The Effect of Proton Pump Inhibitors on Barrett’s Esophagus

Dunbar, Kerry B.; Souza, Rhonda F.; Spechler, Stuart J.

doi:10.1016/j.gtc.2015.02.010

Cited by 21 publications

(11 citation statements)

References 43 publications

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“…High-dose PPI treatment in patients with BE that results in effective esophageal acid suppression has been shown to decrease the markers of cell proliferation and inflammation and increase apoptosis [17]. PPI treatment reduces the acidity and the volume of the refluxate, which may diminish the exposure of esophagus to cytotoxic bile acids [18]. Therefore, modulation of bile acid composition with the UDCA intervention may not result in any further improvement in histology and the selected tissue biomarkers.…”

Section: Discussionmentioning

confidence: 99%

Clinical Study of Ursodeoxycholic Acid in Barrett's Esophagus Patients

Banerjee

Shaheen

Martinez

et al. 2016

Cancer Prevention Research

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Prior research strongly implicates gastric acid and bile acids, two major components of the gastroesophageal refluxate, in the development of Barrett’s esophagus (BE) and its pathogenesis. Ursodeoxycholic acid (UDCA), a hydrophilic bile acid, has been shown to protect esophageal cells against oxidative stress induced by cytotoxic bile acids. We conducted a pilot clinical study to evaluate the clinical activity of UDCA in patients with BE. Twenty-nine BE patients received UDCA treatment at a daily dose of 13–15 mg/kg/day for six months. The clinical activity of UDCA was assessed by evaluating changes in gastric bile acid composition and markers of oxidative DNA damage (8-hydroxydeoxyguanosine, 8OHdG), cell proliferation (Ki67), and apoptosis (cleaved caspase 3, CC3) in BE epithelium. The bile acid concentrations in gastric fluid were measured by liquid chromatography-mass spectrometry. At baseline, UDCA (sum of unchanged and glycine/taurine conjugates) accounted for 18.2% of total gastric bile acids. Post UDCA intervention, UDCA increased significantly to account for 93.39% of total gastric bile acids (p<0.0001). The expression of markers of oxidative DNA damage, cell proliferation, and apoptosis was assessed in the BE biopsies by immunohistochemistry. The selected tissue biomarkers were unchanged after 6 months of UDCA intervention. We conclude that high dose UDCA supplementation for six months resulted in favorable changes in gastric bile acid composition but did not modulate selected markers of oxidative DNA damage, cell proliferation, and apoptosis in the BE epithelium.

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Section: Discussionmentioning

confidence: 99%

Clinical Study of Ursodeoxycholic Acid in Barrett's Esophagus Patients

Banerjee

Shaheen

Martinez

et al. 2016

Cancer Prevention Research

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“…In BE, ongoing acid reflux can lead to neoplastic progression by increasing proliferation, decreasing apoptosis, production of reactive oxygen species (ROS), DNA damage, and stimulating esophageal production of proinflammatory and proproliferative cytokines. 42 Several studies demonstrated a greater frequency of pathological esophageal acid exposure among patients with BE compared with those with erosive esophagitis. 43 – 45 PPIs, through acid-suppressive effects and by modulation of antioxidant and proinflammatory cytokine production, may potentially reduce carcinogenesis.…”

Section: Proton-pump Inhibitorsmentioning

confidence: 99%

Chemoprevention in Barrett’s esophagus and esophageal adenocarcinoma

Alkhayyat

Kumar

Sanaka

et al. 2021

Therap Adv Gastroenterol

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There has been a dramatic increase in the incidence of Barrett’s esophagus and esophageal adenocarcinoma over the past several decades with a continued rise expected in the future. Several strategies have been developed for screening and surveillance of patients with Barrett’s esophagus and endoscopic treatment of Barrett’s associated dysplasia and early esophageal cancer; however, they have not made a substantial impact on the incidence of cancer. Herein, chemoprevention becomes an attractive idea for reducing the incidence of cancer in Barrett’s patients. Several agents appear promising in preclinical and observational studies but very few have been evaluated in randomized controlled trials. Strongest evidence to date is available for proton-pump inhibitors and Aspirin that have been evaluated in a large randomized controlled trial. Other agents such as statins, metformin, ursodeoxycholic acid, and dietary supplements have insufficient evidence for chemoprevention in Barrett’s patients.

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“…A significant association of PPI treatment with a decreased risk of high-grade dysplasia and adenocarcinoma has been shown in clinic-based cohort studies for patients with Barrett’s esophagus (29–31). The indirect evidence supporting PPIs as a a cancer-preventative promises a cost-effective treatment for all patients with Barrett’s esophagus after they have been informed of the potential risks of long-term PPI therapy (32). There is some controversy as prolonged PPI use possibly promotes progression to EAC through increased gastric pH associated with bile salt toxicity (33).…”

Section: Preventionmentioning

confidence: 99%

Esophageal cancer: The latest on chemoprevention and state of the art therapies

Bras

Farooq

Falk

et al. 2016

Pharmacological Research

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Esophageal cancer is currently the 8th most common cancer worldwide and the 6th leading cause of cancer-related mortality. Despite remarkable advances, the mortality for those suffering from esophageal cancer remains high, with 5-year survival rates of less than 20%. In part, because most patients present with late-stage disease, long-term survival even after resection and therapy is disappointingly low. As we will discuss in this review, multiple characteristics specific to the disease stage and patient must be considered when choosing a treatment plan. This article will summarize current standard therapies, potential application of chemoprevention drugs and the promise and partial failure of personalized medicine, as well as novel treatments addressing this disease.

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The Effect of Proton Pump Inhibitors on Barrett’s Esophagus

Cited by 21 publications

References 43 publications

Clinical Study of Ursodeoxycholic Acid in Barrett's Esophagus Patients

Clinical Study of Ursodeoxycholic Acid in Barrett's Esophagus Patients

Chemoprevention in Barrett’s esophagus and esophageal adenocarcinoma

Esophageal cancer: The latest on chemoprevention and state of the art therapies

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