Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aims of this study were to assess the effect of pneumatic dilation on gastroesophageal reflux in achalasia, differentiate esophageal acid due to lactate from acid due to gastroesophageal reflux, and determine if chest pain and heartburn are reliable indicators of gastroesophageal reflux. Eight untreated achalasia patients underwent pre- and postdilation esophageal fluid/food residue lactate and pH analysis, esophageal manometry, 24-hr pH monitoring, and symptom assessment. All patients had a successful clinical outcome and a decrease in lower esophageal sphincter pressure from 29.1 +/- 12.7 to 14.7 +/- 3.8 mm Hg (mean +/- SD; P = 0.04). Abnormal acid exposure was present in two patients before and two patients after dilation. Postdilation acid exposure was mild. Lactate was detected before dilation in all patients. A lactate concentration >2 mmol/liter was associated with acidic residue and one abnormal 24-hr pH profile. There was no correlation between an abnormal 24-hr pH test and age, lower esophageal sphincter pressure, or duration of symptoms prior to treatment. Chest pain and heartburn were unrelated to drops in pH. Gastroesophageal reflux is rare in untreated achalasia and esophageal acidity may result from ingestion of acidic foods or production of lactate. Mild gastroesophageal reflux occurs after dilation but is of no clinical significance. Chest pain and heartburn are not indicators of acid reflux in achalasia.
 ...
PMID:Effect of pneumatic dilation on gastroesophageal reflux in achalasia. 914 54

The esophagus is lined by a moist stratified squamous epithelium. In humans, this epithelium, as evidenced by the Bernstein test, has considerable capacity to resist damage even upon direct contact of high concentrations of luminal acid. This intrinsic property of the epithelium to defend itself against luminal acid is called "tissue resistance." Tissue resistance is comprised of a number of important structures and functions, the individual functions of which are described in this review. Moreover, when luminal acidity is sufficiently noxious, tissue resistance can be overcome, leading to heartburn and ultimately cell necrosis. Herein are described the mechanisms by which acid overcomes the epithelial defense to produce these typical signs and symptoms of gastroesophageal reflux disease.
 ...
PMID:Mechanisms of reflux-induced epithelial injuries in the esophagus. 1071 61

Gastroesophageal reflux symptoms are common and occur in all of us from time to time. In others, reflux may be associated with ulcerative esophagitis. The symptoms may be aggravated by large meals, coffee, smoking and position. Physiological and pathological reflux can be separated by the frequency and duration of the exposure of the lower esophagus to acid. Pathological reflux results in symptoms and also esophagitis and ulceration in some patients. Although gastroesophageal reflux disease (GERD) is considered to result from a disorder of motility in the esophagus, gastric acid and peptic activity are deemed pivotal to the initiation and continuation of the esophageal damage and the development of symptoms. Acid exposure in the esophagus is normally less than 4 percent of the 24 hours with a pH below 4. An increase over 4 percent of the time with a pH less than 4 is considered pathological. Hence, antisecretory drugs have become the principle approach to the treatment of reflux symptoms and esophagitis since they reduce the acidity, of gastric juice and the activity of pepsin. Importantly, they also reduce the volume of gastric juice available for reflux into the esophagus. There is a clear relationship between the degree and duration of acid suppression and the relief of heartburn and healing of esophagitis. Pharmacodynamic studies with different dose regimens of the H2-receptor antagonists and the proton pump inhibitors show a difference in the degree and duration of the antisecretory effect, and this correlates closely with the results of clinical trials with respect to the healing of esophagitis and the relief of symptoms. Proton pump inhibitors achieve healing rates by week four, which are not achieved by H2-receptor antagonists even after 12 weeks of treatment. The advantage of proton pump inhibitors over H2-receptor antagonists is due to the greater degree, longer duration of effect and more complete inhibition of acid secretion that maintains intragastric pH above 4 for a maximal duration. Although there is no significant difference between proton pump inhibitors with respect to healing of esophagitis, symptom relief occurs earlier with lansoprazole than omeprazole, and this is probably due to the greater oral bioavailability and faster onset of action of lansoprazole when compared to omeprazole.
 ...
PMID:pH, healing rate, and symptom relief in patients with GERD. 1078 May 80

