Effect of atropine on gastro-oesophageal reflux and transient lower oesophageal sphincter relaxations in patients with gastro-oesophageal reflux disease

Background—Atropinereduces the rate of reflux episodes in normal subjects by inhibition oftransient lower oesophageal sphincter (LOS) relaxations. The aim ofthis study was to investigate the effect of atropine on the rate andmechanisms of reflux in patients with reflux disease.
Methods—Oesophagealmotility and pH were recorded for one hour after a meal in 15 patientswith reflux disease. On separate days, atropine (15 µg/kg bolusintravenously, 4 µg/kg/h infusion) or saline were given andmaintained for the recording period.
Results—Atropinesignificantly reduced basal LOS pressure from 7.1 (2.2) to 2.9 (1.3) mmHg (mean (SEM)). Atropine also reduced the rate of reflux episodes from5.0 (2.0-8.75) to 1.0 (0-6.25) per hour (median (interquartilerange)) largely because of a decrease in the rate of transient LOSrelaxations from 2.0 (0-4.75) to 0 (0-0) per hour and abolition ofreflux during swallow induced LOS relaxation. There was no change inthe rate of reflux episodes because of absent basal LOS pressure.
Conclusions—Atropineinhibits reflux in patients with reflux disease largely by inhibitionof transient LOS relaxations and swallow induced LOS relaxation. Thesefindings suggest that pharmacological control of reflux through controlof transient LOS relaxations is possible in patients with reflux disease.

Keywords:gastro-oesophageal reflux; lower oesophagealsphincter; manometry; diaphragm; atropine; pharmacology

     

Influence of endoscopic variceal ligation on oesophageal motility

BACKGROUND: To determine the change of oesophageal manometry in patients with oesophageal varices before and after oesophageal variceal ligation (EVL). METHODS: Forty-five patients who had liver cirrhosis and oesophageal varices with high risk of bleeding were managed by EVL. Oesophageal manometry was performed just prior to the ligation and 4-6 weeks after obliteration of varices. Another 45 age- and sex-matched patients without hepatic, oesophageal or systemic disease served as the control group. RESULTS: At 5 cm above the lower oesophageal sphincter (LES), the amplitude of the contractive wave was significantly lower in patients before EVL (56.9 +/- 31.8 vs 80.1 +/- 30.1, P< 1.05) and returned to the level of control subjects after EVL (76.5 +/- 37.0 vs 80.1 +/- 30.1, P> 0.05). At 10 cm above LES, the amplitude of the contractive wave was significantly lower in patients before and after EVL than the control group (54.3 +/- 29.2 vs 68.1 +/- 29.5, 54.2 +/- 26.0 vs 68.1 +/- 29.5, respectively, P< 0.05). The percentage of tertiary waves was significantly higher in patients before and after EVL than in the control group (31.4 +/- 36.6 vs 5.8 +/- 15.1, 26.9 +/- 32.9 vs 5.8 +/- 15.1, respectively, P< 0.05). However, no significant swallowing disturbance was noted in patients after EVL. There was significantly greater LES length in patients before EVL (4.0 +/- 0.9 vs 3.4 +/- 0.7, P<0.05) but there was no significant difference in the LES length after EVL as compared with the control group. Eighty-six per cent (39/45) of patients developed paraoesophageal varices and 31% (14/45) developed new varices 6 months after variceal obliteration. However, there was no significant difference in manometry at the time of variceal obliteration between patients with variceal recurrence and those without. CONCLUSIONS: The presence of varices affected oesophageal motility. However, such abnormality had little clinical significance. Endoscopic variceal ligation normalized oesophageal motility and may not induce abnormal oesophageal motility. The manometric change can not be used to predict the recurrence of varices in cirrhotic patients after variceal obliteration.     

