Oesophagitis, Signs of Reflux, and Gastric Acid Secretion in Patients with Symptoms of Gastro-Oesophageal Reflux Disease

Johansson, Karl‐Erik; Ask, Per; Boeryd, B; Fransson, Sven-Göran; Tibbling, Lita

doi:10.3109/00365528609011128

Cited by 154 publications

(71 citation statements)

References 29 publications

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“…Although the inhibition of gastric acid secretion is known to decrease the time that the oesophageal pH < 4, 8,[36][37][38] gastric acidity has received limited attention with respect to its potential underlying role in oesophageal acid exposure in GERD. [39][40][41][42][43][44][45] The present finding that cisapride decreases post-prandial oesophageal acid exposure in subjects with GERD agrees with previous findings by others, [11][12][13][14][15] who have attributed this action of cisapride to its motility effects on the lower oesophageal sphincter pressure, oesophageal peristalsis and gastric emptying. [11][12][13][14][15] Our present results, however, indicate that the decrease in oesophageal acidity can be explained by a cisapride-induced decrease in gastric acidity.…”

Section: Discussionsupporting

confidence: 92%

Cisapride inhibits meal‐stimulated gastric acid secretion and post‐prandial gastric acidity in subjects with gastro‐oesophageal reflux disease

Gardner¹,

Rodriguez–Stanley

Robinson

et al. 2002

Aliment Pharmacol Ther

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Summary Background and aims : KCNQ1 potassium channels in human gastric parietal cells are thought to be involved in gastric acid secretion. As cisapride can inhibit similar channels in other tissues and is an effective treatment for nocturnal heartburn, we examined the effects of cisapride on gastric and oesophageal acidity, gastric emptying and heartburn severity in subjects with gastro‐oesophageal reflux disease. Methods : Subjects (n=11) had suffered from heartburn four times or more per week for at least 6 months. Gastric pH and oesophageal pH were measured before, during and after a standard meal ingested over 15 min. Each subject received placebo or 10 mg cisapride orally, 30 min before the beginning of the meal. Meal‐stimulated gastric acid secretion was calculated from the amount of HCl required to titrate the homogenized standard meal to pH 2 in vitro and the time required for the pH of the ingested meal to decrease to pH 2 in vivo. Heartburn severity was assessed at 15‐min intervals beginning at the end of the meal. Gastric emptying of solids was measured using a [13C]‐octanoic acid breath test. Results : Cisapride significantly decreased meal‐stimulated gastric acid secretion by 20%, decreased integrated gastric and oesophageal acidity by 50–60% and transiently increased the expiration of 13CO2. Cisapride did not significantly alter heartburn severity. Conclusions : The cisapride‐induced decreases in meal‐stimulated gastric acid secretion, gastric acidity and oesophageal acidity in subjects with gastro‐oesophageal reflux disease can account for its beneficial clinical effects. These results also raise the possibility that gastric KCNQ1 potassium channels are important in meal‐stimulated gastric acid secretion and possibly in the pathophysiology of gastro‐oesophageal reflux disease.

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Section: Discussionsupporting

confidence: 92%

Cisapride inhibits meal‐stimulated gastric acid secretion and post‐prandial gastric acidity in subjects with gastro‐oesophageal reflux disease

Gardner¹,

Rodriguez–Stanley

Robinson

et al. 2002

Aliment Pharmacol Ther

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“…GERD clinical symptoms can be typical or atypical (20,38) . Only half of GERD patients present with esophageal erosions (7,8,16,18) . The prevalence of liver cirrhosis is also large, with high morbidity and mortality (11) .…”

Section: Introductionmentioning

confidence: 99%

Gastroesophageal reflux in cirrhotic patients with esophageal varices without endoscopic treatment

Schechter

Lemme

Coelho

2007

Arq. Gastroenterol.

