The influence of cholecystectomy on the duodenogastric reflux of bile

The effect of cholecystectomy on postprandial duodenogastric bile reflux was studied by biliary excretion scintigraphy in a group of 20 patients examined before and after gallbladder removal. Dyspeptic complaints were correlated with the presence of postprandial duodenogastric reflux in 37 patients admitted to the hospital for cholecystectomy. The removal of the gallbladder, whether functional or not, in patients presenting with gallstones, did not seem to influence the occurrence of postprandial duodenogastric bile reflux. Dyspeptic complaints were positively correlated with postprandial gastric reflux. This reflux was observed in 90% of dyspeptic patients, while only 7% of the patients without dyspepsia had reflux. The role of duodenogastric reflux in the production of dyspeptic complaints is open to discussion, but the removal of the gallbladder does not seem to interfere with the occurrence of bile reflux into the stomach after a milk meal.     

十二指肠胃反流与胆囊切除术关系的临床研究

目的　通过对胆石症和胆囊切除术后出现胆汁反流性胃炎患者的血清胃动素 (MTL)和胆囊收缩素 (CCK)检测 ,探讨十二指肠胃反流 (DGR)的发生机制。方法　对确诊胆汁反流性胃炎的胆囊切除术后患者 (A组 ,30例 )和胆石症合并胆汁反流性胃炎患者 (B组 ,2 2例 ) ,以及对照组 (C组 ,2 0例 )即胃镜无胆汁反流现象 ,病理示慢性浅表性胃炎患者 ,分别抽血测空腹血清MTL和CCK含量。结果　A组血清CCK为 5 86pg/mL± 2 .78pg/mL ,较C组 3 80pg/mL± 1.10pg/mL有显著性升高 ,A组血清MTL为310 31pg/mL± 118 2 1pg/mL ,较C组 32 6 0 0pg/mL± 5 8 0 0pg/mL的降低无显著性差异 ,B组与C组相比CCK变化无显著性差异 ,MTL较C组有显著性降低 ,值为 2 2 8 30pg/mL± 72 2 0pg/mL。结论　DGR是胆道疾患的多见病理现象。胃运动功能障碍和幽门括约肌功能不全是病理性DGR的一个重要原因 ,胃十二指肠收缩不协调可导致DGR发生。MTL和CCK对胃排空和十二指肠运动起重要调节作用 ,胆囊切除术后和胆石症患者发生病理性DGR时存在CCK和MTL分泌不协调 ,调节紊乱的现象     

Gallstones, cholecystectomy, and duodenogastric reflux of bile acid

It has earlier been suggested that cholecystectomy, by eliminating the reservoir function of the gallbladder, will induce reflux of bile to the stomach. In the present study 23 patients were studied for duodenogastric reflux of bile acid before and 3 months after cholecystectomy. At the test the gastric contents were continuously aspirated via a nasogastric tube, collected at 15-min intervals for 2 h in the fasting patient, and analyzed for volume and bile acid concentration. The results were compared with those in 14 control subjects. Significant duodenogastric reflux of bile acid (greater than 100 mumol/h) was seen more frequently in gallstone patients than in controls. This is explained by a high prevalence of bile acid reflux in patients with a reduced or absent opacification of the gallbladder at cholecystography. Cholecystectomy increased the prevalence of bile acid reflux in the patients with well-opacified gallbladders at cholecystography. The duodenogastric reflux of bile acid in patients with a poor filling of the gallbladder at cholecystography was not further enhanced by cholecystectomy. It is concluded that gallstone patients have an increased tendency to duodenogastric reflux of bile acid. This tendency is further enhanced by removal of a functioning gallbladder. The findings may explain some of the symptoms in patients with gallstones. The reflux may also be responsible for symptoms in the so-called postcholecystectomy syndrome.     

