Ambulatory 24-h Esophageal pH Monitoring Research Articles

The effect of lifestyle changes on results of 24-h ambulatory oesophageal pH monitoring

Twenty-four-hour pH monitoring is the 'gold standard' investigation of gastro-oesophageal reflux disease. It has been suggested that results may be influenced by lifestyle alteration during the study. The aim of this study was to determine the influence of lifestyle alteration and anxiety on outcome in pH monitoring. One hundred consecutive patients attending for pH monitoring were recruited. Post-intubation anxiety was quantified (STAI form Y-1). On completion a questionnaire was recorded comprising six questions regarding alteration to eating/drinking (FOOD) (score 0-6) and six regarding posture and activity (ACTIVITY) (score 0-6). The higher the score the greater the alteration of lifestyle. A 10-point visual analogue scale (VAS) scored the degree of distress caused by the experience. pH studies were positive if exposure times at pH < 4 were greater than established normal values or if the Symptom Index was > 50%. Comparisons were made between patients with positive and negative studies regarding FOOD, ACTIVITY, VAS and STAI scores. Patients with positive pH studies had mean FOOD (2 vs 2; P> 0.05), ACTIVITY (2 vs 2; P> 0.05), VAS (3 vs 3; P> 0.05) and STAI (31 vs 32; P> 0.05) scores which were not significantly different from those of patients with negative pH studies. Lifestyle alteration was minimal in patients undergoing pH monitoring, nor was the experience distressing. There was no difference in lifestyle alteration and anxiety between those with positive and negative pH profiles.

Failure of oesophageal acid control in candidates for Barrett's oesophagus reversal on a very high dose of proton pump inhibitor.

Normalization of oesophageal acid exposure using high dose proton pump inhibitors in patients who are candidates for ablation therapy has been suggested to be essential for successful Barrett's reversal. However, the success rate for achieving pH normalization has not been determined. Patients with Barrett's oesophagus (2-6 cm in length) who were found to be eligible for ablation therapy using multipolar electrocoagulation were included in this prospective study. Patients underwent an upper endoscopy to determine Barrett's length and other anatomic characteristics. Biopsies were obtained to rule out dysplasia. Subsequently, patients were treated with omeprazole 40 mg b.d. Twenty-four hour oesophageal pH monitoring was performed after a mean period of 8.4 +/- 0.6 days of therapy. Twenty-five patients were enrolled into the study. The pH test was abnormal in four (16%) of the study subjects. An additional two (8%) patients had abnormal supine percentage time with pH less than 4. There was no significant difference in oesophageal acid control between patients with long vs. short segment Barrett's oesophagus. Elderly (> 60 years) patients tended to have less acid control than younger (</= 60 years) patients. Failure of oesophageal acid control in candidates for Barrett's oesophagus reversal on very high dose of proton pump inhibitor is not uncommon. Our study suggests that ambulatory 24-h oesophageal pH monitoring should be considered in all candidates for Barrett's reversal who are treated with high dose proton pump inhibitor to ensure normalization of oesophageal acid exposure.

The omeprazole test is as sensitive as 24-h oesophageal pH monitoring in diagnosing gastro-oesophageal reflux disease in symptomatic patients with erosive oesophagitis.

Ambulatory 24-h oesophageal pH monitoring and a short course of high dose omeprazole can be used as diagnostic modalities for GERD. However, comparative studies of the diagnostic accuracy and reliability of both strategies have not been performed. To compare the omeprazole test to ambulatory 24-h oesophageal pH monitoring in diagnosing GERD in symptomatic patients using endoscopically proven erosive oesophagitis as a gold standard. Patients with heartburn underwent an upper endoscopy. Only those with erosive oesophagitis were included in the study. Subsequently, patients underwent ambulatory 24-h oesophageal pH monitoring and an 'omeprazole test.' Daily symptoms were recorded during the first week (baseline) and repeated during the second week on therapy (omeprazole 40 mg in the morning and 20 mg in the evening). Thirty-five patients were included in the study. The omeprazole test was significantly more sensitive in diagnosing GERD than total acid contact time on 24-h oesophageal pH monitoring (83% vs. 60%; P < 0.03). However, the sensitivity of the pH test increased to 80% after adding patients with a positive symptom index, and patients with abnormal acid exposure in the supine or erect positions despite normal total acid contact time. Patients with a normal pH test were significantly younger (49 +/- 2.6 years) than those with abnormal test (59 +/- 1.8; P=0.002). In this study an omeprazole test was at least as sensitive as ambulatory 24-h oesophageal pH monitoring in diagnosing GERD in patients with erosive oesophagitis.

