Patients With Barrett’s Esophagus and Confirmed Persistent Low-Grade Dysplasia Are at Increased Risk for Progression to Neoplasia

2017 ◽  
Vol 152 (5) ◽  
pp. 993-1001.e1 ◽  
Author(s):  
Lucas C. Duits ◽  
Myrtle J. van der Wel ◽  
Cary C. Cotton ◽  
K. Nadine Phoa ◽  
Fiebo J.W. ten Kate ◽  
...  
Author(s):  
K Y Song ◽  
A J Henn ◽  
A A Gravely ◽  
H Mesa ◽  
S Sultan ◽  
...  

SUMMARY Patients with Barrett's esophagus (BE) and low-grade dysplasia (LGD) are at increased risk of esophageal adenocarcinoma (EAC), although many regress to nondysplastic BE. This has significant clinical importance for patients being considered for endoscopic eradication therapy. Our aim is to determine the risk for progression in patients with confirmed persistent LGD. We performed a single-center retrospective cohort study of patients with BE and confirmed LGD between 2006 and 2016. Confirmed LGD was defined as LGD diagnosed by consensus conference with an expert GI pathologist or review by an expert GI pathologist and persistence as LGD present on subsequent endoscopic biopsy. The primary outcome was the incidence rate of HGD (high-grade dysplasia)/EAC. Secondary outcomes included risk factors for dysplastic progression. Risk factors for progression were assessed using univariate and multivariate analysis with logistic regression. Of 69 patients (mean age 65.2 years) with confirmed LGD were included. In total, 16 of 69 patients (23.2%) with LGD developed HGD/EAC during a median follow-up of 3.74 years (IQR, 1.24–5.45). For persistent confirmed LGD, the rate was 6.44 (95% confidence interval (CI), 2.61–13.40) compared to 2.61 cases per 100 patient-years (95% CI, 0.83–6.30) for nonpersistent LGD. Persistent LGD was found in only 29% of patients. Persistent LGD was an independent risk factor for the development of HGD/EAC (OR 4.18; [95% CI, 1.03–17.1]). Persistent confirmed LGD, present in only 1/3 of patients, was an independent risk factor for the development of HGD/EAC. Persistence LGD may be useful in decision making regarding the management of BE.


2016 ◽  
Vol 2016 ◽  
pp. 1-4
Author(s):  
Megan Murphy ◽  
Christina Tofani ◽  
Kunjal Gandhi ◽  
Anthony Infantolino

Background. Barrett’s esophagus is associated with an increased risk of adenocarcinoma. Dysplasia in Barrett’s esophagus is a precursor to adenocarcinoma. Rarely, dysplastic polypoid lesions are superimposed on Barrett’s esophagus. Most reported cases of polypoid dysplasia in Barrett’s esophagus have been advanced on presentation and treated with esophagectomy. We describe two cases of polypoid changes in Barrett’s esophagus and treatment with polypectomy followed by radiofrequency ablation.Cases. A 75 yo male presented with esophageal polyps, which on biopsy showed gastric cardia/foveolar mucosa with focal intestinal metaplasia without dysplasia. Biopsy of intervening flat mucosa was consistent with nondysplastic Barrett’s esophagus. Extensive hot snare polypectomies were performed followed by RFA. One year later, repeat EGD revealed no evidence of Barrett’s esophagus. A 61 yo male presented with esophageal polyps, which on biopsy showed gastric cardia/foveolar mucosa with intestinal metaplasia and foci of low-grade dysplasia. Extensive hot snare polypectomies were performed followed by RFA. At repeat EGD, four months later, an esophageal mass was found. Biopsy of the mass showed invasive adenocarcinoma. The patient was referred for esophagectomy.Conclusion. This case series shows two outcomes, one with successful eradication of dysplasia and the other with disease progression to invasive adenocarcinoma requiring esophagectomy.


2021 ◽  
Author(s):  
EA Nieuwenhuis ◽  
SN van Munster ◽  
BLAM Weusten ◽  
L Alvarez Herrero ◽  
A Bogte ◽  
...  

2015 ◽  
Vol 61 (1) ◽  
pp. 158-167 ◽  
Author(s):  
Kavel Visrodia ◽  
Prasad G. Iyer ◽  
Cathy D. Schleck ◽  
Alan R. Zinsmeister ◽  
David A. Katzka

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