Effect of sucralfate granules in suspension on endoscopic variceal sclerotherapy induced ulcer: analysis of the factors determining ulcer healing

Oesophageal ulcers commonly occur after endoscopic variceal sclerotherapy and usually cause complications and a delay in further sclerotherapy. The aims of this study are to investigate the effect of sucralfate granules in suspension on the treatment of endoscopic variceal sclerotherapy induced ulcer and analyse the factors determining the ulcer healing. Fifty-two patients with oesophageal variceal bleeding received elective endoscopic variceal sclerotherapy. After endoscopically proved oesophageal ulcers, they were randomized to receive either sucralfate granules in suspension (n = 22) or antacid (n = 23). Follow-up endoscopy was performed weekly. Ulcer healing rates were compared between the groups using the log-rank test. Forty-one ulcers receiving sucralfate and 48 ulcers receiving antacid treatment were evaluated. The clinical characteristics of the ulcers were similar in both groups. The ulcers in patients receiving sucralfate healed faster than those receiving antacid (P<0.02). On analysis of factors affecting ulcer healing, ulcers smaller than 1 cm2 (n = 59) appeared to heal faster than those larger than 1 cm2 (n = 30; P= 0.059) and shallow ulcers (n = 46) healed faster than deep ulcers (n = 43; P<0.001). On multifactorial analysis, ulcer depth was the only factor determining ulcer healing. The ulcer healing effects of sucralfate became more prominent when the ulcer was larger than 1.0cm2 (1.7+/-0.6 weeks vs 2.3+/-0.6 weeks, P= 0.011) and deep (1.7+/-0.7 weeks vs 2.5+/-1.0 weeks, P= 0.013) when compared with those receiving antacid. Sucralfate granules in suspension speed the healing of endoscopic variceal sclerotherapy induced ulcer, especially deep and large ulcers.     

急诊内镜下套扎与硬化治疗食管静脉曲张破裂出血的比较

目的比较食管静脉曲张破裂出血急诊内镜下套扎与硬化治疗的疗效和安全性。方法对210例食管静脉曲张破裂出血患者,急诊情况下行内镜下套扎或硬化治疗,并分析比较两组急诊止血成功率、近期再出血率、急诊治疗曲张静脉消失率、不良反应、并发症、病死率等情况。结果急诊止血成功率套扎组达95.4%,硬化组达96.0%;近期再出血率分别为4.8%和4.1%;套扎组急诊治疗曲张静脉消失率明显优于硬化组（P〈0.01）。两组不良反应、并发症及病死率无差别。临床疗效与肝功能呈正相关。结论急诊内镜下套扎与硬化治疗食管静脉曲张出血均为有效、安全的止血方法。临床上可结合患者实际情况综合考虑后选择。     

Preservation of postural control of transient lower oesophageal sphincter relaxations in patients with reflux oesophagitis

INTRODUCTION: In normal subjects, transient lower oesophageal sphincter relaxations (TLOSRs) and gas reflux during belching are suppressed in the supine position. Supine reflux, however, is a feature of reflux disease. AIMS: To investigate whether postural suppression of TLOSRs and gas reflux is impaired in patients with reflux disease. PATIENTS: Ten patients with erosive oesophagitis. METHODS: Oesophageal manometry was performed during gastric distension with 750 ml carbon dioxide. Measurements were made for 10 minutes before and after distension in both sitting and supine positions. RESULTS: In the sitting position gastric distension substantially increased the rate of gas reflux (median (interquartile range)), as evidenced by increases in oesophageal common cavities from 1 (0-1)/10 min to 7 (5-10)/10 min and TLOSRs from 1 (1-1.5)/10 min to 6 (2.5-8)/10 min. However, this effect was suppressed in the supine position in all but one patient (TLOSRs 0 (0)/10 min to 1 (0-4.5)/10 min, common cavities 0 (0)/10 min to 0.5 (0-2)/10 min). CONCLUSIONS: Postural suppression of TLOSRs and gas reflux is generally preserved in reflux disease.     

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.     