Barrett's esophagus, gastroesophageal acid reflux and duodenogastric reflux during the digestive and postprandial period]

Pathologic gastroesophageal acid reflux appears to be involved in the pathogenicity of Barrett's esophagus. The possible pathogenic role of duodenogastric reflux, however, has been suggested by several studies. The aim of this prospective study was to assess the prevalence of acid or duodenogastric reflux in patients with Barrett's esophagus. Nine patients with histologically proven Barrett's esophagus (mean length: 7.7cm; range: 2-13 cm) were studied by esophageal manometry and 24 hour pHmetry. Duodenogastric reflux was measured in the interdigestive period by aspiration and during the postprandial period using an isotopic method. The results of these different investigations were compared with healthy volunteers (n = 20 to 27). Three patients had complicated Barrett's esophagus (Barrett's ulcer: n = 2, high-grade dysplasia: n = 1). The results of the different investigations showed that a) all patients had abnormal acid exposure and an esophageal motor dysfunction (decrease in lower esophageal sphincter pressure, amplitude and duration of contractions and increase in percentage of peristaltic dysfunction); b) none of the patients had any pathologic duodenogastric reflux neither in the interdigestive nor in the postprandial period. These results a) confirm the high prevalence of acid reflux in patients with Barrett's esophagus, b) show that bile or pancreatic secretions are not involved in the pathogenicity of Barrett's esophagus.     

Effect of cimetidine on gastric secretion and duodenogastric reflux.

In 19 subjects (four controls, one gastric ulcer and 14 duodenal ulcer) maximal gastric secretion was evoked with histamine 0.13 mumol/kg/h (0.04 mg/kg/h) for two to two and a half hours. A slow intravenous bolus dose of 200 mg cimetidine was given at the beginning of the last hour. Gastric secretion was measured before and after cimetidine administration and expressed both as mean acid output (mmol H+/h) and 'pyloric loss and duodenogastric reflux corrected' volume (Vg, ml/h). Mean reduction by acid output was 86%; mean reduction by corrected volume (Vg) was only 64%. The discrepancy, which is significant (p less than 0.01), is caused by a marked increase in duodenogastric reflux after cimetidine.     

Effect of bethanechol on gastroesophageal reflux

In this study we determined the acute effect of bethanechol (5 mg SC) on gastroesophageal reflux (GER) and lower esophageal sphincter pressure (LESP) in 27 patients with symptomatic esophagitis. The effect of bethanechol on esophageal acid clearance was also determined in 7 of the patients. Intraluminal pH monitoring prior to bethanechol administration demonstrated free or stress-induced reflux episodes in 18 of the 27 patients. Following bethanechol (1) LESP increased significantly, (2) GER diminished or ceased in many of the patients, and (3) acid clearance times decreased significantly. Some individuals, however, continued to reflux despite LESP elevation to 30 mm Hg or more. This latter finding suggests that LESP alone is not the sole factor governing LES competency. Other factors such as improved esophageal emptying may also contribute to the beneficial therapeutic effect of bethanechol in patients with heartburn.This work was supported in part by a grant (PR-58) from the Clinical Research Centers Program of the Division of Research Resources, NIH, and by USPHS Research Grant No. RO1 AM 15540-03.Abstracted in part in Clinical Research 22605, 1974 and presented in part at the American Federation for Clinical Research, Midwest Section, Chicago, Illinois, October 31, 1974.     

脂肪对胃食管酸反流的影响和体重指数与胃食管酸反流的关系

目的评估饮食脂肪对胃食管酸反流的影响和体重指数（BMI）与胃食管酸反流的关系。方法选择23例健康志愿者和22例胃食管反流病（GERD）患者,记录受试者基本情况,先行食管测压,先后两次服用低脂餐和高脂餐,每次监测餐后6h食管pH值。结果健康志愿者和GERD患者在两种热量相等的低脂餐和高脂餐后,pH〈4总反流时间百分率,反流时间〉5min的反流次数及总反流次数的比较,均无显著性差异（P〉0．05）;BMI≥25受试者的pH〈4总反流时间百分率和反流时间〉5min的反流次数高于BMI〈25受试者,两者有显著性差异（P〈0．01）。结论在同热量含量下,食物中脂肪含量对健康志愿者和GERD患者餐后6h酸反流无影响;而肥胖可能会增加胃食管酸反流。     

A prospective study on duodenogastric reflux and on histological changes in gastric mucosa after cholecystectomy.

