Cisapride: influence on oesophageal and gastric emptying and gastro-oesophageal reflux in patients with reflux oesophagitis

A preliminary, double-blind placebo controlled trial of cisapride in reflux oesophagitis was conducted. Eighteen patients were allocated to treatment with either placebo or cisapride, 10 mg three times daily, orally, before meals. Gastric emptying of a scrambled egg meal, oesophageal transit of a liquid bolus and ambulatory monitoring of oesophageal pH were assessed before and after four weeks' therapy. Overall, gastric emptying rates were not influenced by cisapride, although a small but significant reduction in gastric isotope retention, 20 minutes after meal ingestion was observed in patients on the active drug. Oesophageal transit times were not altered by cisapride. A small but significant reduction in the duration of gastro-oesophageal reflux followed cisapride therapy when compared with placebo.     

The role of delayed gastric emptying and impaired oesophageal body motility

Delayed gastric emptying in a variable proportion of patients with gastro-oesophageal reflux disease has been observed in most series, however a relationship between delayed gastric emptying and increased gastro-oesophageal reflux has not been convincingly demonstrated. Enhanced postprandial accommodation and delayed emptying of the proximal stomach have been described, but some controversy exists. Impaired primary peristalsis is often present especially in patients with oesophagitis and its prevalence increases with increasing severity of inflammatory mucosal lesions. Patients with gastro-oesophageal reflux disease often have defective triggering of secondary peristalsis independently of presence of oesophagitis. It is presently unclear if impaired oesophageal motility is a primary defect or an irreversible consequence of inflammation. Attempts at pharmacological improvement of impaired oesophageal motility have been so far disappointing. Patients with partially preserved neuromuscular structures need to be identified in order to select them for new prokinetic therapy.     

Gastric and oesophageal emptying in insulin-dependent diabetes mellitus

Abstract Gastric emptying of a digestible solid and liquid meal and oesophageal emptying of a solid bolus were measured with scintigraphic techniques in 45 randomly selected insulin-dependent diabetics and in 22 control subjects. In the diabetics, the relationships between oesophageal emptying, gastric emptying, age, duration of diabetes mellitus, upper gastrointestinal symptoms, glycaemic control and the complications, autonomic neuropathy, peripheral neuropathy and retinopathy were examined. The lag period before solid food left the stomach was not significantly different in diabetics compared with control subjects, but the percentage retention of solid food at 100 min was greater ( P < 0.001) in the diabetic subjects. Both the early phase (percentage retention at 10 min) and the 50% emptying time for liquid gastric emptying were delayed ( P < 0.001) in the diabetic subjects. Of the diabetics, 58% had delayed gastric emptying of either the solid and/or the liquid meal; oesophageal emptying was delayed in 42%. Upper gastrointestinal symptoms correlated poorly with both gastric and oesophageal emptying. Oesophageal emptying, solid gastric emptying and the liquid 50% emptying time correlated with the severity of autonomic nerve dysfunction ( P < 0.05). The early phase of liquid emptying (retention at 10 min) was significantly slower ( P < 0.05) in patients with mean plasma glucose concentrations of > 15 mmol/l during the gastric emptying test and the lag period for solid emptying correlated with both the glycosylated haemoglobin and mean plasma glucose concentrations.     

Oesophageal dysmotility, delayed gastric emptying and autonomic neuropathy correlate to disturbed glucose homeostasis