Dysphagia after prophylactic endoscopic injection sclerotherapy for oesophageal varices: not fatal but a distressing complication

BACKGROUND: Although dysphagia resulting from oesophageal strictures induced by endoscopic injection sclerotherapy (EIS) is not a fatal complication, it is often quite distressing for the patients. The aim of the current study was to clarify the relationship between dysphagia resulting from oesophageal stricture following prophylactic EIS and the volume of sclerosant consumed in the EIS series. METHODS: Fifty-two patients with oesophageal varices, who had been treated by prophylactic EIS, were selected as the subjects. RESULTS: Seventeen (32.7%) patients developed dysphagia following prophylactic EIS, and five patients with a severe stricture required bougie dilatation to take meals. The volume of sclerosant used in the initial session of EIS for patients with subsequent dysphagia (24.9 +/- 4.0 mL) was significantly larger than that for patients without dysphagia (18.4 +/- 5.1 mL; P < 0.001). The mean volume of sclerosant consumed per session during the EIS series for patients with dysphagia (16.5 +/- 3.0 mL) was also significantly larger than that for patients without dysphagia (13.1 +/- 3.8 mL; P < 0.01). CONCLUSIONS: The injection of a superfluous amount of sclerosant in prophylactic EIS brings about distressing dysphagia with oesophageal stricture in the patients with oesophageal varices who had no such complaint or symptoms before the therapy.     

An ambulant porcine model of acid reflux used to evaluate endoscopic gastroplasty

BACKGROUND: There is a lack of suitable models for testing of therapeutic procedures for gastro-oesophageal reflux disease. Endoscopic sewing methods might allow the development of a new less invasive surgical approach to treatment of gastrointestinal disorders. AIMS: To develop an animal model of gastro-oesophageal reflux for testing the efficacy of a new antireflux procedure, endoscopic gastroplasty, performed at flexible endoscopy without laparotomy or laparoscopy. METHODS: At endoscopy a pH sensitive radiotelemetry capsule was sewn to the oesophageal wall, 5 cm above the lower oesophageal sphincter, in six large white pigs. Ambulant pH recordings (48-96 hours; total 447 hours) were obtained. The median distal oesophageal pH was 6.8 (range 6.4-7.3); pH was less than 4 for 9.3% of the time. After one week, endoscopic gastroplasty was performed by placing sutures below the gastro-oesophageal junction, forming a neo-oesophagus of 1-2 cm in length. Postoperative manometry and pH recordings (24-96 hours; total 344 hours) were carried out. RESULTS: Following gastroplasty, the median sphincter pressure increased significantly from 3 to 6 mm Hg and in length from 3 to 3.75 cm. The median time pH was less than 4 decreased significantly from 9.3% to 0.2%. CONCLUSIONS: These are the first long term measurements of oesophageal pH in ambulant pigs. The finding of spontaneous reflux suggested a model for studying treatments of reflux. Endoscopic gastroplasty increased sphincter pressure and length and decreased acid reflux.     

Oesophageal pH monitoring in infants: elimination of gastric buffering does not modify reflux index

