Helicobacter pylori eradication lowers esophageal sphincter pressures in functional dyspepsia patients

BACKGROUND/AIMS: Helicobacter pylori infection is the most common cause of gastroduodenal diseases. The role H. pylori eradication in functional dyspepsia patients is contradictory. We performed this study to determine the effects of H. pylori eradication in functional dyspepsia patients with respect to physiological and histological parameters including esophageal sphincter functions. METHODOLOGY: We studied 20 functional dyspepsia patients, whose H. pylori infection was confirmed by histology and urease test. We also confirmed eradication using the same methods after three months. We performed 24-hour esophageal pH monitoring, esophageal manometry, meal stimulated gastrin release test and measured dyspepsia severity score and gastric emptying time before and three months after eradication. Eradication regimen consisted of omeprazol 20 mg b.i.d., clarithromycin 500 mg b.i.d. and metranidazol 500 mg b.i.d., for two weeks. Gastric inflammation and H. pylori density within biopsy samples from the antrum (n = 4), corpus (n = 4), cardia (n = 2), fundus (n = 2), duodenum (n = 2) and distal esophagus (n = 1) were assessed. RESULTS: Dyspepsia severity score (P < 0.001), meal stimulated gastrin levels, upper (P = 0.01) and lower (P = 0.06) sphincter pressures were decreased after eradication irrespective of gastric histology; but gastric emptying times (P = 0.87) and pH < 4.5% reflux (P = 0.91) were not changed significantly. CONCLUSIONS: H. pylori eradication results in decreased esophageal sphincter pressures irrespective of gastric histology in functional dyspepsia patients. These decreases are not associated with increased objective reflux or reflux symptomatology. The clinical significance of these finding deserves further evaluations.     

Effects of a pH electrode across the lower esophageal sphincter

Recent studies have suggested that combined monitoring of the esophagus and stomach for prolonged periods may be the best method for investigating patients with upper gastrointestinal complaints. However, the effects of an electrode across the LES on esophageal reflux parameters have not been extensively studied. We studied 10 healthy volunteers and 10 patients with GERD twice with 24-hr pH monitoring. In phase 1, two glass electrodes were placed 1 cm below the UES and 5 cm above the LES. One week later in phase 2, patients were restudied with one electrode 5 cm above and one 5 cm below the LES. Although total acid exposure remained the same in healthy volunteers, three volunteers who spontaneously refluxed at night had abnormal prolongation of their supine acid exposure during phase 2 of the study. In patients with GERD, the electrode across the LES resulted in significant (P=0.01) increase in supine acid exposure and showed a strong tendency for the number of reflux episodes >5 min supine (P=0.02) and longest reflux episode supine (P=0.06) to increase without a change in the number of reflux episodes. In conclusion, a small glass electrode across the LES results in prolongation of supine acid exposure in both healthy volunteers spontaneously refluxing at night and the majority of patients with GERD. This results from the electrode interfering with clearance of refluxed acid in the supine position. Thus, combined esophageal and gastric pH monitoring may have important limitations in investigating gastroesophageal symptoms.     

The possible role of Helicobacter pylori in GERD

A variety of abnormalities contribute to the development of gastroesophageal reflux disease (GERD) including transient lower esophageal sphincter relaxation, low esophageal sphincter pressure, presence of a hiatal hernia, diminished esophageal clearance of refluxed gastric contents, and alterations in esophageal mucosal resistance. Helicobacter pylori infection clearly plays a role in the pathogenesis of peptic ulcer disease and mucosa associated lymphoma of the stomach and is a definite risk factor for distal gastric cancer. The role of H. pylori infection in GERD remains controversial and incompletely understood. Although H. pylori infection does not cause reflux disease, circumstantial evidence suggests that it may protect against the development of GERD and its complications in some patients. The most likely mechanism whereby H. pylori infection protects against GERD is by decreasing the potency of the gastric refluxate in patients with corpus predominant gastritis. A variety of implications of H. pylori infection on GERD treatment have also arisen in recent years. These focus on the risk of gastric atrophy while on proton pump inhibitor therapy and the efficacy of proton pump inhibitors before and after eradication of H. pylori. This article puts into perspective our current understanding of the complex, incompletely understood relationship between H. pylori infection and GERD.     