Aims/hypothesis Among diabetic patients, glucose homeostasis may be affected by abnormal gastrointestinal motility and autonomic neuropathy. This study analysed whether oesophageal dysmotility, delayed gastric emptying or autonomic neuropathy affect glucose homeostasis.Materials and methods Oesophageal manometry and gastric emptying scintigraphy were performed in 20 diabetic patients. Heart-rate variation during deep breathing (expiration/inspiration [E/I] ratio) and continuous subcutaneous glucose concentrations for a period of 72 h were also monitored in the same patients.Results Oesophageal dysmotility was found in eight of 14 patients. Eleven of 20 patients had delayed gastric emptying (abnormal gastric emptying half-time [T ₅₀]) and nine of 18 had an abnormal E/I ratio. Complaints of abdominal fullness were predictive of delayed gastric emptying. A low peristaltic speed of the oesophagus was associated with impaired T ₅₀ (r _s =−0.67; p=0.02). One hour after breakfast, subcutaneous glucose levels decreased in patients with delayed gastric emptying but continued to rise in those with normal emptying. Consequently, the median glucose level 2.5 h after breakfast was lower in the former (9.1 [4.2–12.5] vs 14.3 [11.2–17.7] mmol/l; p<0.05). Glucose fluctuations during the 72 h were significantly higher in patients with an abnormal E/I ratio than in those with a normal E/I ratio (coefficient of variation: 41 [46–49] vs 28 [27–34]%; p=0.008).Conclusions/interpretation Abdominal fullness predicted delayed gastric emptying that was associated with diminished glucose uptake after breakfast. Low oesophageal peristaltic speed was associated with slow gastric emptying whereas parasympathetic neuropathy was associated with increased glucose variations.These results were presented as an oral presentation at the EASD meeting in Athens 2005.     

Gastroesophageal reflux disease and Helicobacter pylori: lack of influence of infection on oesophageal manometric, 3-hour postprandial pHmetric and endoscopic findings

AIM: To investigate the relationship between Helicobacter pylori and gastro-oesophageal reflux disease according to manometric and pHmetric findings. METHOD: Fifty-nine consecutive patients with reflux symptoms and endoscopic evidence of mild oesophagitis, were recruited. Manometry and ambulatory pHmetry were performed in all patients, as well as the 3-hour postprandial pHmetry, as a more flexible and well tolerable test. RESULTS: There were no significant differences between Helicobacter pylori positive and negative patients regarding age, sex ratio and endoscopic severity of oesophagitis. There was no difference in prevalence of abnormal oesophageal peristalsis between the two groups (Fisher's exact test, p=NS). Differences were also not found regarding lower oesophageal sphincter pressure between the two groups (mean PLOS 12.86+/-4.39 mmHg and 13.1+/-4.61 mmHg respectively; p=0.840). Finally, the mean values of DeMeester score were 60.38+/-48.04 and 67.64+/-51.04 respectively (p=0.576). CONCLUSION: Helicobacter pylori infection does not influence oesophageal peristalsis, the lower oesophageal sphincter pressure and the acidity of refluxates into the oesophageal lumen, in patients with established gastro-oesophageal reflux disease (esophagitis grade A and B).     

Helicobacter pylori-induced duodenal ulcer frequently coincides with gastro-oesophageal reflux disease

BACKGROUND: The relationship between Helicobacter pylori infection and gastro-oesophageal reflux disease is complicated. Evidence does not support a causal link. There have been reports, which have implicated successful eradication of Helicobacter pylori, in patients with a duodenal ulcer, with the subsequent development of gastro-oesophageal reflux disease. However, eradication of Helicobacter pylori in these patients with improvement in their condition and a return to normal lifestyle, weight gain and discontinuation of antacids may unmask pre-existing gastro-oesophageal reflux disease. AIMS: To determine the true prevalence of gastro-oesophageal reflux disease in patients with Helicobacter pylori-related duodenal ulceration. METHOD: Dyspeptic patients undergoing endoscopy were prospectively screened for the presence of a duodenal ulcer. Concomitant oesophagitis, when present, was recorded. All subjects with a Helicobacter pylori-related duodenal ulcer without endoscopic evidence of gastro-oesophageal reflux disease were invited to undergo a 24-hr ambulatory oesophageal pH assessment prior to receiving treatment. RESULTS: A total of 97 patients with a duodenal ulcer were identified and 83.5% were Helicobacter pylori positive. Overall, 27.8% had associated endoscopic evidence of oesophagitis, 70% grade I-II and 30% grade III-IV. Of those without evidence of oesophagitis at endoscopy, 68% underwent a 24-hr pH assessment. An additional 17% were identified by this means as having gastro-oesophageal reflux disease. Overall, 44% of symptomatic subjects with Helicobacter pylori and a duodenal ulcer were found to have coexistent gastro-oesophageal reflux disease. CONCLUSION: Gastro-oesophageal reflux disease is frequently found to coexist with Helicobacter pylori-related duodenal ulcer. In addition, almost 20% of symptomatic patients without endoscopic evidence of oesophagitis will have an abnormal oesophageal pH exposure. It is plausible that the development of gastro-oesophageal reflux disease following successful eradication of Helicobacter pylori represents unmasking of existing disease rather than de novo development.     