BACKGROUND: Oesophageal pH monitoring is considered to be the gold standard investigation in the diagnosis of gastro-oesophageal reflux disease. Results of pH monitoring in regurgitating infants, however, may be within normal ranges. Therefore it was hypothesized that prolonged buffering of gastric acidity caused by milk-feeding may falsely normalize the pH data. Therefore, it may be relevant to omit the periods of gastric acid buffering in the analysis of the oesophageal pH monitoring data. METHODS: Combined gastric and oesophageal pH monitoring (Digitrapper Mark III, two-channel antimony electrode, Synectics) was performed in 90 consecutive infants, 0.5-10 months old, who were referred to the unit by outdoor paediatricians for pH measurement. The data were analysed in three different ways. The reflux index (RI), or the percentage time that the pH in the oesophagus was < 4.0, was calculated in three different ways: (i) the total duration of the investigation; (ii) excluding 90-min postprandial periods, starting from the beginning of a feeding; and (iii) excluding all periods with a gastric pH > 4.0, which are the periods of gastric buffering with a theoretical impossibility of recording an oesophageal pH < 4.0. RESULTS: The mean duration of the pHmetries was 19.20+/-2.01h (A; mean +/- 1 SD), with a RI of 5.38+/-5.39% (B; median 3.45%). If the 90-min postprandial periods were not considered, the mean duration decreased to 12.21+/-2.41h (C; P(A vs C) < 0.001), with an oesophageal RI of 6.82+/-6.57% (D; median: 4.65; P(B vs D) = NS; r (B vs D) = 0.97). If all periods with a gastric pH > 4.0 were elminated, the duration available for analysis of the data with a gastric pH < 4.0 was 12.53+/-4.00 h (E; P(A vs E) < 0.001; P(C vs E) = NS), with an oesophageal RI of 7.06+/-7.52% (F; median: 4.50; P(B vs D vs F) = NS; r(B vs F), (D vs F) = 0.96). CONCLUSION: Overall the data do not support a benefit from including periods of gastric buffering in the routine analysis of oesophageal pH monitoring data. Therefore standard oesophageal pH monitoring should be with a single electrode and should not include periods of gastric buffering.     

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.     

Effects of endoscopic variceal sclerotherapy on azygos vein blood flow and systemic haemodynamics*

The present study was designed to determine the systemic haemodynamic effects of obliterating oesophageal varices by endoscopic sclerotherapy. We evaluated systemic and splanchnic haemodynamics before and after the first course of sclerotherapy in cirrhotic patients. The baseline cardiac index was significantly correlated with baseline azygos vein blood flow (r = 0.64; P< 0.01) and the azygos vein blood flow and cardiac index significantly decreased (-33% and -16%, respectively; P< 0.01) following sclerotherapy. The systemic vascular resistance index was also increased significantly (+20%; P<0.01) in these patients. Moreover, the per cent change in azygos vein blood flow was directly correlated with that of the cardiac index (r=0.51; P< 0.03). We conclude from these findings that the obliteration of portosystemic collaterals by sclerotherapy significantly reverses hyperdynamic circulation in such patients via a decrease in cardiac preload. The blood flow of the portosystemic shunt per se is a leading contributor to the hyperdynamic circulation observed in patients with well-developed portal systemic collateral vessels.     

Patterns of gas and liquid reflux during transient lower oesophageal sphincter relaxation: a study using intraluminal electrical impedance

Background—Belching has beenproposed as a major mechanism underlying acid gastro-oesophageal refluxin normal subjects. However, the presence of oesophageal gas hasnot been measured directly but only inferred from manometry.
Aims—To investigate, usingintraluminal electrical impedance, the patterns of gas and liquidreflux during transient lower oesophageal sphincter (LOS) relaxations,the main mechanism of acid reflux in normal subjects.
Methods—Impedance changesassociated with the passage of gas were studied in vitro, and in vivoin cats. Oesophageal manometry, pH, and intraluminal electricalimpedance measurements were performed in 11 normal subjects after a meal.
Results—Gas reflux caused asudden increase in impedance that propagated rapidly to the proximaloesophagus whereas liquid reflux induced a retrogressively propagatedfall in impedance. Impedance showed gas or liquid reflux during most(102/141) transient LOS relaxations. When acid reflux occurred,impedance showed evidence of intraoesophageal retrograde flow of liquidin the majority (78%) of events. Evidence of gas retroflow was foundin almost half (47%) of acid reflux episodes. When present together,however, liquid preceded gas on 44% of occasions. Overall, gas refluxoccurred as the initial event in only 25% of acid reflux episodes.
Conclusions—These findings suggestthat in upright normal subjects, although belching can precipitate acidreflux, most acid reflux occurs as a primary event.