Gastroesophageal reflux before and after Helicobacter pylori eradication. A prospective study using ambulatory 24-h esophageal pH monitoring

The aim of this study was to assess prevalence of GERD before and after Helicobacter pylori (HP) eradication utilizing 24-h esophageal pH/manometry studies. Helicobacter pylori status was confirmed by the Campylobacter like organism test. Those testing positive underwent 24-h pH/manometry followed by HP eradication therapy and urea breath test. Patients were followed up at 6 months and then at 1 year when they underwent a repeat 24-h pH/manometry. Twenty patients, 10 with non-ulcer dyspepsia (NUD) and 10 with duodenal ulcer (DU) were enrolled, though only 10 patients attended for a repeat 24-h pH/manometry study. The patients were well matched, though patients with NUD had a significantly higher symptom score at entry compared with the DU group (8.5 vs 5.7, P < 0.05). The pH and esophageal manometry data were similar in the two groups. Overall nine patients (45%; DU = 5, NUD = 4) had evidence of GERD prior to HP eradication and it persisted one year after cure of the infection. The reflux disease occurred in the presence of normal LES pressure (mean 15.6 +/- 3.3 mmHg). New onset GERD was uncommon after cure of HP infection, occurring in only one patient with NUD. Overall HP eradication had no impact on percentage of time pH < 4 (4.69 +/- 3 vs 4.79 +/- 3), episodes > 5 min (9.8 +/- 16 vs 15.5 +/- 25.3) and Johnson DeMeester Score (16.8 +/- 7.5 vs 26.8 +/- 18). In addition successful cure of HP produced no significant changes in LES pressure (17.9 +/- 3.8 mmHg vs 19.3 +/- 4.6 mmHg), and other esophageal manometry data. Half of HP-positive patients with NUD and DU have evidence of GERD before HP eradication. This persists after successful cure of the infection. New onset GERD occurs very uncommonly one year after HP eradication.     

Behaviour of acid secretion, gastrin release, serum pepsinogen I, and gastric emptying of liquids over six months from eradication of helicobacter pylori in duodenal ulcer patients. A controlled study.

The behaviour of basal and stimulated acid secretion, gastrin release, serum pepsinogen I, and gastric emptying of liquids was studied in 19 consecutive patients with Helicobacter pylori positive duodenal ulcer, over a follow up period of six months. Eleven patients were studied before and at three and six months after eradication with lansoprazole plus amoxicillin and tinidazole (case group), whereas the remainder, with persistent H pylori infection, were studied before and after three and six months from ulcer healing, thus constituting the control group. In the case group, three months after eradication, fasting serum pepsinogen I fell from (mean (SEM)) 91.9 (6.9) (pretreatment) to 72.2 (5.1) ng/l and the integrated gastrin response to a meal reduced from 11,470 (1174) (pretreatment) to 8130 (608) pg/ml/h (p < 0.05). Fasting serum gastrin concentrations and maximal acid output reduced significantly only six months after eradication. In contrast, no significant change of any of these measurements was seen in the control group either at three or six months from healing compared with the pretreatment values. Gastric emptying of liquids did not change over the entire period of follow up in both study groups. In conclusion, eradication of H pylori in duodenal ulcer patients is accompanied by a rapid fall in serum pepsinogen I and plasma gastrin concentrations, whereas a slight but significant reduction of maximal acid secretion takes place later on. In contrast, gastric emptying of liquids does not seem to be influenced by H pylori status.     

GERD and H. pylori: is there a link?

The incidence of gastroesophageal reflux disease (GERD) and esophageal adenocarcinoma have increased in recent years as the incidence of peptic ulcer disease and distal gastric cancer have declined. Given the simultaneous decline in Helicobacter pylori infection, it is tempting to propose a relationship between H. pylori infection and these opposing time trends. Although H. pylori infection clearly does not cause GERD, it may protect certain susceptible individuals from developing GERD and its complications. The most likely mechanism in which H. pylori infection protects against GERD is by decreasing the potency of the gastric refluxate in patients with corpus predominant gastritis. A variety of implications of H. pylori infection on GERD treatment have also arisen in recent years. These focus on the risk of gastric atrophy while on proton pump inhibitor therapy and the efficacy of proton pump inhibitors before and after eradication of H. pylori. This article puts into perspective our current understanding of the complex, incompletely understood relationship between H. pylori infection and GERD.     