Manometric and pH-metric features in gastro-oesophageal reflux disease patients with and without Helicobacter pylori infection

BACKGROUND: The role of Helicobacter pylori in the pathogenesis and evolution of gastro-oesophageal reflux disease is still debated. AIM: To investigate the impact of Helicobacter pylori infection on the oesophageal function and on intra-gastric and intra-oesophageal pH in patients with gastro-oesophageal reflux. METHODS: Fifty patients with non-complicated-gastro-oesophageal reflux disease classified according to Savary-Miller in: grade O, n=24; grade 1, n=19; grade 2, n=6; grade 3, n=1. Of these patients, 24 were Helicobacter pylori positive and 26 negative. Patients underwent, on two different days, stationary oesophageal manometry and 24-hour gastro-oesophageal pH-metry. RESULTS: No difference was observed between Helicobacter pylori infected and non-infected individuals with regard to lower oesophageal sphincter function, oesophageal peristalsis and gastrooesophageal reflux. These parameters were more impaired in individuals with erosive gastro-oesophageal reflux disease but this result was not dependent on the Helicobacter pylori status. Helicobacter pylori did not influence the pattern of gastric pH; however, considering only individuals with non-erosive gastro-oesophageal reflux disease, gastric pH was significantly higher in infected individuals, who, histologically, also showed a corpus predominant gastritis. CONCLUSIONS: In patients with gastro-oesophageal reflux disease, Helicobacter pylori does not affect the oesophageal motility or the gastro-oesophageal reflux. These parameters are strictly related to the severity of gastro-oesophageal reflux disease as assessed at endoscopy. In patients with non-erosive gastro-oesophageal reflux disease, a corpus predominant Helicobacter pylori gastritis could be responsible for the less severe gastro-oesophageal reflux.     

Gastro-oesophageal reflux in the irritable bowel syndrome.

Symptomatic assessment and oesophageal investigations were done in 25 consecutive patients with the irritable bowel syndrome attending a gastroenterological clinic. Symptoms of gastro-oesophageal reflux, dysphagia, and a globus sensation were significantly commoner than in a control group of fracture clinic patients. Ambulatory oesophageal pH monitoring showed clearly abnormal reflux in 11 of 22 patients (50%). Nine patients had macroscopic endoscopic changes and a further 11 biopsy changes alone, of oesophagitis which was thus present in 80% overall. Lower oesophageal sphincter pressure was significantly less in irritable bowel patients than in age and sex matched controls, but upper oesophageal sphincter pressure was comparable in the two groups and disordered peristalsis was not found. Oesophageal symptoms in the irritable bowel syndrome are mainly caused by gastro-oesophageal reflux predisposed to by a subnormal lower oesophageal sphincter pressure, rather than by oesophageal spasm.     

Oesophageal function in patients with angina pectoris: a comparison of patients with normal coronary angiograms and patients with coronary artery disease

Oesophageal function was assessed in 52 patients with angina pectoris whose coronary angiograms were completely normal and in 21 patients with angina pectoris who had significant coronary artery disease. During a standard oesophageal manometric study, abnormalities were found in 23 (44%) patients with normal coronary angiograms but in only 2 (10%) patients with coronary artery disease (p less than 0.01). Twenty-four (46%) patients with normal coronary angiograms were found to have gastro-oesophageal reflux disease during 24-hour oesophageal pH monitoring. Of the 52 patients with normal coronary angiograms, 19 (37%) had gastro-oesophageal reflux disease and abnormal oesophageal motility, 5 (10%) had gastro-oesophageal reflux disease alone, and 7 (13%) had oesophageal motility disorder alone. The use of provocation procedures, including intravenous edrophonium during oesophageal manometry and treadmill exercise testing during pH monitoring, enabled the oesophageal abnormality to be demonstrated simultaneously with chest pain in 25 of these 31 patients. Typical angina pectoris, coincident with abnormal oesophageal motility, was precipitated in a subgroup of patients who had been shown to have oesophageal manometric abnormalities and gastro-oesophageal reflux disease by the infusion of hydrochloric acid into the oesophagus; both the chest pain and manometric abnormality resolved following the oral administration of antacid.     

