Gastric and esophageal acidity during continuous treatment with H2-antagonists in uncomplicated esophagitis

Twenty-four-hour gastric and esophageal pH were monitored simultaneously in 19 patients with moderate esophagitis before and after a randomized crossover treatment with 40 mg famotidine or 300 mg ranitidine. Gastroesophageal reflux in patients with esophagitis was compared with that in 22 healthy controls. Patients with esophagitis had more esophageal acidity than controls; the percentage of time with esophageal pH less than 4 was significantly greater during a 24-h period (p less than 0.01) both in the upright (p less than 0.01) and in the supine (p less than 0.01) position. In esophagitis patients the percentage of time with pH less than 4 during the total 24-h period correlated closely with acid reflux in the upright (p less than 0.001) and supine (p less than 0.01) position. This indicates that daytime reflux is probably as injurious to the esophagus as nighttime reflux. Famotidine and ranitidine decreased gastric acidity during the entire 24-h period (p less than 0.001) but not during the daytime or early evening. The inhibitory effect lasted slightly longer with famotidine (12 h) than with ranitidine (10 h). Famotidine and ranitidine reduced esophageal acidity during the entire 24-h period (p less than 0.001) and particularly during the nighttime (p less than 0.001) but not during the daytime. Famotidine and ranitidine also did not modify the esophageal acid clearance. Nightly doses of famotidine or ranitidine were ineffective in reducing GER during daytime hours.     

Effect of Omeprazole on Gastroesophageal Reflux in Barrett''s Esophagus

Pattern of gastric and esophageal acidity were evaluated in 14 patients with endoscopically and histologically proven Barrett's esophagus, in 46 with slight-to-moderate esophagitis, and in 22 healthy subjects. In patients with Barrett's esophagus, LES pressure was considerably lower and percentage exposure to acid was considerably higher than in either patients with esophagitis or controls (p less than 0.001). Percentage of time with esophageal pH below 4 was 33.2% in patients with Barrett's esophagus, 14% in patients with slight-to-moderate esophagitis (p less than 0.001), and 3.4% in controls (p less than 0.001). In patients with Barrett's esophagus, the esophageal exposure to acid was similar in upright and supine positions, and the number of refluxes that lasted longer than 5 min was also greater in these patients than in uncomplicated esophagitis or controls (p less than 0.001). Accordingly, their acid-clearing capacity was markedly reduced (p less than 0.001 vs. control). Omeprazole 20 mg, given once daily, reduced both percentage of time with pH below 4 (p less than 0.001) and the number of episodes longer than 5 min (p less than 0.001), but had no effect on acid clearance. In patients with Barrett's esophagus, omeprazole lowered intragastric acidity by 77.8% (p less than 0.001). Median intragastric pH was 1.9 (1.7-2.1) pretreatment, and 4.5 (4.2-5) during omeprazole (p less than 0.001).     

24-hour intragastric acidity and plasma gastrin during long-term treatment with omeprazole or ranitidine in patients with reflux esophagitis

The reduction in intragastric acidity and the subsequent increase in plasma gastrin were compared during long-term treatment with either omeprazole or ranitidine in 19 patients with erosive reflux esophagitis. The patients received 40 mg omeprazole in the morning or 300 mg ranitidine twice daily. After healing, half the dose was given as maintenance treatment for 1 year. Intragastric acidity and plasma gastrin were measured 24 h before entry and monthly with the high dose and after 1, 6, and 12 months with the low dose. Omeprazole reduced intragastric acidity more effectively than ranitidine (p less than 0.001). This difference in efficacy was more pronounced during the daytime. Plasma gastrin increased more after omeprazole than after ranitidine (p less than 0.01), and both drugs showed a normal postprandial response and approached fasting levels before the next dose. During long-term treatment with 20 mg omeprazole in the morning no progressive alterations were observed in 24-h intragastric acidity or plasma gastrin.     

