In the Journals

Barrett's esophagus, persistent low-grade dysplasia increase high-grade dysplasia, cancer risk

The risk for progression to high-grade dysplasia and esophageal adenocarcinoma was found to be increased in patients with both Barrett’s esophagus and confirmed persistent low-grade dysplasia.

Peter D. Siersema

The researchers defined confirmed LGD as a pathologist-confirmed diagnosis, and persistent LGD as disease detected at both the first and follow-up endoscopy (median, 11.7 months). Patient data were evaluated until the following: the patient was treated for high-grade dysplasia (HGD); esophageal adenocarcinoma (EAC) was detected; or the last biopsy was collected with endoscopy through July 2014. The researchers then used uni- and multivariable Cox regression analyses to determine risk for malignant progression. 

In patients with confirmed LGD at the first endoscopy (10%) the incidence of HGD and/or EAC was 5.18/100 person-years (95% CI, 4.32-8.1/100 person-years) compared with 1.85/100 person-years (95% CI 1.52-2.22/100 person-years) in patients without a confirmed diagnosis of LGD at first endoscopy. The incidence of EAC alone was 2.51/100 person-years (95% CI, 1.46-3.99/100 person-years), compared with 1.01/per 100 person-years (95% CI, 0.41-2.1/100 person-years).

At first follow-up, persistent LGD was found in 30% of patients with confirmed LGD, while no dysplasia was found at first follow-up in 51% of patients with confirmed LGD. Patients with persistent LGD were found to be at higher risk for the development of HGD and/or EAC, with a HR of 3.5 (95% CI, 1.48-8.28). The incidence of HGD and/or EAC was 7.65/100 person-years (95% CI, 4.45-12.34) for patients with persistent LGD, compared with 2.32/100 person-years (95% CI, 1.08-4.4/100 person-years) for patients without persistent LGD, making persistent LGD an independent HGD and EAC risk factor. 

“In this large nationwide cohort of BE patients with LGD, we demonstrate that confirmed and persistent LGD identifies a subgroup of patients with an increased risk of malignant progression. In addition, in half of these patients LGD was no longer detected during follow-up and a quarter of them exhibited persistent [no dysplasia] BE. We therefore believe that endoscopic treatment of LGD BE is indicated in patients with confirmed and persistent LGD. In patients in whom confirmed LGD does not persist, it may well be that a wait and see policy is justified,” the researchers wrote.

Disclosures: The researchers report no relevant financial disclosures.

The risk for progression to high-grade dysplasia and esophageal adenocarcinoma was found to be increased in patients with both Barrett’s esophagus and confirmed persistent low-grade dysplasia.

Peter D. Siersema, MD, PhD, chief of the department of gastroenterology and hepatology at the University Medical Center, Utrecht, the Netherlands, and colleagues conducted a retrospective study using a nationwide registry of histopathology diagnoses in the Netherlands (PALGA). Information was examined on 1,579 patients with Barrett’s esophagus (BE) and confirmed low-grade dysplasia (LGD) from 2005 through 2010.

Peter D. Siersema

The researchers defined confirmed LGD as a pathologist-confirmed diagnosis, and persistent LGD as disease detected at both the first and follow-up endoscopy (median, 11.7 months). Patient data were evaluated until the following: the patient was treated for high-grade dysplasia (HGD); esophageal adenocarcinoma (EAC) was detected; or the last biopsy was collected with endoscopy through July 2014. The researchers then used uni- and multivariable Cox regression analyses to determine risk for malignant progression. 

In patients with confirmed LGD at the first endoscopy (10%) the incidence of HGD and/or EAC was 5.18/100 person-years (95% CI, 4.32-8.1/100 person-years) compared with 1.85/100 person-years (95% CI 1.52-2.22/100 person-years) in patients without a confirmed diagnosis of LGD at first endoscopy. The incidence of EAC alone was 2.51/100 person-years (95% CI, 1.46-3.99/100 person-years), compared with 1.01/per 100 person-years (95% CI, 0.41-2.1/100 person-years).

At first follow-up, persistent LGD was found in 30% of patients with confirmed LGD, while no dysplasia was found at first follow-up in 51% of patients with confirmed LGD. Patients with persistent LGD were found to be at higher risk for the development of HGD and/or EAC, with a HR of 3.5 (95% CI, 1.48-8.28). The incidence of HGD and/or EAC was 7.65/100 person-years (95% CI, 4.45-12.34) for patients with persistent LGD, compared with 2.32/100 person-years (95% CI, 1.08-4.4/100 person-years) for patients without persistent LGD, making persistent LGD an independent HGD and EAC risk factor. 

“In this large nationwide cohort of BE patients with LGD, we demonstrate that confirmed and persistent LGD identifies a subgroup of patients with an increased risk of malignant progression. In addition, in half of these patients LGD was no longer detected during follow-up and a quarter of them exhibited persistent [no dysplasia] BE. We therefore believe that endoscopic treatment of LGD BE is indicated in patients with confirmed and persistent LGD. In patients in whom confirmed LGD does not persist, it may well be that a wait and see policy is justified,” the researchers wrote.

Disclosures: The researchers report no relevant financial disclosures.