The effect of Helicobacter pylori eradication on gastroesophageal reflux disease

BACKGROUND: The effect of Helicobacter pylori (H. pylori) eradication on gastroesophageal reflux disease is controversial. We aimed to investigate the effect of H. pylori eradication in this group of patients. MATERIALS AND METHODS: Thirty-four consecutive patients with H. pylori infection and reflux esophagitis (grade 1 or 2) were enrolled into the study. Twenty-four hour intra-esophageal pH recording and esophageal manometry were performed before and 3 months after eradication of H. pylori, which was achieved using lansoprazole 30 mg b.i.d., amoxycillin 1 g b.i.d., and clarithromycin 500 mg b.i.d. for 14 days. H. pylori was evaluated in biopsy specimens taken from the antrum and corpus by rapid urease test and by histopathologic examination before and 3 months after eradication. RESULTS: Eighteen patients (11 men and 7 women, median age 42 years) completed the study. Three months after the treatment, there was no significant change in any of the 24-hour esophageal pH recording parameters and mean lower esophageal sphincter resting pressure (P > 0.05). The percentage of total time esophageal pH <4 increased in 10 patients, and decreased in 8 patients. There was a significant decrease in the scores of heartburn and regurgitation (P < 0.01). Esophagitis persisted in 16 patients and disappeared in 2 patients. Esophagitis score decreased in 6 patients, and did not change in 12 patients (P < 0.05). CONCLUSION: H. pylori eradication does not have any effect on gastroesophageal acid reflux in patients with reflux esophagitis 3 months after eradication, but significant improvement is achieved in some reflux associated symptoms.     

Eradication of Helicobacter pylori does not increase acid reflux in patients with mild to moderate reflux oesophagitis

BACKGROUND: A substantial minority of patients with gastro-oesophageal reflux disease (GERD) are infected with Helicobacter pylori, but there is controversy as to whether these patients should be treated for their infection. We hypothesized that H. pylori eradication increases gastro-oesophageal acid reflux in such patients with time. METHODS: Thirty-five consecutive H. pylori-infected patients (16 M and 19 F) with mild or moderate reflux oesophagitis were enrolled. Twenty-four-hour intra-oesophageal (n = 35) and intragastric (n = 12) pH-metry was recorded before and 15 months after H. pylori eradication. Gastric biopsy specimens from the antrum and corpus were obtained from 10 consecutive patients before and 15 months after H. pylori eradication. RESULTS: Fifteen months after eradication of H. pylori there was a significant decrease in percentage time oesophageal pH < 4 in the recumbent position only (P = 0.04). Despite a marked reduction in the severity of gastritis, there was no significant change in gastric acidity, total intra-oesophageal acid exposure or symptom score. Heartburn improved in 12, worsened in 7. and remained unchanged in 16 patients (P = 0.36) without any significant relationship to individual changes in acid exposure (P = 0.60). CONCLUSIONS: H. pylori eradication does not increase gastric acidity or gastro-oesophageal acid reflux in patients with mild to moderate reflux oesophagitis over the first 15 months.     

Motion--Helicobacter pylori causes or worsens GERD: arguments against the motion.

Data from large epidemiological studies show that Helicobacter pylori is less prevalent in patients with gastroesophageal reflux disease (GERD) than in control subjects. The more virulent cagA-positive strains of the organism are also less commonly seen in patients with erosive esophagitis and in those with Barrett's esophagus than in those with less severe forms of GERD. Although the relationship between H pylori and gastric physiology is complex, the organism has little effect on acid secretion in most North American or Western European subjects, and has a net suppressive effect, especially in elderly subjects, in other parts of the world. Thus, the organism has a potential protective effect against GERD, which is exacerbated by gastric acidity. H pylori has no proven effect on other gastric factors that might provoke reflux, including delayed gastric emptying or inappropriate relaxation of the gastric fundus. Two well-designed interventional studies have found that eradication of H pylori either provoked GERD or had no effect. A third smaller study, which seemed to demonstrate that persistent infection was associated with GERD, was flawed, in that the two treatment groups were not comparable. The evidence thus does not support the idea that H pylori infection provokes or aggravates GERD.     