Ambulatory Esophageal pH Recording in Gastroesophageal Reflux: Relevance to the Development of Esophagitis

In a group of 60 patients with symptomatic gastroesophageal reflux (GER), we carried out upper gastrointestinal (GI) endoscopy and 24-h ambulatory esophageal pH monitoring to assess the relationship between acid reflux and esophagitis. The results of 24-h pH measurement were compared with those of 15 asymptomatic control subjects who were studied with ambulatory 24-h esophageal pH monitoring only. Thirty-two patients (53.3%) had a normal esophagus macroscopically, and 28 patients (46.7%) had some degree of esophagitis. There was no significant difference between the two groups with and without esophagitis, regarding male:female ratio, age, and duration of symptoms. The group with esophagitis was more symptomatic (p less than 0.001) than the group without, and differed significantly in relation to all pH variables, i.e., number of GER episodes per hour, duration of mucosal exposure to acid (pH less than 4), and number of GER episodes requiring more than 5 min to clear per hour for the upright, supine, and 24-h periods, compared with the control group (p less than 0.001) and the group without esophagitis (p less than 0.001). In the group with esophagitis, comparison of the above pH variables in the upright and supine periods showed significantly higher values in the upright than in the supine period for the total number of reflux episodes per hour (p less than 0.001) and the number of episodes greater than 5 min/h (p less than 0.05). We conclude that the presence of esophagitis is related to both frequency and duration of GER episodes. Our findings also stress the importance of daytime acid exposure in the pathogenesis of esophagitis.     

The effect of omeprazole or ranitidine treatment on 24-hour esophageal acidity in patients with reflux esophagitis

Twenty-two consecutive patients with gastroesophageal reflux and erosive or ulcerative esophagitis entered a double-blind, randomized study comparing the effect of 20 mg omeprazole once daily with that of 150 mg ranitidine twice daily on esophageal acidity. Ambulatory 24-h esophageal pH measurements were performed within 1 month before inclusion and after 3 weeks of medication. Omeprazole significantly (p less than 0.05) reduced the number of reflux (pH less than 4) episodes, the number of refluxes lasting greater than 5 min, and the total reflux time. In contrast, ranitidine significantly reduced only the total reflux time. When the two treatment groups were compared, a significant difference in favor of omeprazole was found for daytime and total reflux values, except for the longest reflux and the number of reflux episodes lasting greater than 5 min. Substantial differences, also in favor of omeprazole, were found with regard to the effect on endoscopic healing of the esophagitis.     

24-Hour Intragastric Acidity and Plasma Gastrin during Long-Term Treatment with Omeprazole or Ranitidine in Patients with Reflux Esophagitis

The reduction in intragastric acidity and the subsequent increase in plasma gastrin were compared during long-term treatment with either omeprazole or ranitidine in 19 patients with erosive reflux esophagitis. The patients received 40 mg omeprazole in the morning or 300 mg ranitidine twice daily. After healing, half the dose was given as maintenance treatment for 1 year. Intragastric acidity and plasma gastrin were measured 24 h before entry and monthly with the high dose and after 1, 6, and 12 months with the low dose. Omeprazole reduced intragastric acidity more effectively than ranitidine (p < 0.001). This difference in efficacy was more pronounced during the daytime. Plasma gastrin increased more after omeprazole than after ranitidine (p < 0.01), and both drugs showed a normal postprandial response and approached fasting levels before the next dose. During long-term treatment with 20 mg omeprazole in the morning no progressive alterations were observed in 24-h intragastric acidity or plasma gastrin.     