Symptom severity and oesophageal chemosensitivity to acid in older and young patients with gastro-oesophageal reflux.

elderly patients appear to have a more aggressive form of gastro-oesophageal reflux disease than younger patients. Reduced pain perception with age is a possible underlying mechanism. to compare the extent of oesophageal mucosal injury, acid exposure, symptom severity and perception thresholds for acid infusion in older (aged 60 or older) and younger patients with gastro-oesophageal reflux. twenty-five younger and 23 older patients completed the study. We determined acid exposure and oesophageal mucosal injury by ambulatory 24-h oesophageal pH monitoring and upper endoscopy, respectively. We determined chemosensitivity by infusing 0.1 N hydrochloric acid into the mid-oesophagus for 10 min at 10 ml/min after a 2-min infusion of normal saline at a similar rate. We quantified acid perception thresholds by the lag time to initial typical symptom perception, intensity rating at the end of acid infusion and an acid perfusion sensitivity score, calculated from the fractional duration of symptom perception and intensity rating. mean percentage of total time with pH <4 was higher in the older (15.8+/-2.4) than in the younger patients (11.9+/-1.8; P = 0.18). Of the older group, 74% had erosive oesophagitis versus 64% in the younger group. Frequency of symptoms (heartburn, acid regurgitation and dysphagia) was lower in the elderly group. Older patients perceived heartburn and acid regurgitation as much less severe than younger patients (P < 0.05).Younger patients had a significantly shorter lag time to initial symptom perception (P < 0.05) and a higher sensory intensity rating (P < 0.08). The acid perfusion sensitivity score was significantly lower in the older group (P < 0.05). older patients with gastro-oesophageal reflux disease have reduced symptom severity for heartburn despite a tendency towards increased severity of oesophageal mucosal injury and acid exposure. Age-related reduction in chemosensitivity to acid is a possible underlying mechanism.

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.

Does progesterone fluctuation across the menstrual cycle predispose to gastroesophageal reflux?

OBJECTIVE: Gastroesophageal reflux (GER) occurs in 30–50% of all pregnancies. The progressive rise in plasma progesterone has been suggested as a possible mediator of GER during pregnancy. It is not known whether progesterone, at physiological concentrations, has an effect on acid contact time. We sought to evaluate the relationship between progesterone concentrations, lower esophageal sphincter pressure (LESP), and acid contact time across the normal menstrual cycle. METHODS: LESP, 24-h ambulatory esophageal pH monitoring, and serum progesterone levels were determined in 19 healthy women known to have normal menstrual cycles. All tests were performed during the follicular phase (days 2–7) and the luteal phase (days 22–28) of one or two consecutive menstrual cycles. RESULTS: Despite marked oscillations in progesterone levels between the follicular phase (0.37 ± 0.3 ng/ml) and luteal phase (4.64 ± 2.92 ng/ml) we observed no significant differences in LESP (29.82 ± 9.49 vs 30.45 ± 8.56 mm Hg) or 24-h ambulatory pH levels (pH < 4) in total time (3.04 ± 0.3% vs 3.18 ± 2.51%), upright time (4.41 ± 3.54% vs 4.18 ± 3.36%), or supine time (0.77 ± 1.32% vs 1.42 ± 2.18%). CONCLUSIONS: The fluctuations in progesterone levels across the normal menstrual cycle have no significant impact on LESP and 24-h ambulatory pH parameters. Progesterone, at physiological concentrations, does not predispose to GER in healthy menstruating women.

Does progesterone fluctuation across the menstrual cycle predispose to gastroesophageal reflux?