The authors carried out a prospective study to evaluate variations with time in postcholecystectomy duodenogastric reflux (expressed as "fasting bile reflux" in mumol/h) and in gastric mucosal damage. Ten patients underwent (before cholecystectomy, 6 months after surgery and after a median period of 4 years from surgery) a gastric drainage to assess total (enzymatic method) and single (high performance liquid chromatography) intragastric bile acids, and a gastroscopy with biopsies of the antrum and gastric body to assess histological damage to the mucosa. The results showed that there was a progressive increase in the fasting bile reflux of total bile acids with time (precholecystectomy median value 0.295 mumol/h; 6 months control median value 12.045 mumol/h; late control medial value 19.9 mumol/h; Friedman test, P = 0.0022). Examination of the gastric mucosa at the three moments of the study showed that histological damage worsened progressively. In fact chronic atrophic gastritis of the antrum was present in 10 percent of cases before surgery and in 50 percent 4 years after, and the prevalence of chronic superficial gastritis of the body progressed from 0 to 40 percent. Studies on larger groups of patients are necessary to evaluate whether these two phenomena are correlated.     

Effect of omeprazole on antral duodenogastric reflux in Barrett oesophagus

BACKGROUND: The effect of long-term acid suppression therapy in Barrett oesophagus remains unknown, but the high intragastric pH generated has been shown to increase the cytotoxicity of duodenal refluxate on foregut mucosa. However, recent work suggests that duodenogastric reflux (DGR) may be reduced by omeprazole. AIM: To investigate the effect of omeprazole on the reflux of duodenal contents into the gastric antrum in Barrett patients and healthy subjects. METHOD: Fifteen patients with Barrett oesophagus and 14 healthy subjects underwent oesophageal manometry followed by 24-h ambulatory oesophageal and gastric pH and gastric bilirubin monitoring. The bilirubin sensor (modified by the addition of a weighted tip to facilitate manoeuvrability) was sited in the gastric antrum under fluoroscopic control. Combined ambulatory pH and bilirubin monitoring was repeated after 2 weeks on omeprazole 20 mg b.d. RESULTS: Changes in oesophageal acid reflux and gastric alkaline shift due to omeprazole were as expected (P < 0.001). There was no difference in total antral DGR between the Barrett and control groups (P = 0.56), and omeprazole had no significant effect on DGR in either group (P = 0.77 and 0.27, respectively). CONCLUSIONS: DGR into the antrum is of a similar level in Barrett patients and healthy controls. Omeprazole does not reduce the reflux of duodenal contents across the pylorus. Further work is required on the increased cytotoxic potential of continuing DGR in those on long-term acid suppression.     

Ulcer disease and duodenogastric reflux

The intragastric concentrations of lysolecithin and bile acids were determined in 44 chronic peptic ulcer patients and 35 healthy volunteers. Normal reflux values were found in the prepyloric ulcer (Johnson type III) (n = 15) Elevated reflux amounts could be observed in the type I gastric ulcer (n = 15), there was a three-to fourfold increase compared to the controls. - Slightly elevated reflux concentrations were found in the duodenal ulcer patients (n = 14), but only under fasting conditions. The increase of reflux concentration in chronic gastric ulcer type I is shown to be in the same range as in acute stress ulcer. Compared to the three-to four times higher reflux concentrations of the resected stomach, the duodenogastric reflux in ulcer disease is very moderate. It's role in ulcerogenesis has to be analyzed further.     