Comparison of omeprazole and ranitidine in treatment of refractory gastroesophageal reflux disease in patients with gastric acid hypersecretion

Secretion of gastric acid and volume, serum gastrin concentration, and ambulatory 24-hr esophageal pH monitoring were evaluated prospectively in 12 patients with idiopathic gastric acid hypersecretion (basal acid output greater than 10.0 meq/hr) undergoing treatment for refractory chronic long-standing pyrosis. Treatment lasted six months and consisted of three months of ranitidine (mean 2150 mg/day, range 1200–3000 mg/day), followed by three months of omeprazole (mean 33 mg/day, range 20–60 mg/day). Both ranitidine and omeprazole significantly reduced gastric acid output (P<0.001) and gastric volume output (P<0.001) compared to a basal evaluation and resulted in complete disappearance of pyrosis. Total reflux time (percent 24 hr intraesophageal pH less than 4) was significantly reduced by ranitidine (P<0.02) and omeprazole (P<0.001) compared to basal evaluation; however, the effects of omeprazole were significantly greater than ranitidine (P<0.05). Omeprazole caused a significant increase in serum gastrin concentration compared to both basal and ranitidine (P<0.05). Endoscopically documented erosive esophagitis was present in nine of the 12 patients, and seven of the 12 patients had Barrett's epithelium. All 12 patients had complete resolution of pyrosis and healed esophagitis by six months, but no significant endoscopic regression was observed in the extent of Barrett's epithelium. No side effects occurred with these high doses of ranitidine or omeprazole. These results indicate that high-dose ranitidine and omeprazole are effective therapy for refractory gastroesophageal reflux disease. However, with omeprazole, total reflux times are reduced more than with ranitidine, often into the normal range. That marked reduction of gastric acid secretion with omeprazole, which greatly reduces total reflux times, accounts for the significant elevation of serum gastrin concentration seen during omeprazole therapy.     

Gastric acid hypersecretion in refractory gastroesophageal reflux disease

We prospectively evaluated gastric acid output (mEq/h), gastric volume output (ml/h), ambulatory 24-h esophageal pH monitoring, and the endoscopic appearance of the esophagus in 23 patients undergoing treatment of chronic long-standing pyrosis. Twelve of these 23 individuals (52%) remained symptomatic after 3 mo of standard antisecretory treatment with ranitidine, 150 mg twice daily. When compared with initial responders, those patients who did not experience complete symptomatic relief on therapy had significantly higher basal acid output (p less than 0.001), basal volume output (p less than 0.02), and basal upright (but not supine) reflux time (p less than 0.05). Nine of the 12 patients who did not respond to initial treatment had gastric acid hypersecretion (basal acid output greater than 10 mEq/h), and 10 of the 12 had Barrett's epithelium compared with only 1 patient in the initial-responder group (p less than 0.001). All 12 nonresponders were treated for an additional 3 mo with increased doses of ranitidine (mean, 1280 mg/day; range, 600-1800 mg/day), and complete disappearance of pyrosis occurred in 10 of the 12, although no significant endoscopic regression was observed in the extent of the underlying columnar mucosa in those with Barrett's esophagus over the 6-mo duration of the study. A significant correlation was shown between the daily ranitidine dose required to eliminate symptoms and the pretreatment basal acid output (r = 0.81, p less than 0.001); gastric acid output had to be almost totally suppressed (i.e., less than 1 mEq/h) for pyrosis to disappear completely. No side effects occurred with any of these high doses of ranitidine. We conclude that a subgroup of patients with long-standing symptomatic gastroesophageal reflux disease who do not respond to standard ulcer-healing doses of histamine2-receptor antagonists are hypersecretors of basal gastric acid and require increased acid-suppressive therapy. Many of these individuals also have underlying Barrett's epithelium.     

Stability of gastric secretory inhibition during 6-month treatment with omeprazole in patients with gastroesophageal reflux disease