Keywords:belching; gastro-oesophageal reflux disease; oesophageal manometry; intraluminal electrical impedance; loweroesophageal sphincter

     

Influence of posture on transient lower oesophageal sphincter relaxation and gastro-oesophageal reflux in the dog

The hypothesis that suppression of transient lower oesophageal sphincter relaxation (TLOSR) in recumbent postures in the dog is dependent upon the sensing of a gastric pool of liquid in proximity to the lower oesophageal sphincter was examined. Constant gastric insufflation with air (80 ml/min) was used to evoke TLOSR in unsedated, fasting animals. Oesophageal motility was monitored with a perfused manometric sleeve catheter assembly. Gastrooesophageal flow was recognized manometrically and by oesophageal pH recording. TLOSR occurred significantly less frequently in three recumbent positions (right lateral, left lateral and supine) than when the dog stood on four legs, but was more likely to be associated with acid reflux when they occurred in recumbent positions. Aspiration of the gastric pool was found to have no effect on triggering of TLOSR although it reduced the frequency with which acid reflux was associated with TLOSR. It is concluded that the low rate of occurrence of TLOSR in recumbent positions is unlikely to be explained by the presence of a gastric pool of liquid in proximity to the lower oesophageal sphincter.     

Patterns of gastritis in patients with gastro-oesophageal reflux disease

BACKGROUND: The cause of inflammation in cardiac mucosa at the gastro-oesophageal junction (GOJ) is unclear, both gastro-oesophageal reflux disease (GORD) and Helicobacter pylori having been implicated. AIMS: To describe patterns of gastritis in patients with symptomatic GORD. METHODS: In 150 patients (126 normally located Z-line, 24 Barrett's oesophagus) with symptoms of GORD, biopsies were taken of the GOJ, corpus, and antrum. Inflammation was assessed using the updated Sydney System. RESULTS: For the 126 patients with a normally located Z-line, biopsies of the GOJ revealed cardiac mucosa in 96, fundic mucosa in 29, and squamous mucosa in one. Inflammation in glandular mucosa at the GOJ was present in 99/125 specimens (79%), including 87/96 (91%) with cardiac mucosa and 12/29 (41%) with fundic mucosa. Inflammation in fundic mucosa was closely related to H pylori and active inflammation was only seen in its presence. Inflammation in cardiac mucosa was less closely linked to H pylori. When H pylori was present in cardiac mucosa (28/96, 29%) active inflammation was usually present (25/28, 89%). However, active inflammation was also found in 34/68 (50%) cardiac mucosa specimens without H pylori. Overall, 28/87 (32%) biopsies with carditis were colonised with H pylori and 59/87 (68%) were not. In H pylori colonised patients, inflammation was seen throughout the stomach, while in non-colonised patients, it was confined to cardiac mucosa. CONCLUSIONS: Patients with symptomatic GORD had a high prevalence of carditis. This was of two types, H pylori associated and unassociated. Except on Giemsa staining, the two were morphologically identical, suggesting mediation by a similar immunological mechanism.     

Oesophageal perforation following endoscopic variceal ligation and balloon tamponade

Endoscopic variceal ligation (EVL) related complication is rarely reported. A case is presented of a 74 year old man with oesophageal variceal bleeding who developed oesophageal perforation following EVL and balloon tamponade. An oesophageal wall defect was induced by EVL and tissue repair was hindered by decompensated liver reserve and shock status; concomitant balloon tamponade precipitated oesophageal perforation. The case is reported to draw attention to oesophageal perforation after concurrent use of balloon tamponade and EVL.     

Perforation of esophagus after endoscopic variceal sclerotherapy

To determine the true incidence of endoscopic variceal sclerotherapy (EVS) -related esophageal perforation, a retrospective analysis of 900 EVS procedures using sodium tetradecyl sulfate performed on 170 patients during a five-year period (1980–1985) was carried out. Autopsy data of all patients who received EVS and who died (32 patients, 100%) during this period were available to confirm the diagnosis of perforation. Esophageal perforation was confirmed in 5 (2.9%) and was seen in patients with advanced alcoholic liver disease. Importantly, most patients did not manifest features of an esophageal leak, but presented instead as a deterioration in condition and died after a mean (±sd) 14±5.2 days. Analysis of the clinical and EVS data reveals that the risk of developing perforation is high when EVS is performed during active bleeding. The extravariceal location of sclerosant and microabscesses may be important predisposing factors. In our experience largedose injection, deep ulceration, and balloon tamponade are less likely predisposing factors of this complication.     