Nonsteroidal antiinflammatory drugs: Effect on pyloric sphincter and duodenogastric reflux

We have investigated the effect of nonsteroidal antiinflammatory drugs on canine pyloric sphincter pressure, mucosal potential difference (PD), and duodenogastric reflux in 5 dogs. Only intragastric aspirin at doses of 30 and 100 mg/kg caused a significant (P<0.05) decrease in pyloric sphincter pressure, an increase of duodenogastric reflux, and changed the mucosal PD. Neither intravenous aspirin, intragastric phenylbutazone, or intrarectal indomethacin produced these changes. The mechanism for the aspirin effect may be mediated by local pathways related to changes in mucosal PD. We postulate that increased duodenogastric reflux may be an aggravating factor for the gastric mucosal damage caused by intragastric aspirin.     

Effect of gastroesophageal reflux on esophageal speech

Gastroesophageal reflux has been incriminated as a factor-inhibiting acquisition of esophageal speech after laryngectomy. Fourteen proficient esophageal speakers and 10 nonproficient speakers underwent esophageal manometry, esophageal pH probe testing, and Bernstein acid perfusion testing. Additionally, 175 laryngectomized members of Lost Chord Clubs answered mailed questionnaires about the frequency of reflux symptoms. Nonproficient and proficient esophageal speakers had a similar frequency of gastroesophageal reflux by pH probe testing, esophageal mucosal acid sensitivity by Bernstein testing, lower esophageal sphincter pressures, and gastroesophageal reflux symptoms. Gastroesophageal reflux does not appear to be a major factor in preventing esophageal speech.     

Effect of hyoscine N-butylbromide on gastroesophageal reflux in normal subjects and patients with gastroesophageal reflux disease

OBJECTIVES: Recent studies have shown that atropine reduces gastroesophageal reflux in normal subjects and patients with gastroesophageal reflux. The aim of the study has been to assess the effects of an atropine derivative, hyoscine N-butylbromide in normal subjects and patients with gastroesophageal reflux disease by recording esophageal and gastric pH-metry for a 24-h period. METHODS: Ten normal subjects and 10 patients with gastroesophageal reflux disease were evaluated. PH-metry was performed using two glass pH flexible probes with distal incorporated electrodes. The two catheters were introduced nasally under fluoroscopy. One probe was positioned in the gastric body; the other was placed 5 cm above the lower esophageal sphincter which had been evaluated manometrically before the study. Recording lasted without interruption for 48 h. Patients and normal subjects were assigned to receive hyoscine N-butylbromide (10 mg p.o. t.i.d.) for 24 h followed by a placebo for another 24 h or vice versa in a random manner. The pH was analyzed for a total number of acid refluxes and percentage of the period with pH <4 in the esophagus and the mean gastric pH in 24 h, before and after treatment with hyoscine N-butylbromide. RESULTS: The number of reflux episodes was significantly greater with hyoscine N-butylbromide in comparison with a placebo in patients with gastroesophageal reflux disease and normal subjects (p < 0.02). The percentage of time with pH <4, was also significantly greater in patients with gastroesophageal reflux disease and in controls (p < 0.05). The mean 24-h gastric pH after hyoscine N-butylbromide was not different from placebo in gastroesophageal reflux disease and controls. CONCLUSIONS: Hyoscine N-butylbromide, an anticholinergic agent, increases the total number of esophageal acid refluxes in patients with gastroesophageal reflux disease and in controls, therefore it is not recommended in the treatment of gastroesophageal reflux disease.     