OBJECTIVE: A trend toward relapse of reflux symptoms and esophagitis during long-term treatment with proton pump inhibitors has been reported. The purpose of this study was to evaluate the existence of tachyphylaxia to the effect of proton pump inhibitors on gastric acidity and gastroesophageal reflux over time. METHODS: A total of 23 patients with reflux esophagitis underwent 24-h intragastric and intraesophageal pH-metry after 7, 90, and 180 days of continued dosing with 20 mg of omeprazole once daily before breakfast. RESULTS: The total median percentages of time gastric pH <4 (interquartile range) were 49% (35-70%), 60% (36-76%), and 42% (26-66%) after 7, 90, and 180 days (p = 0.14). Percentages of time gastric pH <3 were 41%, 54%, and 34%, respectively (p = 0.19). The median percentages of total time esophageal pH <4 were 1.1%, 2.5%, and 1.1%, respectively (p = 0.70). Healing of esophagitis was achieved in 84% of the patients after 6 months. Heartburn improved in six, worsened in three, and was unchanged in 10 patients (p = 0.16). There was no statistical significant relationship between change in esophageal acid exposure and change in severity of heartburn. CONCLUSIONS: A dose of 20 mg of omeprazole once daily consistently controlled patients' symptoms and kept gastric acidity at a stable level over a period of 6 months. There is no evidence of diminution in the effects of 20 mg of omeprazole over time that could indicate the development of tolerance.     

Control of Nocturnal Gastric Acidity: A Role for Low Dose Bedtime Ranitidine to Supplement Daily Omeprazole

In some patients, proton pump inhibitors do not abolish nocturnal gastric acidity and additional evening antisecretory medication may be required. In 16 subjects with chronic heartburn, 24-hr gastric and esophageal pH were measured at baseline and again after six days of 20 mg omeprazole alone at 08:00 hr followed by placebo, 75 mg ranitidine, or 20 mg omeprazole at 22:00 hr. Integrated acidity was calculated from the cumulative, time-weighted mean acid concentrations (derived from pH values for each second). Baseline integrated gastric acidity increased progressively over 24 hr, whereas integrated esophageal acidity increased only until 22:00 hr. Morning omeprazole nearly abolished 24-hr esophageal acidity and significantly decreased overall gastric acidity but did not abolish nocturnal gastric acidity. Adding evening ranitidine or omeprazole nearly eliminated the nocturnal increase in gastric acidity. Integrated acidity was more sensitive than time pH < 4 in assessing gastric and esophageal acidity as well as their inhibition by omeprazole and ranitidine. In conclusion, integrated acidity provides novel information regarding the synergy of omeprazole plus ranitidine. Adding low-dose ranitidine helps control nocturnal gastric acidity that can occur with conventional omeprazole administration. Although the heartburn patients in the present study had nocturnal gastric acidity without accompanying nocturnal esophageal acid reflux, other patients who do have nocturnal esophageal reflux might profit from addition of bedtime ranitidine or another gastric antisecretory agent.     

Letter to the Editor: Triticum moncoccum and celiac disease

Twenty-two consecutive patients with gastroesophageal reflux and erosive or ulcerative esophagitis entered a double-blind, randomized study comparing the effect of 20 mg omeprazole once daily with that of 150 mg ranitidine twice daily on esophageal acidity. Ambulatory 24-h esophageal pH measurements were performed within 1 month before inclusion and after 3 weeks of medication. Omeprazole significantly (p < 0.05) reduced the number of reflux (pH < 4) episodes, the number of refluxes lasting >5 min, and the total reflux time. In contrast, ranitidine significantly reduced only the total reflux time. When the two treatment groups were compared, a significant difference in favor of omeprazole was found for daytime and total reflux values, except for the longest reflux and the number of reflux episodes lasting >5 min. Substantial differences, also in favor of omeprazole, were found with regard to the effect on endoscopic healing of the esophagitis.     

Omeprazole or ranitidine in the treatment of reflux esophagitis. Results of a double-blind, randomized, Scandinavian multicenter study

One hundred and fifty-two patients with endoscopically verified erosive and/or ulcerative esophagitis entered a double-blind, randomized study comparing 20 mg omeprazole given once daily and ranitidine 150 mg twice daily. The efficacy and safety of 4 to 8 weeks' treatment were studied. Macroscopic healing of esophagitis was defined as complete epithelialization of all esophageal erosive and/or ulcerative lesions. One hundred and forty-four patients completed the first 4 weeks of treatment in accordance with the protocol. The healing rate was 67% in the omeprazole group and 31% in the ranitidine group (p less than 0.0001). The corresponding figures after 8 weeks' treatment were 85% and 50%, respectively (p less than 0.0001). The higher healing rate for omeprazole was also accompanied by a significantly faster and more substantial improvement in reflux symptoms. In the patient's own overall evaluation of symptoms, these had resolved in 51% of the omeprazole-treated patients already at the end of the 1st week of treatment, compared with 27% of those given ranitidine (p = 0.009). Both omeprazole and ranitidine were well tolerated, and there were no adverse events or clinically significant changes in the laboratory values attributable to the trial medication.     