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-Background -Portal hypertension in patients with liver cirrhosis causes manifestations such as esophageal varices, ascites and edema. Some studies have been conducted about the role of esophageal varices in the development of esophageal motor disorders and abnormal gastroesophageal reflux in these patients. Ascites could be a factor promoting gastroesophageal reflux and it has been questioned whether reflux would favor the rupture of varices. However there are a few studies using ambulatory esophageal pH recording in the evaluation of these patients. Aims -Evaluate gastroesophageal reflux by pH recording in cirrhotic patients with esophageal varices and possible predictors. Methods -Fifty one patients (28 men, 23 women, mean age of 54 years) with liver cirrhosis, diagnosed by clinical, laboratorial, image and histological findings were prospectively evaluated. All patients had esophageal varices confirmed by endoscopy and were submitted to a questionnaire about typical gastroesophageal reflux disease symptoms (heartburn and or acid regurgitation). pH recording was performed with the probe placed 5 cm above the superior lower esophageal sphincter limit, as determined by manometry. Abnormal reflux (% total time with pH <4 >4.5%) was related to the size of varices, congestive gastropathy, ascites, severity of cirrhosis and typical gastroesophageal reflux disease symptoms. Results -The caliber of the varices was considered to be small in 30 patients (59%), medium in 17 (33%) and large in 4 (8%), 21 (41%) congestive gastropathy. Ascites was observed in 17 (33%), 32 patients (63%) were classified as Child-Pugh A, 17 (33%) Child-Pugh B and 2 (4%) Child-Pugh C. Twenty seven patients (53%) presented with typical gastroesophageal reflux disease symptoms. Abnormal reflux at pH recording was found in 19 patients (37%). One of them presented with erosive esophagitis at endoscopy. There was no relation between ascites, variceal size, congestive gastropathy and Child-Pugh score and abnormal reflux. There was a correlation between typical gastroesophageal reflux disease symptoms and abnormal reflux. Conclusions -Abnormal gastroesophageal reflux was found in 37% of the patients with hepatic cirrhosis and esophageal varices. Only typical gastroesophageal reflux disease symptoms predicted these findings.

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“…Chronic exposure is associated with serious complications including esophageal stricture in 4%-20% of patients [4] and Barrett's esophagus in up to 15% of patients with GERD [4][5][6][7] . Healing of reflux esophagitis is directly correlated with the intragastric pH > 4.0 [8,9] . The efficacy of antisecretory drugs in healing reflux esophagitis depends on the strength and duration of acid suppression within a 24 h period, and the duration of the treatment [10] .…”

Section: Introductionmentioning

confidence: 99%

Comparative study of omeprazole, lansoprazole, pantoprazole and esomeprazole for symptom relief in patients with reflux esophagitis

Zheng¹

2009

WJG

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AIM:To clarify whether there is any difference in the symptom relief in patients with reflux esophagitis following the administration of four Proton pump inhibitors (PPIs). METHODS:Two hundred and seventy-four patients with erosive reflux esophagitis were randomized to receive 8 wk of 20 mg omeprazole (n = 68), 30 mg of lansoprazole (n = 69), 40 mg of pantoprazole (n = 69), 40 mg of esomeprazole (n = 68) once a day in the morning. Daily changes in heartburn and acid reflux symptoms in the first 7 d of administration were assessed using a six-point scale (0: none; 1: mild; 2: mild-moderate; 3: moderate; 4: moderate-severe; 5: severe). RESULTS:The mean heartburn score in patients treated with esomeprazole more rapidly decreased than those receiving other PPI. Complete resolution of heartburn was also more rapid in patients treated with esomeprazole for 5 d compared with omeprazole (P = 0.0018, P = 0.0098, P = 0.0027, P = 0.0137, P = 0.0069, respectively), lansoprazole (P = 0.0020, P = 0.0046, P = 0.0037, P = 0.0016, P = 0.0076, respectively), and pantoprazole (P = 0.0006, P = 0.0005, P = 0.0009, P = 0.0031, P = 0.0119, respectively). There were no significant differences between the four groups in the rate of endoscopic healing of reflux esophagitis at week 8. CONCLUSION:Esomeprazole may be more effective than omeprazole, lansoprazole, and pantoprazole for the rapid relief of heartburn symptoms and acid reflux symptoms in patients with reflux esophagitis.

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Oesophagitis, Signs of Reflux, and Gastric Acid Secretion in Patients with Symptoms of Gastro-Oesophageal Reflux Disease

Cited by 154 publications

References 29 publications

Cisapride inhibits meal‐stimulated gastric acid secretion and post‐prandial gastric acidity in subjects with gastro‐oesophageal reflux disease

Cisapride inhibits meal‐stimulated gastric acid secretion and post‐prandial gastric acidity in subjects with gastro‐oesophageal reflux disease

Gastroesophageal reflux in cirrhotic patients with esophageal varices without endoscopic treatment

Comparative study of omeprazole, lansoprazole, pantoprazole and esomeprazole for symptom relief in patients with reflux esophagitis

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