Gastric and oesophageal emptying in patients with Type 2 (non-insulin-dependent) diabetes mellitus

Summary Gastric emptying of a digestible solid and liquid meal and oesophageal emptying of a solid bolus were measured with scintigraphic techniques in 20 randomly selected Type 2 (non-insulin-dependent) diabetic patients receiving oral hypoglycaemic therapy and 20 control subjects. In the diabetic patients, the relationships between oesophageal emptying, gastric emptying, gastrointestinal symptoms, autonomic nerve function and glycaemic control were examined. The percentage of the solid meal remaining in the stomach at 100 min (p<0.001), the 50% gastric emptying time for the liquid meal (p<0.05) and oesophageal emptying (p<0.05) were slower in the diabetic patients compared to the control subjects. Scores for upper gastrointestinal symptoms and autonomic nerve dysfunction did not correlate significantly (p>0.05) with oesophageal, or gastric emptying. The 50% gastric emptying time for the liquid meal was positively related (r=0.58, p<0.01) to the plasma glucose concentration at the time of the performance of the gastric emptying test and the lag period, before any solid food emptied from the stomach, was longer (p<0.05) in subjects with plasma glucose concentrations during the gastric emptying measurement greater than the median, compared to those with glucose concentrations below the median. These results indicate that delayed gastric and oesophageal emptying occur frequently in Type 2 diabetes mellitus and that delayed gastric emptying relates, at least in part, to plasma glucose concentrations.     

Gastric dysrhythmias occur in gastro-oesophageal reflux disease complicated by food regurgitation but not in uncomplicated reflux

AIM: To investigate gastric pacemaker activity in gastro-oesophageal reflux disease using the electrogastrogram. PATIENTS: Forty patients with gastro-oesophageal reflux disease (20 with acid reflux, 20 with the additional symptom of food regurgitation) and 30 asymptomatic controls. METHODS: Patients were studied using an electrogastrogram, oesophageal manometry, and 24 hour ambulatory oesophageal pH analysis. RESULTS: An abnormal electrogastrogram was recorded in two (7%) controls, two (10%) patients with acid reflux, and 10 (50%) patients with food regurgitation. Food regurgitators had significantly more gastric dysrhythmias (tachygastrias) both before (p<0.02) and after (p<0.01) a test meal. Gastric pacemaker activity was also significantly less stable following the test meal in food regurgitators (p<0.003). Patients with food regurgitation and an abnormal electrogastrogram had higher oesophageal acid exposure than those with a normal electrogastrogram (p<0.05). CONCLUSIONS: The electrogastrogram is usually normal in gastro-oesophageal reflux disease but an abnormal rhythm occurred in half of our patients with the additional symptom of food regurgitation. Furthermore, an abnormal electrogastrogram is associated with increased oesophageal acid exposure.     

Autonomic nerve dysfunction in pathologically obese patients

BACKGROUND: Obese patients frequently present clinical symptoms related to gastrointestinal motility alterations and autonomic nervous system dysfunction. AIM: To evaluate the possible correlation between cardiovascular autonomic nervous dysfunction and oesophageal motility in pathologically obese patients. PATIENTS AND METHODS: Enrolled in the study were 22 patients with a body mass index of 45.72 +/- 7.48 and 10 control subjects, all within 20% of their ideal weight. Oesophageal motility was measured by stationary manometry and scintigraphic transit. Tests for the evaluation of autonomic nervous system were: Valsalva ratio, deep breathing, sustained handgrip, sudormotor axon reflex test and spectral analysis of the variability of R-R interval. RESULTS: The mean pressure of oesophageal peristaltic waves in patients and controls was 39.36 +/- 14 mmHg and 73 +/- 12 mmHg, respectively The scintigraphic mean transit time was 22.96 +/- 16.26 seconds in patients and 10.23 +/- 16.26 seconds in controls (p < 0.001). Spectral analysis of the variability of the R-R interval showed an increase in the parasympathetic component both in the lying and standing position compared to controls. The other autonomic nervous system function tests showed no significant difference between obese patients and controls. CONCLUSIONS: These results suggest that obese patients present a reduction of oesophageal transit and autonomic nervous system dysfunction albeit no direct correlation was found between these phenomena.     