Nocturnal acid breakthrough: clinical significance and correlation with esophageal acid exposure

OBJECTIVES: Previous studies suggest that the addition of H2 receptor antagonist (H2RA) therapy is more effective than proton pump inhibitor (PPI) therapy alone in reducing nocturnal acid breakthrough (NAB). However, the clinical significance of NAB with respect to esophageal acid control has not been investigated. The aim of this study was to evaluate prospectively the degree of upright and supine esophageal and gastric acid suppression using various PPI regimens in comparison to the addition of an H2RA at bedtime. METHODS: A total of 22 subjects (13 with gastroesophageal reflux disease and nine who served as control subjects) were prospectively evaluated by serial combined esophageal and gastric 24-h pH monitoring. Studies were performed at baseline off antireflux medical therapy and subsequent to completion of the following four drug regimens: 1) omeprazole 20 mg b.i.d. for 2 wk; 2) omeprazole 20 mg b.i.d. plus ranitidine 300 mg HS for 4 wk; 3) omeprazole 20 mg QAM and QHS for 2 wk; and 4) omeprazole 20 mg every 8 h for 2 wk. A dual pH probe was placed 5 cm above and 10 cm below the manometrically defined LES for a minimum of 18 h. Median total, upright, and supine pH values were compared among treatment regimens. All subjects underwent Helicobacter pylori serology testing. RESULTS: A total of 17 men and eight women (mean age 37 yr +/- 2.4 yr, range 22-71 yr) were enrolled in the study. Total, upright, and supine median percentage of the time that gastric pH was <4 were significantly less than baseline values in all treatment regimens. Although patients treated with Q8 h omeprazole had significantly (p < 0.01) more gastric acid suppression, there was a high degree of overlap among regimens. Treatment regimens resulted in NAB elimination of 9-41%. However, no single treatment regimen resulted in more significant NAB suppression than the others. Despite continued NAB with all treatment regimens, esophageal acid reflux (90%) and patient symptoms (100%) were well controlled. In addition, there were no differences in the esophageal median percentage of time that pH was <4 for any treatment regimen. CONCLUSIONS: NAB is an isolated gastric phenomenon that is poorly controlled even with most aggressive acid suppressive therapy. Esophageal acid suppression and symptom control are not dependent on the degree of NAB elimination.     

Circadian Variations in Gastric Acid and Pepsin Secretion and Intragastric Bile Acid in Patients with Reflux Esophagitis and in Healthy Controls

Objectives : Duodenogastric reflux is a physiological phenomenon in both fasting and postprandial state. Because this suggests that bile acids may reflux into the esophagus together with the acid in patients with reflux esophagitis, we investigated the circadian variations of acid and pepsin secretion and intragastric bile acid concentrations in 25 patients with reflux esophagitis and in 15 healthy controls. Methods : Between-meal, nocturnal gastric and meal-stimulated acid and pepsin secretion and bile acid concentrations were measured by continuous gastric aspiration and intragastric titration. Results : Bile acids were found in 85 and 59% of gastric samples ( p < 0.05). Intragastric bile acid concentrations were 6–8-fold higher in esophagitis patients than controls during the day. Approximately 10% of gastric samples from reflux esophagitis patients had a pH greater than 7, and all contained more than 500 μmol/L bile acids. Bile acids and pepsin were simultaneously revealed in 98% of the gastric samples from patients with reflux esophagitis with pH less than 4. Mean daily acid output (meal excluded) averaged 3.5 ± 0.1 in healthy subjects and 2.7 ± 0.2 mmol/30 minutes in esophagitis patients ( p < 0.05); meal-induced acid secretions were similar. Total (24-h) acid secretion averaged 192.3 ± 12.4 and 162.4 ± 10.5 mmol/24 h ( p < 0.05). There were no differences in the daily pepsin output. Conclusions : Our data indicate that almost all "acid" gastroesophageal refluxes should be considered as "mixed" refluxes. Because bile acids are found in the stomach irrespective of whether the environment was acid or alkaline, pH-metry provides no useful information on the pattern of duodenogastric reflux into the esophagus. Variability in the composition of the gastroesophageal refluxate may explain why the severity of esophageal lesions differs in patients with similar pattern of acid refluxes.     