Gastroesophageal reflux (GER) occurs in 30-50% of all pregnancies. The progressive rise in plasma progesterone has been suggested as a possible mediator of GER during pregnancy. It is not known whether progesterone, at physiological concentrations, has an effect on acid contact time. We sought to evaluate the relationship between progesterone concentrations, lower esophageal sphincter pressure (LESP), and acid contact time across the normal menstrual cycle. LESP, 24-h ambulatory esophageal pH monitoring, and serum progesterone levels were determined in 19 healthy women known to have normal menstrual cycles. All tests were performed during the follicular phase (days 2-7) and the luteal phase (days 22-28) of one or two consecutive menstrual cycles. Despite marked oscillations in progesterone levels between the follicular phase (0.37 +/- 0.3 ng/ml) and luteal phase (4.64 +/- 2.92 ng/ml) we observed no significant differences in LESP (29.82 +/- 9.49 vs 30.45 +/- 8.56 mm Hg) or 24-h ambulatory pH levels (pH < 4) in total time (3.04 +/- 0.3% vs 3.18 +/- 2.51%), upright time (4.41 +/- 3.54% vs 4.18 +/- 3.36%), or supine time (0.77 +/- 1.32% vs 1.42 +/- 2.18%). The fluctuations in progesterone levels across the normal menstrual cycle have no significant impact on LESP and 24-h ambulatory pH parameters. Progesterone, at physiological concentrations, does not predispose to GER in healthy menstruating women.

Gastroesophageal reflux in diabetes mellitus

OBJECTIVE: Although abnormal gastroesophageal (GE) reflux is the most frequent alteration of the gastrointestinal tract, its prevalence in diabetes mellitus (DM) is not widely known. The objective of this study was to analyze both the presence of abnormal GE reflux in diabetic patients with no esophageal symptoms and the influence of cardiovascular autonomic neuropathy (CVAN) in the development of abnormal GE reflux. METHODS: Fifty insulin-dependent diabetic patients, averaging 29.2 ± 9.0 yr of age, who had had diabetes for > 5 yr and showed no symptoms or history of gastroesophageal disease, were compared with a control group composed of 36 healthy volunteers (18 men, 18 women) whose average age was 35.9 ± 10.1 yr. The cardiovascular autonomic nervous system was examined in the diabetics and control subjects who complied with inclusion criteria. Long-term (24-h) ambulatory esophageal pH monitoring was performed, as well as a manometric study of the lower esophageal sphincter. RESULTS: The parameters obtained from the monitoring showed significant differences ( p < 0.01) between DM and control subjects. Abnormal GE reflux, defined as any percentage of time with esophageal pH < 4 exceeding 3.5% of total time (8.7 ± 5.6%; range, 4.1–24.4%), was detected in 14 patients. Diabetic subjects were classified according to cardiovascular autonomic neuropathy tests (without CVAN [n = 19, 38%] and with abnormal CVAN tests [n = 31, 62%]). The pH monitoring parameters showed significant differences between these two groups ( p < 0.05). CONCLUSIONS: A higher prevalence (28%) of abnormal GE reflux appeared among asymptomatic diabetic patients than among the general population. The presence of abnormal GE reflux in diabetic patients was associated with the existence of cardiovascular autonomic neuropathy (abnormal GE reflux = 38.7% in diabetic patients with abnormal CVAN tests vs 10.5% in diabetic patients without CVAN).

Investigation of oesophageal reflux symptoms after gastric surgery with combined pH and bilirubin monitoring.

Little is known about the role of bile in gastro-oesophageal reflux disease in patients with previous gastric surgery. This has partly been due to a lack of suitable techniques for identifying bile reflux objectively. Some 28 patients with reflux symptoms and previous gastric surgery underwent oesophageal manometry, and 24-h ambulatory oesophageal pH and bilirubin monitoring. A wide variety of operations had been performed, most commonly Pólya gastrectomy (seven patients), vagotomy and pyloroplasty (six) and vagotomy and gastrojejunostomy (four). Three patients had isolated acid reflux, eight had isolated bile reflux, six had combined acid and bile reflux, and 11 patients had no reflux. Two-thirds of heartburn symptoms were not associated with reflux. However, one-quarter were associated with acid reflux and only 7 per cent with bile reflux. Erosive oesophagitis was present in five patients: two with combined acid and bile reflux, and three with isolated bile reflux. Acid and/or bile reflux can be present after a wide variety of gastric operations. Symptoms are more frequently associated with acid reflux than with bile reflux. Erosive oesophagitis can occur in the presence of isolated bile reflux. Combined pH and bilirubin monitoring determines the nature of the refluxate, and may help in the management of these patients.