Relationship between acceleration of gastric emptying and oesophageal acid exposure in patients with endoscopy-negative gastro-oesophageal reflux disease

OBJECTIVE: A delay in gastric emptying has been reported in patients with gastro-oesophageal reflux disease (GORD), but its role in increasing the number of reflux episodes is still debated. The aim of this study was to assess the relationship between acceleration of gastric emptying and gastro-oesophageal reflux in patients with endoscopy-negative GORD and pathological oesophageal acid exposure. MATERIAL AND METHODS: Twelve patients (7 M, age range 24-65 years) underwent 6-h postprandial (2.1 MJ meal) combined gastric emptying by real-time ultrasonography and intra-oesophageal pH monitoring after cisapride (20 mg b.i.d.) and placebo for 3 days, on two separate occasions at least 7 days apart in double-blind randomized order. Gastric emptying after placebo was also measured in 12 healthy volunteers (7 M, age range 25-54 years). RESULTS: In the patients' group, the area under the emptying time curve was greater (p<0.01), and half and total emptying times prolonged (p<0.01) compared to the healthy subjects, 115 min (mean)+/-6 (SEM) versus 86+/-6 and 232 min+/-16 versus 160+/-7, respectively. Cisapride accelerated both half- and total gastric emptying (p<0.02): -22 min (mean); -10 to -34 (95% CI) and -48 min; -10 to -85, respectively, decreased both percentage of time at pH < 4 (p<0.01) and number of reflux episodes (p<0.05). However, no relationship was found between changes in gastric emptying and in the reflux variables by linear regression analysis (R2<0.005). CONCLUSION: The emptying rate of the whole stomach is not a major determinant of gastro-oesophageal reflux.     

Role of autonomic dysfunction in patients with functional dyspepsia

BACKGROUND: The role of autonomic dysfunction in patients with functional dyspepsia is not completely understood. AIMS: 1. to prospectively assess abnormalities of autonomic function in patients with functional dyspepsia, 2. to assess whether autonomic dysfunction in these patients is associated with a. visceral hypersensitivity or b. delayed gastric emptying or c. severity of dyspeptic symptoms. PATIENTS: A series of 28 patients with functional dyspepsia and 14 healthy volunteers without gastrointestinal symptoms were studied. METHODS: All patients and controls were submitted to a battery of five standard cardiovascular autonomic reflex tests, dyspeptic questionnaire, gastric barostat tests and gastric emptying tests. RESULTS: 1. Autonomic function tests showed that both sympathetic and parasympathetic scores of dyspeptic patients were significantly higher than in controls; 2. visceral hypersensitivity was confirmed in dyspeptics in response to proximal gastric distension, demonstrating lower pain threshold; 3. delayed gastric emptying occurred more frequently in patients with functional dyspepsia than in controls; 4. epigastric pain and epigastric burning were significantly more prevalent in patients with definite evidence of autonomic dysfunction; 5. No significant association was found between presence of autonomic dysfunction and presence of visceral hypersensitivity or presence of delayed gastric emptying in patients with functional dyspepsia. CONCLUSIONS: We concluded that a possible role of autonomic dysfunction in eliciting dyspeptic symptoms could not be determined from alterations in visceral hypersensitivity or delayed gastric emptying. Autonomic dysfunction might not be the major explanation for symptoms associated with functional dyspepsia.     

Smoking delays gastric emptying of solids.

