Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some methodological in vitro observations concerning bile reflux monitoring (Bilitec) suggested that Bilitec monitoring is underestimating reflux in an acid environment. Moreover, other studies showed that the area above the cutoff level of bilirubin absorbance would provide an adequate quantitative marker for reflux of duodenal contents. Our aim was to study whether correction for intraesophageal acidity and the area above cutoff during Bilitec monitoring affects the results and the correlation with pH measurement and esophageal lesions. In 84 patients (46 men; mean age 46 +/- 2.7 years) evaluated for suspected gastroesophageal reflux disease, we performed ambulatory 24-hr esophageal pH and Bilitec monitoring after an upper gastrointestinal endoscopy. We obtained total area, percent total time, and correction by computer software. The correction factor for bilirubin absorbance was based on literature data for acidified bile (0.06 for pH < 3.6; 0.21 for pH < 2.6). Endoscopy revealed esophagitis grade 1-2 (E1-2) and 3-4 (E3-4) in 23 and 16 patients, respectively. A progressive increase of mixed (acid + bile) reflux occurred with increasing severity of endoscopic lesions (E3-4 vs no esophagitis, P < 0.05). A pathologic Bilitec monitoring result was present in the same 35 patients before and after correction and the correlation between the pH measurement and percent time of bile reflux was not improved by correction for intraesophageal pH (r = 0.386 and r = 0.391; P < 0.05). The total area of bilirubin absorbance above 0.14 (abs x min) was 7.8 +/- 2.2 in patients without esophagitis, and 11.7 +/- 4.4 and 17.0 +/- 4.2 in the E1-2 and E3-4 groups, respectively (E3-4 vs no esophagitis, P < 0.05). The correlation between the Bilitec monitoring and pH measurement regarding percent (r = 0.427, P < 0.01) or area of time below 4 (r = 0.280, P < 0.05) was not improved by considering the area of bilirubin absorbance above the cutoff level. Correction for intraesophageal pH has only a minor effect on the results of ambulatory Bilitec monitoring. Taking into account the surface rather than the percent of time above the cutoff level for bilirubin absorbance does not improve the correlation of Bilitec with acid reflux and with esophageal lesions.
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PMID:Analysis of ambulatory duodenogastroesophageal reflux monitoring. 1125 76

The suppression of gastric acid secretion with anti-secretory agents has been the mainstay of medical treatment for patients with acid-related disorders. Although the majority of Helicobacter pylori -related peptic ulcers can be healed with antibiotics, ulcer healing and symptom control can be significantly improved when antibiotics are given with anti-secretory agents, especially with a proton pump inhibitor. There is a dynamic relationship between the suppression of intragastric acidity and the healing of peptic ulcer and erosive oesophagitis and control of acid-related symptoms. The suppression of gastric acid secretion achieved with H(2)-receptor antagonists has, however, proved to be suboptimal for effectively controlling acid-related disorders, especially for healing erosive oesophagitis and for the relief of reflux symptoms. H(2)-receptor antagonists are also not effective in inhibiting meal-stimulated acid secretion, which is required for managing patients with erosive oesophagitis. Furthermore, the rapid development of tolerance to H(2)-receptor antagonists and the rebound acid hypersecretion after the withdrawal of an H(2)-receptor antagonist further limit their clinical use. Although low-dose H(2)-receptor antagonists are currently available as over-the-counter medications for self-controlling acid-related symptoms, their pharmacology and pharmacodynamics have not been well studied, especially in the self-medicating population. Proton pump inhibitors have been proved to be very effective for suppressing intragastric acidity to all known stimuli, although variations exist in the rapidity of onset of action and the potency of acid inhibition after oral administration at the approved therapeutic doses, which may have important clinical implications for the treatment of gastro-oesophageal reflux disease and perhaps for eradicating H. pylori infection when a proton pump inhibitor is given with antibiotics. Once-daily dosing in the morning is more effective than dosing in the evening for all proton pump inhibitors with respect to the suppression of intragastric acidity and daytime gastric acid secretion in particular, which may result from a better bio-availability being achieved with the morning dose. When higher doses are needed, these drugs must be given twice daily to achieve the optimal suppression of 24 hour intragastric acidity. Preliminary results have shown that esomeprazole, the optical isomer of omeprazole, given at 40 mg, is significantly more effective than omeprazole 40 mg, lansoprazole 30 mg or pantoprazole 40 mg for suppressing gastric acid secretion. However, more studies in different patient populations are needed to compare esomeprazole with the existing proton pump inhibitors with regard to their efficacy, cost-effectiveness and long-term safety for the management of acid-related disorders.
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PMID:Pharmacological and pharmacodynamic essentials of H(2)-receptor antagonists and proton pump inhibitors for the practising physician. 1140 32