Complete elimination of reflux symptoms does not guarantee normalization of intraesophageal acid reflux in patients with Barrett’s esophagus

Objective: Normalization of intraesophageal acid exposure is increasingly recognized as a desired goal in the management of Barrett’s esophagus. In this prospective trial, we studied patients with Barrett’s esophagus by 24-h intraesophageal pH monitoring after having completely eliminated their reflux symptoms with lansoprazole, to determine whether they had achieved normalization of intraesophageal pH. Methods: Thirty patients with Barrett’s esophagus, all of whom had presented with reflux symptoms, were treated with lansoprazole (15–30 mg/day) until they were asymptomatic. Twenty-four-hour ambulatory pH monitoring was performed while they were receiving lansoprazole and were asymptomatic. Results: Twelve patients (40%) showed persistent bipositional, pathologic acid reflux while on therapy, with a mean DeMeester score of 52.8 (95% CI: 33.8–71.8); the remaining 18 (60%) exhibited normalization of intraesophageal acid exposure with a score of 4.4 (95% CI: 2.3–6.6, p < 0.001). This inadequate control of intraesophageal pH is most likely due to incomplete gastric acid suppression induced by the drug and is associated with a variable acid (distal > proximal) exposure within the esophagus. The two groups were not different in regard to their symptom frequency and severity before therapy, amount of lansoprazole dosage required to eliminate symptoms, length of Barrett’s metaplasia, presence of hiatal hernia, lower esophageal sphincter resting tone and length, or esophageal peristaltic function. Conclusion: Complete symptom eradication with lansoprazole (15–30 mg daily) in patients with Barrett’s esophagus does not guarantee normalization of intraesophageal pH profile. If the goal of therapy in such patients is to achieve complete intraesophageal acid suppression, 24-h ambulatory esophageal pH monitoring should be performed to titrate therapy.

Complete elimination of reflux symptoms does not guarantee normalization of intraesophageal acid reflux in patients with Barrett's esophagus.

Normalization of intraesophageal acid exposure is increasingly recognized as a desired goal in the management of Barrett's esophagus. In this prospective trial, we studied patients with Barrett's esophagus by 24-h intraesophageal pH monitoring after having completely eliminated their reflux symptoms with lansoprazole, to determine whether they had achieved normalization of intraesophageal pH. Thirty patients with Barrett's esophagus, all of whom had presented with reflux symptoms, were treated with lansoprazole (15-30 mg/day) until they were asymptomatic. Twenty-four-hour ambulatory pH monitoring was performed while they were receiving lansoprazole and were asymptomatic. Twelve patients (40%) showed persistent bipositional, pathologic acid reflux while on therapy, with a mean DeMeester score of 52.8 (95% CI: 33.8-71.8); the remaining 18 (60%) exhibited normalization of intraesophageal acid exposure with a score of 4.4 (95% CI: 2.3-6.6,p < 0.001). This inadequate control of intraesophageal pH is most likely due to incomplete gastric acid suppression induced by the drug and is associated with a variable acid (distal > proximal) exposure within the esophagus. The two groups were not different in regard to their symptom frequency and severity before therapy, amount of lansoprazole dosage required to eliminate symptoms, length of Barrett's metaplasia, presence of hiatal hernia, lower esophageal sphincter resting tone and length, or esophageal peristaltic function. Complete symptom eradication with lansoprazole (15-30 mg daily) in patients with Barrett's esophagus does not guarantee normalization of intraesophageal pH profile. If the goal of therapy in such patients is to achieve complete intraesophageal acid suppression, 24-h ambulatory esophageal pH monitoring should be performed to titrate therapy.

How Standard Is a Standard Day during a Standard Ambulatory 24-Hour Esophageal pH Monitoring?