Oesophageal transit and gastric emptying of liquids and solids was measured in eight normal subjects with a single test meal containing In113 labelled water and an omelette labelled with Tc99m sulphur colloid. Each volunteer was studied, basally, whilst continuously smoking, and while chewing nicotine gum. Neither liquid, nor solid oesophageal transit were affected by smoking, or gum. Liquid gastric emptying occurred exponentially and clearance was not affected by smoking nor gum (mean basal t1/2 17.4 (2.7) (SEM) min, smoking t1/2 16.6 (7.4) min, gum t1/2 12.5 (2.9) min). Gastric emptying of solid had three components. An initial mean lag phase increased from 17.5 (2.7) min, to 27.5 (6.1) min (p less than 0.05) during smoking, but was not prolonged by nicotine gum (17.5 (1.1) min). A subsequent linear emptying phase was also slowed by smoking from a mean of 1.01 (0.15)% min to 0.80 (0.15)% min (p less than 0.05), but was not affected by nicotine gum, 1.06 (0.2)% min. A third complex phase of solid gastric emptying was not analysed. Smoking delays gastric emptying of solids, but not liquids; nicotine is not responsible for this effect. This observation may partly explain the adverse effect of smoking in patients with gastro-oesophageal reflux.     

Oesophageal dysmotility, delayed gastric emptying and gastrointestinal symptoms in patients with diabetes mellitus.

AIMS: Gastroparesis is a common gastrointestinal complication in diabetes mellitus, whereas dysfunction in the other gastrointestinal organs has been less thoroughly investigated. Furthermore, it is not known whether there is any relationship between motility and dysmotility between these organs. The aim of this study was to examine whether diabetic patients with gastrointestinal symptoms also have motility disturbances in the oesophagus and stomach and, if so, whether there are any associations between these disturbances. METHODS: Thirty-one patients with diabetes mellitus who complained of gastrointestinal symptoms were asked to complete a questionnaire about their symptoms. They were further investigated with oesophageal manometry and gastric emptying scintigraphy. RESULTS: Fifty-eight per cent of the patients had abnormal oesophageal function, and 68% had delayed gastric emptying. Abdominal fullness was the only symptom that related to any dysfunction, and it was associated with delayed gastric emptying (P = 0.02). We did not find any relationship in motility or dysmotility between the oesophagus and the stomach. CONCLUSION: Oesophageal dysmotility, as well as gastroparesis, are common in patients with diabetes who have gastrointestinal symptoms. It is important to investigate these patients further, to be able to reach an accurate diagnosis and instigate appropriate treatment. Our findings indicate that the oesophagus and the stomach function as separate organs and that pathology in one does not necessarily mean pathology in the other.     

Rapid gastric emptying is more common than gastroparesis in patients with autonomic dysfunction

OBJECTIVES: Autonomic dysfunction is associated with a wide variety of gastrointestinal symptoms. It is unclear how many patients with autonomic dysfunction have slow or rapid gastric emptying. The aim of this study was to determine the prevalence of rapid and delayed solid phase gastric emptying in patients with autonomic dysfunction referred for evaluation of gastrointestinal symptoms and the association of emptying rate with clinical symptoms. METHODS: Retrospective review of all patients with autonomic dysfunction who had a gastric emptying test from January, 1996 to March, 2005. Demographic data, clinical symptoms, composite autonomic scoring scale (CASS) score, and gastric emptying parameters were analyzed. RESULTS: Sixty-one subjects (women 49, age 42 [16-74] yr) with autonomic dysfunction were reviewed. Patients had mild-to-moderate (mean CASS score 3) autonomic dysfunction. Twenty-seven, 17, and 17 patients had rapid, normal, and delayed gastric emptying t(1/2), respectively. In addition, 10 patients had initially rapid emptying in phase 1, with subsequent slowing in phase 2 to produce an overall normal or delayed t(1/2). There was no difference in demographic data or CASS score among the three groups. More patients with initial or overall rapid emptying had diarrhea (70%) compared to patients with normal (33%) or delayed (33%) emptying (P= 0.018). CONCLUSIONS: Unexpectedly, more patients with autonomic dysfunction have rapid rather than delayed gastric emptying. The presence of diarrhea in patients with autonomic symptoms should prompt consideration for the presence of rapid gastric emptying. Conversely, the finding of rapid gastric emptying in patients with gastrointestinal symptoms should prompt consideration for the presence of underlying autonomic dysfunction.     