The prevalence of Helicobacter pylori infection is steadily decreasing in developing countries, and this has been paralleled by an increasing incidence of gastroesophageal reflux disease (GERD) and adenocarcinomas of the esophagus and of the esophagogastric junction. The prevalence of H. pylori infection, which is on the decline in Europe and in the United States, is probably related to improvements in sanitary conditions and socioeconomic status. These epidemiological data do not support a role for H. pylori in the pathogenesis of GERD, but at the same time suggest a negative association with the rising incidence in esophageal diseases. While H. pylori infection clearly does not cause GERD, it may protect certain susceptible individuals from the development of GERD and its complications. There are conflicting reports that GERD can develop after H. pylori eradication and that proton pump inhibitors are less effective in suppressing intragastric acidity in H. pylori negative patients--reasons not to eradicate H. pylori in GERD patients. On the contrary, other data suggest an increase in the development of atrophic gastritis in GERD patients (H. pylori positive) on long-term proton pump inhibitor therapy - a reason to eradicate H. pylori. Preexisting lower esophageal sphincter dysfunction, susceptibility to GERD, unmasking of latent GERD, and patterns and severity of gastritis may be important factors contributing to the development of GERD rather than just the presence or absence of infection with H. pylori.
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PMID:Helicobacter pylori: a debated factor in gastroesophageal reflux disease. 1154 22

Acid-related disorders are caused by an imbalance between acid secretion by the gastric parietal cells and the defensive mechanisms of the gastrointestinal tract to protect against the effects of acid. Therapy for acid-related disorders focuses on the control of acidity. Data collected throughout the last decade have demonstrated that PPIs are the most effective therapy for acid-related disorders: PPIs have proven superior to H2RAs and antacids in numerous studies. Five PPIs are currently available in the United States. While all PPIs exert their effect through the same basic mechanism of action, they do not have the same pharmacologic and clinical properties. All PPIs are effective in healing and maintenance of gastric and duodenal ulcers and GERD. The PPIs differ, however, in their ability to control symptoms rapidly and consistently. Due to its more rapid rate of activation, rabeprazole results in a faster onset of action and faster symptom control than other PPIs. Studies comparing rabeprazole to omeprazole found statistically significant differences in the rapidity of symptom relief in patients with gastric ulcer, duodenal ulcer, and GERD. Rapid symptom relief is important to the majority of patients, as their symptoms have an impact on their quality of life. Rapid symptom relief is also important in an environment where patients self-medicate on demand, depending on daily symptoms. Rabeprazole has also been shown to have a more consistent suppression of acid, including at night. Optimizing therapy with PPIs necessitates consideration not only of healing rates of the different available treatments but also of the rapidity and consistency of acid suppression that translate clinically into symptom relief.
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PMID:Optimizing acid-suppression therapy. 1172 43

Most patients with peptic ulcers or gastroesophageal reflex disease develop subjective symptoms of epigastralgia and retrosternal pain during the period of time from the middle of the night to the early dawn (nocturnal pain). Such pain often disappears before breakfast. Disturbed circadian rhythm of gastric acid secretion may have a close relationship with the onset and aggravation of acid-related diseases. On the other hand, Helicobacter pylori has been considered to be an etiological agent of duodenal ulcer, and H. pylori eradication has been conducted in patients with gastritis and peptic ulcers. However, such eradication therapy sometimes results in the onset or deterioration of gastroesophageal reflux diseases. In this context, the question of whether the circadian rhythm of gastric acid secretion varies in accordance with the presence or absence of H. pylori infection is of interest. In the present study, we examined the fluctuation in intragastric acidity via a portable pH meter in 10 H. pylori-positive and 10 H. pylori-negative subjects. As a result, a significant difference in the circadian rhythmicity was observed between the H. pylori-negative and the H. pylori-positive group, with mean values for each parameter of 28.1 and 13.3 for amplitude, 22.7 and 12.4 for the midline-estimating statistic of rhythm (MESOR), and 324.0 and 321.0 for acrophase, respectively (P < 0.001). In both H. pylori-positive and negative groups, a tendency was observed toward an increase in intragastric acidity during the time period from the middle of the night to the early dawn, and toward a decrease in intragastric acidity during the early morning. In the H. pylori-positive group, the values for intragastric acidity over time were lower, and the degree of amplitude was smaller as compared to the H. pylori-negative group. Further, H. pylori-positive individuals were at a more advanced stage of the disease.
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PMID:Intragastric acidity and circadian rhythm. 1177 61

