Effects of omeprazole or anti-reflux surgery on lower oesophageal sphincter characteristics and oesophageal acid exposure over 10 years.

OBJECTIVE: To compare the effect of anti-reflux surgery (ARS) versus proton pump inhibitor therapy on lower oesophageal sphincter (LOS) function and oesophageal acid exposure in patients with chronic gastro-oesophageal reflux disease (GORD) over a decade of follow-up. MATERIAL AND METHODS: In this randomised, prospective, multicentre study we compared LOS pressure profiles, as well as oesophageal exposure to acid, at baseline and at 1 and 10 years after randomisation to either open ARS (n = 137) or long-term treatment with omeprazole (OME) 20-60 mg daily (n = 108). RESULTS: Median LOS resting pressure and abdominal length increased significantly and remained elevated in patients operated on with ARS, as opposed to those on OME. The proportion of total time (%) with oesophageal pH <4.0 decreased significantly in both the surgical and medical groups, and was significantly lower after 1 year in patients treated with ARS versus OME. After 10 years, oesophageal acid exposure was normalised in both groups, with no significant differences, and bilirubin exposure was within normal limits. After 10 years, patients with or without Barrett's oesophagus did not differ in acid reflux control between the two treatment options. CONCLUSIONS: Open ARS and OME were both effective in normalising acid reflux into the oesophagus even when studied over a period of 10 years. Anatomically and functionally the LOS was repaired durably by surgery, with increased resting pressure and abdominal length.

Gastroesophageal Acid Reflux Control 5 Years After Antireflux Surgery, Compared With Long-term Esomeprazole Therapy.

BACKGROUND & AIMS: We compared the ability of laparoscopic antireflux surgery (LARS) and esomeprazole to control esophageal acid exposure, over a 5-year period, in patients with chronic gastroesophageal reflux disease (GERD). We also studied whether intraesophageal and intragastric pH parameters off and on therapy were associated with long-term outcomes. METHODS: We analyzed data from a prospective, randomized, open-label trial comparing the efficacy and safety of LARS vs esomeprazole (20 or 40 mg/d) over 5 years in patients with chronic GERD. Ambulatory intraesophageal and intragastric 24-hour pH monitoring data were compared between groups before LARS or the start of esomeprazole treatment, and 6 months and 5 years afterward. A secondary aim was to evaluate the association between baseline and 6-month pH parameters and esomeprazole dose escalation, reappearance of GERD symptoms, and treatment failure over 5 years in patients receiving LARS or esomeprazole. RESULTS: In the LARS group (n = 116), the median 24-hour esophageal acid exposure was 8.6% at baseline and 0.7% after 6 months and 5 years (P < .001 vs baseline). In the esomeprazole group (n = 151), the median 24-hour esophageal acid exposure was 8.8% at baseline, 2.1% after 6 months, and 1.9% after 5 years (P < .001, therapy vs baseline, and LARS vs esomeprazole). Gastric acidity was stable in both groups. Patients who required a dose increase to 40 mg/d had more severe supine reflux at baseline, and decreased esophageal acid exposure (P < .02) and gastric acidity after dose escalation. Esophageal and intragastric pH parameters, off and on therapy, did not predict long-term symptom breakthrough. CONCLUSIONS: In a prospective study of patients with chronic GERD, esophageal acid reflux was reduced greatly by LARS or esomeprazole therapy. However, patients receiving LARS had significantly greater reductions in 24-hour esophageal acid exposure after 6 months and 5 years. Esophageal and gastric pH, off and on therapy, did not predict long-term outcomes of patients. Abnormal supine acid exposure predicted esomeprazole dose escalation. ClinicalTrials.Gov identifier: NCT00251927 (available: http://clinicaltrials.gov/ct2/show/NCT00251927).

Etiology and risk factors for esophageal carcinoma.

Trends toward increasing incidence rates were observed for esophageal and gastric cardia adenocarcinoma in Western countries and were associated with trends toward stabilizing or declining incidence rates for esophageal squamous cell carcinoma, suggesting that these tumors might be associated with distinct risk factors. Overweight and obesity have been consistently related to esophageal adenocarcinoma, but not to squamous cell carcinoma. Body mass index seems to be inversely related to the risk of esophageal squamous cell carcinoma. The influence of obesity on esophageal adenocarcinoma and gastric cardia adenocarcinoma may be related to higher incidence of gastroesophageal reflux in obese persons since the risk of gastroesophageal reflux is strongly related to the risk for Barrett's esophagus. Tobacco smoking is a strong risk factor for esophageal squamous cell carcinoma, but is only a weak risk factor for esophageal adenocarcinoma. Alcohol consumption is a strong risk factor for esophageal squamous cell carcinoma, but is not consistently related to esophageal adenocarcinoma. Selenium, dietary fiber, fruits, vegetables and antioxidants are seen as protective factors. Male gender seems to be a risk factor for both types of tumors in the region, while infection with human papillomavirus does not seem to play a major part in the development of esophageal cancers. Infection with Helicobacter pylori is, however, an interesting factor to this region of tumors as discussed in many reports. It has been suggested that infection with H. pylori is protective to adenocarcinoma, but might be a risk factor for squamous cell carcinoma, although the role of H. pylori in the etiology of these cancers remains somewhat unclear.