19例胃食管反流病患者根除幽门螺杆菌后食管酸反流的变化

目的：在胃食管反流病(GRED)患者根除幽门螺杆菌(Hp)是否会加重胃食管反流目前存在很大争议。本研究将采用食管内24h pH监测及食管测压检查的方法，定量观察GERD患者根除Hp治疗前后食管酸暴露及食管动力的变化。方法：连续选取我院门诊就诊的Hp阳性GERD患者。Hp感染诊断依据RUT和UBT或UBT和血清学检查。所有入选对象均在内镜检查后1～3d内行食管内24h pH监测和食管测压检查，同时评估反流症状。给予1周三联根除Hp治疗(奥美拉唑20mg，克拉霉素0．25g，阿莫仙1．0g，均bid)。疗程结束3个月后^14C—UBT检查，证实Hp根除者复查食管内24h pH监测和食管测压，同时重新评估反流症状。随访期间不用抑酸剂及促动力剂。结果：共23例Hp阳性GERD患者入选了本研究，其中19例患者完成了根除Hp前后的对比研究。在入选时有6例患者内镜下表现符合反流性食管炎，24h食管内pH监测提示病理性反流者10例。在确定根除Hp3个月后反酸、腹痛症状明显改善，食管24h pH监测各项参数与根除前相比均无显著性差异。LESP根除前10mm Hg(7．7—15．9)，根除后15mm Hg(10—20．6)，前后相比有显著性差异。食管体蠕动无明显改变。结论：本研究在GERD患者根除Hp3个月后反流症状有改善，食管酸暴露情况无明显变化，LESP较根除前增高，提示在GERD患者根除Hp有可能改善胃食管反流症状。     

根除幽门螺杆菌与胃食管反流病的关系研究

目的探讨根除幽门螺杆菌（H．pylori）与胃食管反流病（GERD）的关系。方法本研究采用食管内24hpH监测的方法，定量观察H．pylori阳性GERD患者根除H．pylori和单用兰索拉唑治疗3月后食管酸暴露的变化，以及H．pylori阳性慢性浅表性胃炎（CSG）根除H．pylori和姑息治疗3月后食管酸暴露的变化。RE组：反流性食管炎（RE）表现患者60例，按就诊门诊号随机分为治疗组和对照组。治疗组采用丽珠唯三联＋兰索拉唑方案，对照组单用兰索拉唑。CSG组：慢性浅表性胃炎（CSG）患者60例，按就诊门诊号随机分为治疗组和对照组。治疗组均采用丽珠唯三联方案，对照组不采用药物治疗。以上两组待H．pylori根除后，对比研究H．pylori根除组和对照组3月后食管24hpH监测参数。结果RE组：H．pylori根除和单用兰索拉唑治疗3月后两组24h食管pH监测主要观察5项指标均无显著性差异（P〉0．05）。CSG组：H．pylori根除和姑息治疗3月两组24h食管pH监测主要观察5项指标均无显著性差异（P〉0．05）。结论GERD患者根除幽门螺杆菌后食管酸暴露无明显改变，CSG患者根除幽门螺杆菌后食管酸暴露无明显改变，H．pylori感染可能与GERD的转归和发生无关。     