Effect of intragastric volume and osmolality on mechanisms of gastroesophageal reflux in children with gastroesophageal reflux disease

OBJECTIVE: Both transient lower esophageal sphincter (LES) relaxations (TLESRs) and periods of low/absent LES pressure (LESP) are the main mechanisms of gastroesophageal reflux. These events are believed to be triggered by stimuli from different areas of the upper GI tract. We aimed at investigating the relationship between LESP profile and gastric emptying and distension after meals of different composition in 30 children with gastroesophageal reflux disease (median age 7.0 yr, range 12 months-12 yr). METHODS: Recordings of LESP and intraesophageal pH for 1 h fasting and for 2 postprandial h were performed with a perfused sleeve catheter and flexible electrode, respectively; gastric emptying and distension of antral area were simultaneously recorded with real-time ultrasonography. Ten patients had a standard meal (group A), 10 had a high-volume meal (group B), and 10 had a high-volume and osmolality meal (group C). RESULTS: Postprandial esophageal acid exposure was significantly higher in patients of groups B and C than in patients of group A (p < 0.01); it was also more prolonged in patients of group C than in subjects of group B (p < 0.05). A higher postfeeding rate of reflux episodes caused by TLESRs was detected in patients of groups B and C as compared with patients of group A (p < 0.01). This increase did not statistically differ in patients of groups B and C. Patients of group C exhibited a higher postprandial rate of reflux episodes associated with low/absent tone of the LES as well as a more prolonged gastric emptying time and a higher postfeeding gastric distension as compared with patients of groups A and B (p < 0.01). Finally, a significant correlation was only found between the postprandial rate of reflux events resulting from low/absent LESP and the degree of antral distension in patients of group C (p < 0.01). CONCLUSION: Gastroesophageal reflux is worsened by increasing the volume and osmolality of meals through significant changes of LESP. Meals of high volume and meals with high volume and osmolality cause a comparable increase of reflux episodes as a result of TLESRs. However, meals with high volume and osmolality cause the higher degrees of esophageal acid exposure than meals with high volume resulting from a higher rate of reflux episodes associated with low/absent LESP. This finding correlates with a high postfeeding antral distension.     

Dissociation of duodenogastric marker reflux and bile salt reflux

Duodenogastric reflux of a perfused marker and bile salt reflux, as well as emptying of fasting gastric contents and gastric secretion, were measured simultaneously in six healthy volunteers. Each of the subjects was studied three times in randomized order during intravenous administration of either saline or atropine (40 micrograms/kg/4 hr) or cerulein (360 ng/kg/4 hr). Fractional gastric emptying rate was inhibited from 4.57%/min +/- 0.50 SE to 0.70 +/- 0.15 by atropine (P less than 0.001) and to 1.80 +/- 0.29 by cerulein (P less than 0.005). Atropine increased reflux of duodenally perfused phenol red from 0.95 +/- 0.28 to 26.09 +/- 4.98% (P less than 0.005) without affecting bile salt reflux (0.44 +/- 0.07 vs 0.51 +/- 0.17 mumol/min). In contrast, cerulein did not significantly affect duodenogastric marker reflux (2.23 +/- 0.82%) but increased bile salt reflux to 0.94 +/- 0.16 mumol/min (P less than 0.05). It is concluded that reflux of duodenal contents and reflux of bile salts do not necessarily parallel each other. This may produce considerable confusion by apparently contradictory results in studies on duodenogastric reflux.     

Effect of sucralfate on gastroesophageal reflux in esophagitis

Gastroesophageal reflux was assessed in 18 patients with endoscopically and histologically verified esophagitis, and 15 asymptomatic normal subjects, by a portable receiving system. The qualitative evaluation of the frequency of reflux episodes, normalized mean pH, normalized mean [H+] and the acid clearance rate is found to be indicative of gastroesophageal reflux. Twelve weeks of treatment with sucralfate in an open clinical trial resulted in a significant reduction of gastroesophageal reflux and the elimination of esophageal mucosal damage. Barrett++'s epithelium was found in a rather high proportion and proved to be resistant to treatment. It is suggested that the observed improvement is due to the barrier protecting properties of sucralfate restoring the motor function of the distal esophagus.