pylori (odds ration [OR]: 0.77, 95% confidence interval [CI]: 0.69–0.87). Compared to patients with normal esophageal biopsies, odds of H. pylori were reduced among patients with ≥15 eosinophils per high-power field (eos/hpf) (OR 0.79; 95% CI 0.70–0.88), ≥45 eos/hpf (OR 0.75; 0.61–0.93), ≥75 eos/hpf (OR 0.72; 0.62–0.83), and ≥90 eos/hpf (OR 0.52; 0.31–0.87) (p for trend <0.001). A similar dose-response trend was observed for increasing clinical suspicion for EoE and decreasing prevalence of H pylori. Additionally, severity of histologic effects of H. pylori was inversely associated with esophageal eosinophilia. All trends held in multivariate analysis. Conclusions In a large cross-sectional analysis, H. pylori infection was inversely associated with esophageal eosinophilia. This relationship could have implications for the pathogenesis and epidemiology of EoE.