The changing epidemiology of GERD: geography and Helicobacter pylori

BACKGROUND: Issues have arisen regarding H. pylori infection and GERD that have caused unnecessary confusion among practicing physicians. In the last century GERD became increasingly recognized in the West and it has become evident that the prevalence of GERD is now occurring in many previously underdeveloped countries. METHODS: This review article fosters understanding of the issues by focusing on the esophageal acid load and the factors that control it. In particular, we discuss the effects of the change in the patterns of gastritis that have occurred naturally as well as after H. pylori eradication and correlate those changes with their effects on the esophageal acid load. We show how it is possible to separate gastroesophageal reflux from gastroesophageal reflux disease based on differences in esophageal acid load. We also describe how the practice of assessing gastroesophageal reflux based on the time the intraesophageal pH is less than 4 resulted in investigators systematically discarding data critical to understanding of the effect of their interventions on esophageal acid load. Testable hypotheses are presented to explain the interactions between H. pylori and GERD and between H. pylori and the changing epidemiology of GERD. CONCLUSIONS: We propose that the confusion regarding H. pylori and the changing epidemiology of GERD is based on the failure to critically examine the historical evidence in relation to the other H. pylori-related diseases as well as reliance on techniques that are either unable to measure, or systematically discard data critical for understanding effects of various interventions on the esophageal acid load. This has resulted in propagation of erroneous concepts regarding H. pylori and adenocarcinoma of the esophagus and has resulted in some patients being denied appropriate therapy.     

Gastroesophageal reflux disease and Helicobacter pylori infection

The prevalence of Helicobacter pylori infection has been decreasing while the prevalence of gastroesophageal reflux disease and esophageal adenocarcinoma has been increasing in developed countries since the 1930s. This has raised concerns that H. pylori infection may protect against esophageal disease and that the disappearance of H. pylori from the population might lead to a further increase in gastroesophageal reflux disease. Some studies have suggested that eradication of H. pylori in patients with duodenal ulcer disease results in an increase in the incidence of erosive esophagitis, whereas other studies have shown no such increase. Studies on gastric acid secretion have demonstrated that proton pump inhibitors are more effective in controlling gastric pH in individuals who are infected with H. pylori. Studies on the impact of therapy in patients with erosive esophagitis have been conflicting. This article reviews each of the issues in the debate separately and concludes that there is little evidence to suggest a major effect of H. pylori eradication on the outcome of gastroesophageal reflux disease.     

幽门螺杆菌与胃食管反流病

幽门螺杆菌（Helicobacter pylori，H．pylori）与胃食管反流病（gastroesophageal reflux disease，GERD）的关系各研究结果不尽一致，流行病学研究表明，在GERD中不仅Mpylori感染率较低，而且cagA的检出率也低，二者都与食管疾病严重程度呈负相关。亦有文献报告H．pylori感染与GERD发生无明显关系。H．pylori对食管保护作用机制可能与其能提高LES压力、降低胃内酸度和影响食管对酸的敏感性有关。有研究表明，H．pylori可以提高质子泵抑制剂的抑酸效果，亦有人认为H．pylori并不影响GERD疗效。因此H．pylori与GERD的关系仍需进一步的临床和基础研究来评价。     

The effects of alcohol consumption upon the gastrointestinal tract

Regardless of the type and dose of beverage involved, alcohol facilitates the development of gastroesophageal reflux disease by reducing the pressure of the lower esophageal sphincter and esophageal motility. Fermented and nondistilled alcoholic beverages increase gastrin levels and acid secretion. Succinic and maleic acid contained in certain alcoholic drinks also stimulate acid secretion. Low alcohol doses accelerate gastric emptying, whereas high doses delay emptying and slow bowel motility. Alcohol facilitates the development of superficial gastritis and chronic atrophic gastritis--though it has not been shown to cause peptic ulcer. Alcoholic beverages, fundamentally wine, have important bactericidal effects upon Helicobacter pylori and enteropathogenic bacteria. The main alcohol-related intestinal alterations are diarrhea and malabsorption, with recovery after restoring a normal diet. Alcohol facilitates the development of oropharyngeal, esophageal, gastric, and colon cancer. Initial research suggests that wine may be comparatively less carcinogenic.     

