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Page 4 of 11 Fontan et al. Mini-invasive Surg 2020;4:29 I http://dx.doi.org/10.20517/2574-1225.2020.09

Figure 2. Endoscopy showing changes consistent with Barrett’s esophagus

screening in bariatric surgery patients [23-25] . This patient population is at higher risk of dysplasia and
potential development of esophageal adenocarcinoma, as the risk of cancer in BE patients is estimated to be
[26]
30-125-fold greater than that of the general population .

To date, neither medical nor surgical treatment seems to guarantee histologic regression of BE. Multiple
authors have shown that surgical management results tend to indicate slightly higher resolution and
regression rates when compared to medical therapy arms, but these studies lack statistical power, have
highly heterogeneous cohorts, and use relatively short surveillance periods [27-29] . Some authors claim that
the main advantage of surgery over medical therapy is that surgery also prevents bile reflux, while proton
pump inhibitors control only acid reflux. Other groups have recommended medical treatment because
of the less aggressive nature of these therapies when compared to surgery [30-32] . Regardless, interest in
regression of BE with antireflux therapy vs. medical therapy has waned in recent years with the rising use
of endoscopic ablative techniques such as radiofrequency ablation, which can eradicate the metaplastic
[33]
mucosa directly .

Regarding the effects of bariatric surgery on BE, a meta-analysis of eight studies that included 117 patients
with BE undergoing roux-en-Y gastric bypass (RYGB) found that 56% of these patients had regression of
[34]
their BE after > 1 year of follow up . Regression rates of short segment and long segment BE were similar
in this study. There have only been a few studies looking at the relationship between BE and laparoscopic
[35]
sleeve gastrectomy (LSG). Braghetto et al. reported that, in the short term, 1.2% of their post-LSG
patients developed BE. However, in this study, patients did not continue endoscopic surveillance past one
year if they were asymptomatic. In a study of 110 patients from a single institution in Italy, 17.2% developed
[36]
a new diagnosis of BE after LSG at a median follow up of 58 months . The postoperative incidence
of GERD symptoms and daily PPI use were also significantly increased. Interestingly, of the patients
who had developed BE, 26% had no symptoms of GERD. This finding was also reported in a study by
[37]
Soricelli et al. , in which 21% of post-LSG patients with BE were asymptomatic. Similar rates of “de novo”
[38]
BE after LSG were reported recently (2019) . In a multicenter study, 18.8% of patients had developed BE
after LSG, with follow up of at least five years. In a study where patients had 10 years of follow up, 15% had
[39]
developed BE . Although the malignant transformation potential of BE in post-LSG patients is unknown,
the authors of the aforementioned studies have proposed endoscopic screening and surveillance, even in
patients without GERD symptoms [36-39] .

DIAGNOSIS
According to current standards of care, for low risk patients with symptoms and history consistent with
uncomplicated GERD, empirical therapy with proton pump inhibitors and lifestyle modifications can be