Regional esophageal distribution and clearance of refluxed gastric acid

Regional differences in the esophageal distribution and clearance of refluxed gastric acid was studied in seven asymptomatic volunteers and seven patients with reflux esophagitis. Intraluminal pH was recorded for 3 postprandial hours from the distal, middle, and proximal esophagus on two separate occasions (with subjects in upright and supine positions). With the subjects in a supine position, about half of the acid reflux episodes reached the proximal esophagus in patients as well as in controls. This percentage decreased to 25% in patients and 29% in controls when they were upright. In both groups, the pH drops in the distal esophagus were significantly greater than in the proximal esophagus for both the supine and upright positions. In both patients and controls, a 4-5-fold greater acid exposure occurred in the distal esophagus, than in the proximal esophagus. In both patient and control groups, acid exposure time, as well as the number of reflux episodes in the distal esophagus, were significantly greater than that of the proximal esophagus (P less than 0.05). Spontaneous acid clearance time in the distal esophagus was significantly longer than that of the proximal esophagus in both positions (P less than 0.05) for both subject groups. In conclusion, regional differences exist in the exposure of the esophageal mucosa to refluxed gastric acid. These regional differences are more pronounced when subjects are upright than supine. Regional differences also exist in esophageal acid clearance, with clearance taking longer in the distal esophagus than in the proximal esophagus. The net effect of these phenomena is that acid exposure time in the distal esophagus is greater than that in the remainder of the esophagus.     

Nocturnal intragastric acidity during and after a period of dosing with either ranitidine or omeprazole

The magnitude and duration of changes in nocturnal intragastric acidity caused by 25 days of dosing with the antisecretory drugs ranitidine and omeprazole were investigated in a double-blind study of 22 healthy subjects. Nocturnal intragastric acidity was studied before (twice), during (on day 25), and after (every 3 days for 21 days) dosing with either 300 mg ranitidine at night or 40 mg omeprazole every morning. Three and six days after withdrawal of dosing with ranitidine, median integrated nocturnal intragastric acidity was increased significantly (17% and 14%, P = 0.01 and P = 0.05, respectively) compared with before dosing. Three days after withdrawal of dosing with omeprazole, median integrated nocturnal intragastric acidity was decreased significantly (-23%, P = 0.003). Compared with before dosing, no significant differences were seen in the ranitidine group between days 9 and 21 or the omeprazole group between days 6 and 21 after cessation of dosing. Fasting plasma gastrin concentration was measured on the morning of each study; compared with before treatment, the only significant elevations occurred on the last day of dosing with omeprazole (before, 4 pmol/L; during, 7 pmol/L). It is concluded that rebound intragastric hyperacidity after dosing with 300 mg ranitidine at night or sustained hypoacidity after dosing with 40 mg omeprazole every morning reflect transient disturbances of gastric function that are unlikely to be of clinical importance.     

Double blind comparison of the effects of cimetidine, ranitidine, famotidine, and placebo on intragastric acidity in 30 normal volunteers.