Background: Ambulatory 24-h esophageal pH monitoring is the gold standard method for measuring esophageal exposure to gastric acid. The method has gained acceptability because of its sensitivity, specificity, and accuracy and also because it is easy to perform, well tolerated, and quite physiologic. However, whether ambulatory esophageal pH-metry affects normal lifestyle has not been specifically evaluated. Methods: We investigated 114 consecutive patients admitted to our Unit because of heartburn, acid regurgitation, or non-cardiac chest pain. Patients filled in a diary chart on 2 different days: 1 day while the pH-metry was performed and another normal day, to record the following variables: number, amount, and composition of the meals; time in supine position; number of cigarettes smoked; alcohol intake; degree of physical activity; and number and type of symptomatic episodes. Patients were encouraged to carry out normal activity. Results: When the 2 days were compared, none of the registered variables appeared to differ, with the exception of subjective evaluation of physical activity: 65% of the patients said their physical activity was diminished during the test day relative to their usual standard. Conclusions: Normal habits are not significantly modified by 24-h esophageal pH-metry, with the exception of physical activity, which decreases, possibly owing more to aesthetic than to physical problems.

The preoperative evaluation of patients considered for laparoscopic antireflux surgery.

Few studies address the proper extent of the preoperative testing in patients referred for consideration of antireflux surgery. Our aim was to perform a thorough gastroesophageal evaluation and determine its influence on the therapeutic decisions of such patients. We evaluated 107 consecutive patients in a combined GI/Surgery clinic for severe or refractory gastroesophageal reflux. The patients had an EGD, esophageal manometry, and 24-h ambulatory esophageal pH monitoring. Only patients with gastric symptoms had gastric testing. Nineteen patients were excluded, 12 refused further evaluation and seven were felt to be unfit for antireflux surgery because of medical or psychological reasons. Eighty-eight patients completed the required studies. Fifty-four patients (61%) had typical reflux symptoms and erosive esophagitis on EGD. All these patients had an abnormal pH study. Five of the 34 patients without esophagitis had a normal pH study and did not have surgery. Ten patients had poor peristalsis by esophageal manometry prompting a subtotal fundoplication. One patient had severe delayed gastric emptying, requiring pyloroplasty in addition to the fundoplication. Eighty of 83 patients had good or excellent surgical results. EGD and esophageal manometry are indispensable in the preoperative evaluation. Manometry may identify abnormalities altering surgical decisions in roughly 10% of patients. Routine ambulatory esophageal pH monitoring is of marginal benefit, except in patients without esophagitis or in those patients where the diagnosis is in doubt. Clinically significant gastric abnormalities are rare, and routine testing of gastric function is not indicated.

Glycogenic acanthosis of the esophagus and gastroesophageal reflux.

A nodular appearance of the esophageal mucosa, observed in 3.5% of 2,328 consecutive upper endoscopic examinations, most commonly appeared as multiple, uniformly sized, oval or round elevations usually < 1 cm, involving otherwise normal esophageal mucosa. Endoscopic biopsies in 35 consecutive patients followed prospectively demonstrated the nodules to represent glycogenic acanthosis--a combination of cellular hyperplasia and increased cellular glycogen. When studied by 24-h ambulatory esophageal pH monitoring, 83% of these patients had pathologic gastroesophageal acid reflux; mean percentage of time with pH < 4.0 was 37.3%. Antireflux therapy improved symptoms in all patients but failed to eradicate the lesions of glycogenic acanthosis. Although its etiology and pathogenesis still remain elusive, glycogenic acanthosis may be related to gastroesophageal reflux.

Chronic Persistent Cough and Clearance of Esophageal Acid

Unexplained chronic persistent cough has been shown to be associated with increased episodes of otherwise asymptomatic gastroesophageal reflux; however, normal subjects without cough also exhibit some reflux. We postulate that the prompt clearance of refluxed acid from the esophagus may play an important role in the prevention of cough, and we sought to determine if patients with chronic cough have impaired clearance. Thirty patients with unexplained chronic cough underwent 24-h ambulatory esophageal pH monitoring. Compared to 12 matched control subjects, patients experienced significantly more episodes (all values expressed as median [range]) of reflux per 24 h (88.3 [5.0 to 338.0] vs 5.7 [0 to 13.0]; p < 0.0001) and had impaired clearance of esophageal acid as measured by the duration of individual reflux episodes (3.0 [0.1 to 20.5] min per reflux vs 0.7 [0 to 2.5] min per reflux; p < 0.01). We conclude that patients with chronic persistent cough have impaired clearance of esophageal acid.