Impact of Helicobacter pylori eradication on the anti-secretory efficacy of lansoprazole in gastroesophageal reflux disease patients

BACKGROUND: Helicobacter pylori eradication was recommended for the prevention of atrophic gastritis in gastroesophageal reflux disease (GERD) patients on long-term omeprazole treatment. It has been also shown that the treatment with proton pump inhibitors produces lower intragastric pH after H. pylori eradication in subjects with peptic ulcer and healthy individuals. The aim of the present study was to test the hypothesis of whether the efficacy of lansoprazole is reduced after the eradication of H. pylori in GERD patients with peptic esophagitis. METHODS: Eight-hour intragastric pH recordings were performed before and after an 8-day course of lansoprazole (30 mg once daily) in 10 H. pylori-positive male patients with reflux esophagitis and were repeated after the H. pylori eradication. Intragastric acidity was measured by using an antimony electrode placed 10 cm below the cardia. RESULTS: Baseline median preprandial, post-prandial, total intragastric pH and the percentage of time with pH < 3 were not different before and after H. pylori eradication without lansoprazole treatment. During lansoprazole treatment, median post-prandial intragastric pH was lower (4 vs 2.7; P < 0.05) and the percentage of time with pH < 3 was longer (3.4%vs 41.8%; P < 0.05) after H. pylori eradication. Median total intragastric pH tended to be lower after eradication but no difference was found in preprandial median pH. CONCLUSIONS: In patients with reflux esophagitis treated with lansoprazole, intragastric pH increased significantly when H. pylori was present, especially in the post-prandial period, whereas baseline pH remained unchanged after H. pylori eradication.     

Abnormal acid reflux in asthmatic patients in a region with low GERD prevalence

Background A high prevalence of gastroesophageal reflux disease (GERD) in asthmatic patients has been reported from North America and Europe. However, only a few data from Asia are available. This study evaluated the incidence of abnormal gastroesophageal reflux (GER) in asthmatic patients in Taiwan.Methods Fifty-six consecutive ambulatory patients with clinically stable asthma (41 men and 15 women; age, 57.7 ± 12.4 years; range, 24 to 74 years) were evaluated prospectively. All patients underwent esophagogastroduodenoscopy, esophageal manometry, and 24-h esophageal pH monitoring.Results Twenty-nine patients (51.8%) had abnormal GER, as defined by 24-h esophageal pH monitoring. There were 42 patients without endoscopic evidence of esophagitis, 10 patients with Los Angeles (LA) grade A esophagitis, and 4 patients with LA grade B esophagitis. The esophageal motility function studies revealed 21 patients with normal esophageal motility, 23 patients with ineffective esophageal motility (IEM), and 12 patients with nonspecific esophageal motility disorders other than IEM. Although the lower esophageal sphincter (LES) basal pressure was higher in the patients without GER, the difference was not statistically significant.Conclusions Abnormal GER seems to be a clinically significant problem in asthmatic patients in Taiwan. The most common esophageal motility dysfunction is IEM. However, the status of Helicobacter pylori infection plays no role in abnormal GER.     

反流性食管炎和非糜烂性反流病患者酸暴露与食管压力监测结果分析

目的通过对胃食管反流病（GERD）患者的酸暴露情况、食管下括约肌（LES）压力、食管体部压力、幽门螺杆菌（Hp）感染结果的比较，探讨反流性食管炎（RE）、非糜烂性反流病（NERD）的不同状况，为临床治疗提供科学依据。方法2001年10月至2005年7月，具有反流症状（烧心、反酸）的患者80例，胃镜检出RE31例，NERD45例，Barrett食管（BE）4例。行食管24hpH动态监测，并以De—Meester积分均值将GERD分为轻、中、重度，检测LES、食管体部即LES上方5cm、7cm、13cm（简记为L5、L7、L12）和食管上括约肌（UES）下方1cm、6cm、8cm（简记为U1、U6、U8）压力指标，并进行Hp感染的检查。结果RE、NERD两组患者食管24hpH酸暴露各指标的差异，无统计学意义（P〉0．05），De-Meester积分均值亦无统计学意义（P〉0．05）；轻、中、重度GERD患者食管24hpH监测指标具有统计学意义（P〈0．01）。RE、NERD两组患者LES压力、食管体部的L5、L7、L12、U6和u8压力监测指标无统计学意义（P〉0．05），只有RE组U1压力低于NERD组，差异有统计学意义（P〈0．05）；轻、中、重度GERD患者LES压力和食管体部的压力监测指标差异无统计学意义（P〉0．05）。RE和NERD组患者Hp感染率分别为16．1％和22．2％，其差异无统计学意义（P〉0．05），OR为1．309，95％C10．364～4．705。结论RE和NERD患者酸暴露、LES压力和食管体部压力等相应指标无明显差异；NERD在发病机制中，酸反流的强弱没有起到决定性作用。     