Inflammation at the cardio-oesophageal junction: relationship to acid and bile exposure

BACKGROUND: The aetiology of inflammation in cardiac mucosa at the gastro-oesophageal junction (carditis) is unclear, although gastro-oesophageal reflux has been suggested. OBJECTIVES: To correlate histological features of carditis with oesophageal acid exposure (gastro-oesophageal reflux) and proximal gastric bile exposure (duodenogastric reflux) in patients with symptoms of gastro-oesophageal reflux disease (GORD). METHODS: Sixty-six patients with reflux symptoms underwent endoscopy with biopsy, oesophageal manometry, 24-h oesophageal pH testing and 24-h proximal gastric Bilitec 2000 testing. Inflammation in glandular mucosa was assessed using the updated Sydney System. Fifteen healthy volunteers underwent pH and Bilitec 2000 testing and served as controls. RESULTS: There was no correlation between either the presence or histological grade of carditis and oesophageal acid exposure or proximal gastric bilirubin exposure. Patients with reflux symptoms had as much duodenogastric reflux into the proximal stomach as did control subjects. CONCLUSIONS: We were unable to establish either gastro-oesophageal or duodenogastric reflux as the predominant cause of inflammation in cardiac mucosa.     

Gastric emptying and duodeno-gastro-oesophageal reflux in gastro-oesophageal reflux disease

BACKGROUND: Previous studies present conflicting results regarding relationship between gastric emptying and gastro-oesophageal reflux disease. Reflux of duodenal content to oesophagus is generally considered to be associated with more severe disease. AIM: To assess presence of a gastric emptying disorder in persons with reflux of duodenal contents to oesophagus and to identify any correlation with gastric emptying and oesophageal motility. METHODOLOGY: A total of 15 subjects with (B+) and 15 subjects without (B-) bile reflux to oesophagus determined by 24-hour bilirubin monitoring were studied with scintigraphic solid gastric emptying and 24-hour oesophageal manometry. RESULTS: There was no difference in lag phase [median 23.7 (range 10.8-44.0) vs 24.6 (8.1-40.1) min], half emptying time [74.6 (48.0-93.6) vs 82.8 (54.4-153.9) min] or emptying rate [0.89 (0.59-1.34) vs 0.83 (0.36-1. 15)%/min] for B- and B+ subjects, respectively. In addition, there was no difference in emptying rate of gastric fundus between B- and B+ subjects. Subjects with bile reflux had less effective oesophageal contractions of oesophageal body [9.4(3.3-37)%] compared to subjects without bile reflux [32(19-47)%, p = 0.002]. However, there was no correlation between oesophageal motility and gastric emptying. CONCLUSION: Results suggest that a gastric emptying disorder is a less likely contributing cause of bile reflux to the oesophagus, but bile reflux is associated with less effective oesophageal motility.     

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

Johansson K-E, Ask P, Boeryd B, Fransson S-G, Tibbling L. Oesophagitis, signs of reflux, and gastric acid secretion in patients with symptoms of gastro-oesophageal reflux disease. Scand J Gastroenterol 1986, 21, 837-847

In a study comprising 100 patients referred to a surgical clinic with symptoms suggestive of gastro-oesophageal reflux disease the value of different diagnostic procedures was investigated. Positive acid perfusion and 24-h pH tests were the commonest findings. Forty-nine per cent showed a normal oesophageal mucosa or diffuse oesophagitis at endoscopy. The severity of heartburn and regurgitation did not differ between patients with normal oesophageal mucosa and oesophagitis of various severities. The severity of macroscopic oesophagitis was significantly correlated to the total reflux time, the presence of reflux or a hiatal hernia at radiology, an open cardia or reflux at endoscopy, pressure transmission or reflux and low lower oesophageal sphincter pressure at manometry. Gastric hypersecretion was found in 66% of the patients. Gastric acid secretion was not correlated to the severity of oesophagitis or to the findings at 24-h pH test. In patients with severe oesophagitis the sensitivity for radiologic, manometric, and endoscopic signs of incompetence of the gastro-oesophageal junction was 94%.