Effect of different doses of omeprazole on 24‐hour oesophageal acid exposure in patients with gastro‐oesophageal reflux

To define the optimum doses of omeprazole appropriate for acute and long-term therapy of patients with gastro-oesophageal reflux disease, 24-h oesophageal pH was measured in 12 patients with symptomatic reflux and an abnormal 24-h oesophageal acid exposure time (greater than 6%) in a randomized, double-blind, four-way crossover study comparing the effects of omeprazole 10, 20, or 40 mg/day and placebo. Total reflux time over 24 hours, number of reflux episodes per hour, and the number of reflux episodes lasting greater than 5 minutes were measured by ambulatory 24-h oesophageal pH monitoring. All doses of omeprazole were superior to placebo in decreasing gastro-oesophageal reflux as measured by each index. With placebo, oesophageal acid exposure was 16.3% of the 24 hours, 10 mg omeprazole/day reduced that to 6.3%, 20 mg/day lowered acid exposure to 0.9%, and 40 mg/day to 0.6%. Thus only the 20 and 40 mg doses reduced acid exposure to within the normal range. Similar results were obtained with the other indices of reflux. These data suggest that a rational dose regimen for reflux oesophagitis is 20 mg/day, a regimen that has proved effective in clinical trials. The present study indicates that 24-hour oesophageal pH monitoring is a practical approach to the determination of drug dosage in patients with gastro-oesophageal reflux.

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 < 0.001), basal volume output (p < 0.02), and basal upright (but not supine) reflux time (p < 0.05). Nine of the 12 patients who did not respond to initial treatment had gastric acid hypersecretion (basal acid output >L10 mEq/h), and 10 of the 12 had Barrett's epithelium compared with only 1 patient in the initial-responder group (p < 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 < 0.001); gastric acid output had to be almost totally suppressed (i.e., < 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.

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.

Ambulatory 24-Hour pH-Metry in the Diagnosis of Gastroesophageal Reflux Disease

The results of ambulatory 24-h esophageal pH monitoring in 67 patients with gastroesophageal reflux symptoms (endoscopic esophagitis, n = 44; normal endoscopy, n = 23) were compared with those of 27 normal subjects without reflux symptoms. Patients with reflux symptoms had significantly increased gastroesophageal reflux compared with normal subjects. Acid reflux time was significantly (p less than 0.001) correlated with the severity of endoscopic esophagitis. Linear discriminant analysis was used to differentiate, for each reflux variable, between patients and controls. When the percentage of overall time at pH below 4 was used as a single determinant of gastroesophageal reflux, the sensitivity and specificity were 81% and 85%, respectively, with 4% as upper limit of normal. Pathologic reflux was found in 61% of the patients with negative endoscopy. Long-term ambulatory pH-metry is of clinical value in detecting pathologic reflux in symptomatic patients with negative endoscopy.

Noncardiac Chest Pain: Is the Esophagus Really a Frequent Source?

The occurrence of esophagus-related noncardiac chest pain was investigated in 22 unselected consecutive patients referred by local cardiologists. The investigations included endoscopy, standard manometry, esophageal scintigraphy, a double-blind placebo-controlled edrophonium provocation test on two occasions (during manometry and scintigraphy), an acid perfusion test, and 24-h ambulatory esophageal pH-monitoring. Nine patients had reflux symptoms; none had dysphagia. Abnormal test results were found in 11 patients. In only three of them was a definite relation between chest pain and the esophagus established: the acid perfusion test was positive in these three, as was 24-h pH-monitoring in two of them. All three had symptomatic reflux. The absence of patient selection and, possibly, the exclusion of biasing during the edrophonium tests are considered to be the most important factors for the finding of only few patients with definite esophagus-related noncardiac chest pain in this study. A prudent approach towards patients with noncardiac chest pain, with regard to the evaluation of an esophageal cause, is recommended.