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Pinning Down Cancer Risk in Barrett Esophagus with LGD

Summary and Comment |
June 17, 2014

Pinning Down Cancer Risk in Barrett Esophagus with LGD

  1. David A. Johnson, MD

Annual incidence of EAC in pooled cohort data was 0.54% but varied by LGD prevalence in cohorts, a surrogate for quality of pathology reporting.

  1. David A. Johnson, MD

The estimated rate of progression of Barrett esophagus (BE) with low-grade dysplasia (LGD) to esophageal adenocarcinoma (EAC) ranges widely from <0.2% to >3% annually, in large part because of interobserver variability among pathologists. In the current systematic review and meta-analysis, investigators estimated the incidence of EAC using cohort studies with a minimum mean follow-up of 2 years after diagnosis of BE with LGD and LGD duration >6 months before incidence of high-grade dysplasia (HGD) or EAC.

In 24 studies comprising 2694 patients and 16,672 patient-years of follow-up, the pooled incidence rate (IR) of EAC was 0.54% annually, ranging from 0.02% to 11.43% in individual studies. Significant heterogeneity was observed. The pooled IR of HGD, EAC, or both was 1.73% per year. A ratio of patients with LGD to all patients with BE in each cohort was used as a surrogate for selection bias and quality of pathology reporting. In the 14 studies with LGD:BE ratios <0.15 (the estimated prevalence of BE with LGD), the pooled IR of EAC was 0.76%, with low heterogeneity between studies. In the six studies with two expert GI pathologists, the pooled IR of EAC was 1.6%. Estimated incidence was similar with use of prevalent versus incident BE, unifocal versus multifocal LGD, and long-segment versus short-segment BE. In four studies, cause-specific mortality rates were between 1.0% and 2.2% for EAC and 28.3% for nonesophageal disease.

Comment

These findings will provide guidance for informed discussions and management of patients with BE with LGD. Ideally, all cases of BE with LGD should be confirmed by an expert GI pathologist after any esophageal inflammation is resolved using a course of proton-pump inhibitor therapy. Carefully analyze your local pathologist's expertise. Better data are still needed to distinguish mortality from EAC versus other causes to help guide best strategies and determine cost-effectiveness of surveillance and ablative therapies.

  • Disclosures for David A. Johnson, MD at time of publication Consultant / Advisory board Takeda Pharmaceuticals; Abbott Laboratories; MedScape; Pfizer; CRH Medical; Epigenomics AG; Centocor Speaker's bureau Takeda Pharmaceuticals Editorial boards ACG Education Universe; MedScape Gastroenterology Leadership positions in professional societies GI Quality Improvement Consortium (Director and Treasurer)

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