Evaluation of gastric emptying by electrogastrography and ultrasonography in gastroesophageal reflux disease

Background: It has been suggested that transient lower esophageal sphincter relaxation is involved in the occurrence of gastroesophageal reflux disease (GERD) and that decreased gastric emptying is an exacerbating factor of transient LES relaxation. In addition, the gastric emptying function is considered to be closely related to gastric motility. Methods: Gastric activity was evaluated by electrogastrography (EGG) in 22 patients with endoscopically positive reflux esophagitis (15 with mild esophagitis of Los Angeles grade A or B and seven with severe esophagitis of Los Angeles grade C or D) and 20 normal individuals. The gastric emptying function was also evaluated by abdominal ultrasonography. The sampling cycle of EGG was 1 s, and the measured frequency was 2.1–6.0 cycle/min (c.p.m.). The mean amplitude of EGG was compared by EGG spectral analysis among brady‐gastria cases with a contraction frequency of less than 2.4 c.p.m., normo‐gastria cases with a contraction frequency of 2.4–3.6 c.p.m., and tachy‐gastria cases with a contraction frequency exceeding 3.6 c.p.m. Results: In the patients with GERD, both the frequency of 3‐c.p.m. waves and peak frequency were reduced, and the gastric emptying function examined by ultrasonography had deteriorated, in comparison with normal individuals. Of those with GERD, the ultrasonographic gastric emptying function was significantly reduced in all patients with severe esophagitis compared with those with mild esophagitis, but the differences of the frequency of 3‐c.p.m. waves, the peak frequency, were not significant. Also, no significant difference was observed in the frequency of 3‐c.p.m. waves or the ultrasonographic gastric emptying function between the 16 patients with hiatal hernia and the six patients with no hiatal hernia. However, the mean amplitude in brady‐gastria and tachy‐gastria was significantly increased in the patients with hiatal hernia compared to those without hiatal hernia. Conclusions: Reduced gastric motility was suggested to be involved in the development of reflux esophagitis, and the presence of hiatal hernia was considered to have some effect on gastric motility.     

Gastrin, gastric emptying, and gastroesophageal reflux after ranitidine

In a double-blind study comparing ranitidine to placebo in the treatment of symptomatic gastroesophageal reflux disease (GERD), we assessed gastric emptying time, gastroesophageal reflux, and gastrin response to food. Mean half-time for gastric emptying, measured using 99mTc-sulfur colloid, was 109 minutes in GERD and 102 minutes in nine healthy asymptomatic controls. This difference was not significant, but one-third of GERD had emptying times of 2 S.D.s beyond the mean for the normal controls. The patients with GERD refluxed an average of 2.3% (0.1-10%) of the isotope in 120 minutes compared with only 0.2% (0.0-0.5%) in control subjects. Reflux scans and gastric emptying times did not change with healing of esophagitis or with symptomatic improvement from ranitidine and antacids. There was no relationship between the percentage of the test dose refluxed into the esophagus and the rate of gastric emptying. The mean fasting gastrin concentration in GERD, 133 +/- 12 pg/ml, was higher than in healthy controls, 93 +/- 10 pg/ml (p less than 0.01). After stimulation with a standard meal, the integrated gastrin response (IGR) was similar in controls and GERD patients, but IGR was significantly higher after 6 weeks therapy with ranitidine. These results suggest that: 1) gastric emptying time may be prolonged in some patients with GERD, 2) basal but not food-stimulated gastrin concentrations may be abnormal in GERD, 3) reflux scans have limited use in the investigation of GERD, and 4) ranitidine therapy is associated with an increase in food-stimulated gastrin concentrations.