Continuous measurement of 24 hour intragastric acidity was carried out in 30 normal volunteers during treatment with placebo, cimetidine 800 mg, ranitidine 300 mg, and famotidine 40 mg in a double blind study. Medication was taken after the evening meal (post cenam nocte, PCN). Median 24 hour acidity decreased with all H2-receptor antagonists from 25.1 mmol/l on placebo to 10 mmol/l (-60.1%) during cimetidine, to 3.2 mmol/l (-87.25%) during ranitidine and to 2.5 mmol/l (-90.0%) during famotidine treatment (p less than 0.0005). All drugs significantly inhibited night time acidity but only famotidine decreased acidity during the late morning compared with placebo. Significantly greater acid reduction was seen with famotidine and ranitidine compared with cimetidine but no difference was found between famotidine and ranitidine.     

Comparison of the effects of ranitidine, cimetidine and placebo on the 24 hour intragastric acidity and nocturnal acid secretion in patients with duodenal ulcer.

Twenty-four hour intragastric acidity and nocturnal acid secretion were measured in 10 males with duodenal ulcer in four separate 24 hour studies, during which the subjects ate normal meals, had unrestricted physical activity, and consumed their customary quantities of tobacco. The medication consisted of either placebo, cimetidine 200 mg tds and 400 mg at night, or ranitidine 150 mg bd, or 200 mg bd. Ranitidine 150 mg bd decreased mean 24 hour hydrogen ion activity from 41.8 mmol/l to 13.1 mmol/l (-69%, P less than 0.001) and nocturnal acid output from 6.1 mmol/h to 0.6 mmol/h (-90%, P less than 0.01). This degree of inhibition was significantly greater than that due to cimetidine (P less than 0.001 for 24 hours acidity, less than 0.05 for night time acid output). Plasma concentrations of ranitidine were greater than the IC50 for more than eight hours after the 150 mg dose. Ranitidine 200 mg conferred no additional advantage. Ranitidine 150 mg bd should be tested in therapeutic trials.     

Utility of inpatient 24-hour intraesophageal pH monitoring in diagnosis of gastroesophageal reflux

The aims of the present study were to evaluate the accuracy of 24-hr intraesophageal pH monitoring in the diagnosis of gastroesophageal reflux in the hospital setting and to establish whether there were any differences in terms of reflux events between patients with and without endoscopic esophagitis. Fifteen control subjects and 47 patients with proven gastroesophageal reflux disease were studied. A composite score of reflux events (number of reflux episodes; total, upright, and supine reflux time; number of refluxes lasting more than 5 min; and duration of the longest reflux) provided the best discrimination between controls and patients (94% sensitivity and 100% specificity). Patients with esophagitis showed concurrently a longer total reflux time and supine reflux time, and more prolonged reflux episodes than those without esophagitis. On the other hand the severity of esophagitis was directly related to the duration of both total and supine reflux. The results indicate that inpatient 24-hr pH-metry is very accurate in the diagnosis of gastroesophageal reflux. They also suggest that prolonged esophageal exposure to acid, particularly at night, and slow esophageal acid clearing are factors that determine the appearance and/or perpetuation of esophagitis in patients with reflux.     

Pattern of acid reflux in patients with reflux esophagitis 'resistant' to H2-receptor antagonists

Ambulatory 24-h esophageal pH monitoring was carried out in 54 patients with erosive/ulcerative reflux esophagitis before a 12- to 24-week treatment with either ranitidine, 150 to 300 mg twice daily, or famotidine, 20 to 40 mg twice daily. After this period, 21 patients continued to present endoscopic evidence of esophagitis. Patients who did not respond to the therapy showed a more severe pretreatment pattern of acid reflux than those who healed, with regard to both median percentage time of reflux (16.2% versus 11.0%, respectively, p less than 0.05) and median number of reflux episodes (88.0 versus 55.0; p less than 0.05). Ambulatory 24-h esophageal pH-metry is therefore to be recommended in all patients with acid reflux symptoms, even in those who already show endoscopic lesions of the esophageal mucosa, since this test is a valid prognostic indicator of response to treatment.