Adult asthma and gastro-oesophageal reflux: the effects of omeprazole therapy on asthma

Background: Approximately 40–60% of patients with asthma have gastro-oesophageal reflux (GOR) and it has been postulated that this may worsen asthma severity. Aims: To investigate the effect of the potent gastric acid inhibitor omeprazole 40 mg orally daily on peak expiratory flow rate (PEFR), asthma symptoms and histamine bronchial responsiveness in adult patients with both asthma and GOR. Methods: This was a double blind, randomised, placebo controlled, crossover study. Upper gastrointestinal endoscopy, 24 hour oesophageal pH measurements, spirometry and histamine bronchoprovocation test (HIT) were performed prior to entry. Phase 1:2 week placebo run-in period, with baseline recording of PEFR, asthma and GOR symptoms, and use of inhaled p₂-agonist. Phase 2: patients randomised to receive either placebo or omeprazole 40 mg/d for four weeks. Phase 3: placebo for two weeks. Phase 4: patients crossed over to opposite treatment from that of phase 2. Spirometry, and diary cards were assessed at beginning and end of phases 2 and 4. HIT was performed at the end of phase 2 and at the beginning and end of phase 4. Results: Twenty patients (eight female and 12 male) completed the study. The evening but not morning PEFR (% predicted) were significantly higher on omeprazole vs placebo (82 ± 4% SEM vs 79 ± 4% SEM; p<0.05). No significant differences were found in FEVj, FVC, histamine bronchial responsiveness and diurnal variation of PEFR between placebo and omeprazole treatments. Similarly, there were no significant differences during placebo and omeprazole periods in day time wheeze, cough, breathlessness, p₂-agonist use or night time wheeze and breathlessness. Day and night heartburn symptoms were significantly better on omeprazole vs placebo (p<0.05). Conclusions: Omeprazole 40 mg daily improved evening PEFR in asthma patients with GOR. However, asthma symptoms, inhaled β₂-agonist use and histamine bronchial responsiveness did not change.     

Oesophageal epithelial innervation in health and reflux oesophagitis

BACKGROUND: The response of the oesophagus to refluxed gastric contents is likely to depend on intact neural mechanisms in the oesophageal mucosa. The epithelial innervation has not been systematically evaluated in health or reflux disease. AIMS: To study oesophageal epithelial innervation in controls, and also inflamed and non-inflamed mucosa in patients with reflux oesophagitis and healed oesophagitis. PATIENTS: Ten controls, nine patients with reflux oesophagitis, and five patients with healed oesophagitis. METHODS: Oesophageal epithelial biopsy specimens were obtained at endoscopy. The distribution of the neuronal marker protein gene product 9.5 (PGP), and the neuropeptides calcitonin gene related peptide (CGRP), neuropeptide Y (NPY), substance P (SP), and vasoactive intestinal peptide (VIP) were investigated by immunohistochemistry. Density of innervation was assessed by the proportion of papillae in each oesophageal epithelial biopsy specimen containing immunoreactive fibres (found in the subepithelium and epithelial papillae, but not penetrating the epithelium). RESULTS: The proportion of papillae positive for PGP immunoreactive nerve fibres was significantly increased in inflamed tissue when compared with controls, and non-inflamed and healed tissue. There was also a significant increase in VIP immunoreactive fibres within epithelial papillae. Other neuropeptides showed no proportional changes in inflammation. CONCLUSIONS: Epithelial biopsy specimens can be used to assess innervation in the oesophagus. The innervation of the oesophageal mucosa is not altered in non-inflamed tissue of patients with oesophagitis but alters in response to inflammation, where there is a selective increase (about three- to fourfold) in VIP containing nerves.     

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.