The recent introduction of proton pump inhibitors has extraordinarily improved the therapeutic approach to gastro-oesophageal reflux disease. The concept of decreasing gastric acid secretion and increasing the pH in the lower oesophagus has been demonstrated to be therapeutically effective and the higher the level of pH achieved, the better the results. In spite of the evident efficacy of these molecules, there are still many patients who will continue to have symptoms despite medical treatment. Proton pump inhibitors suppress gastric acidity, but this effect shows a remarkable interindividual variation depending on different reasons. Thus, it is still possible to optimise medical therapy for gastro-oesophageal reflux disease. Esomeprazole, the S-isomer of omeprazole, has an advantageous metabolism and this particular feature translates into superior clinical efficacy. Clinical trials for initial and long-term treatment across the gastro-oesophageal reflux disease spectrum, have clearly demonstrated the superiority of esomeprazole over omeprazole, even if tolerability and safety are very similar.
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PMID:Improving opportunities for effective management of gastro-oesophageal reflux disease. 1178 20

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.
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PMID:Control of nocturnal gastric acidity: a role for low dose bedtime ranitidine to supplement daily omeprazole. 1185 40

Maintenance of intragastric pH > 4 is vital for effective management of gastroesophageal reflux disease (GERD). Esomeprazole 40 mg, the first proton pump inhibitor developed as an optical isomer, demonstrates improved acid inhibition over omeprazole 20 mg. Our aim was to compare esomeprazole 40 mg with omeprazole 40 mg, once-daily, on intragastric acidity in patients with symptoms of GERD. In this open-label, crossover study, 130 patients with symptoms of GERD received esomeprazole 40 mg or omeprazole 40 mg once-daily for five days. The 24-hr intragastric pH was monitored on days 1 and 5 of each treatment period. The mean percentage of the 24-hr period with intragastric pH > 4 was significantly greater (P < 0.001) with esomeprazole 40 mg than with omeprazole 40 mg on days 1 (48.6% vs 40.6%) and 5 (68.4% vs 62.0%). Interpatient variability was significantly less with esomeprazole than omeprazole. Esomeprazole was well tolerated. In conclusion, esomeprazole 40 mg provides more effective acid control than twice the standard dose of omeprazole.
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PMID:Effect of esomeprazole 40 mg vs omeprazole 40 mg on 24-hour intragastric pH in patients with symptoms of gastroesophageal reflux disease. 1201 20

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.
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PMID:Motion--Helicobacter pylori causes or worsens GERD: arguments against the motion. 1236 16

Gastric acid suppression is the most effective medical therapy to control acidic gastro-oesophageal reflux: individuals in whom therapy fails usually have inadequate acid suppression. Twenty-four-hour intragastric pH-metry measures the percentage of time that gastric pH is above 4 or 3, the critical thresholds for tissue damage and symptom generation in the distal oesophagus. Effective medical therapy must control gastric acidity throughout the daytime, including the postprandial period. It is therefore useful to report the percentage of patients in whom gastric acidity is controlled above pH 4 for at least 16 out of 24 h. Esomeprazole was compared with standard-dose proton pump inhibitors in healthy volunteers and patients with gastro-oesophageal reflux disease. Esomeprazole, 40 mg daily, was significantly more effective at controlling gastric acidity above pH 4 for more than 16 h than lansoprazole, 30 mg daily (38% of individuals vs. 5%, respectively). Esomeprazole, 40 mg daily, also suppressed gastric acidity more effectively and in more individuals than pantoprazole, 40 mg daily, and rabeprazole, 20 mg daily. Esomeprazole, 20 mg daily, was significantly more effective at controlling gastric acidity than lansoprazole, 15 mg daily. The improved acid control with esomeprazole compared with other proton pump inhibitors is likely to result in superior healing rates and improved symptom relief, with fewer therapy-resistant patients.
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PMID:Review article: gastric acidity--comparison of esomeprazole with other proton pump inhibitors. 1261


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