Gastroesophageal reflux disease (GERD) affects more than one third of the population. It is generally a chronic condition and has the potential to be serious. Some patients with GERD experience persistent daytime or nighttime heartburn and some sustain severe damage, including ulceration, stricture, and Barrett's esophagus, which can predispose to development of adenocarcinoma. Extraesophageal manifestations of GERD can include otolaryngologic, respiratory, and cardiac problems. Severe GERD responds best to agents that suppress gastric acid secretion. Of these, proton pump inhibitors (PPIs) provide the most effective control of gastric acidity and are, therefore, the medical treatment of choice. In fact, nonresponse to a PPI should raise the suspicion that the diagnosis is not GERD. Proton pump inhibitors are quickly becoming the treatment of choice for GERD, especially for severe or refractory cases. For patients whose GERD is refractory even to PPIs or who are unwilling to face years of PPI therapy, antireflux surgery remains an option.
 ...
PMID:Management of severe gastroesophageal reflux disease. 1115 63

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

Gastroesophageal reflux disease is a common, usually lifelong, disorder resulting from chronic abnormal exposure of the lower esophagus to gastric contents. Motor dysfunction of the lower esophageal sphincter is the primary cause of this disease. At this writing, no medical therapies can completely resolve abnormal lower esophageal sphincter function; therefore, the treatment of gastroesophageal reflux disease centers on suppression of intragastric acid secretion. Available acid-suppressant medications include proton pump inhibitors, H2-receptor antagonists, and antacids. Of these, the proton pump inhibitors are recognized generally as the mainstays of both short-term and long-term therapy for gastroesophageal reflux disease. All have a low incidence of side effects and are well tolerated by most patients. Five proton pump inhibitors are available currently for patients with gastroesophageal reflux disease. Of these, esomeprazole has shown greater efficacy in controlling intragastric acidity than the others. For patients with erosive esophagitis, esomeprazole has demonstrated higher healing rates and more rapid sustained resolution of heartburn than omeprazole or lansoprazole after up to 8 weeks of once-daily treatment. Because new therapies for gastroesophageal reflux disease are highly effective, patients can be reassured that their disease will be well controlled and their symptoms resolved with a safe and appropriate treatment.
 ...
PMID:Gastroesophageal reflux disease: current treatment approaches. 1467 9

Gastroesophageal reflux disease (GERD) is a common chronic disorder in the Western world. The basic cause of GERD has been well characterized--the fundamental defect is a loss of integrity of the gastroesophageal barrier. What is less clear is the most appropriate means of addressing this reflux. GERD has a variety of symptoms, ranging from typical presentations of heartburn and regurgitation (without esophagitis) to atypical presentations, such as severe erosive esophagitis and its associated complications. Because of its symptomatic diversity, physicians may select from a variety of therapeutic approaches. Medical therapy aims at decreasing acidity by suppressing proton secretion and has been well established. Available medications include antacids and alginates, H2-receptor antagonists, motility agents, and proton pump inhibitors (PPIs). Antireflux surgery, commonly performed laparoscopically, aims at reinforcing and repairing the defective barrier through plication of the gastric fundus. The earliest performed successful procedures were the Nissen and Toupet fundoplications, to which several modifications have since been made. It has been demonstrated in preliminary studies and long-term outcomes of such open surgery and preliminary studies of such laparoscopic surgery that antireflux surgery is an effective approach, with overall outcomes superior to those achieved with medications. The precise indications for the surgical treatment of patients with GERD, however, remain controversial. In recent years, endoscopic intraluminal antireflux approaches have attracted the attention of physicians, surgeons, and commercial companies, especially after the approval of two endoscopic intraluminal methods by the United States FDA in 2000. The common element is prevention of acid reflux by construction of a functional or controlled barrier in the lower esophageal sphincter zone. Three main methods are currently employed: endoscopic intraluminal valvuloplasty, endoscopic radiofrequency therapy, and endoscopic injection or implantation of foreign material. The endoluminal suturing method is highly demanding technically, and its short-term results are encouraging, although largely dependent on the experience of the endoscopist. Several prospective cohort studies have shown that the radiofrequency procedure (Stretta) significantly improves GERD symptoms and quality of life while reducing esophageal acid exposure and eliminating the need for antisecretory medications in the majority of patients within 6-12 months. Most recently, some researchers have studied the endoluminal implantation of polymers, such as Plexiglas (polymethyl-methylacrylate), Gatekeeper hydrogel, and Enteryx (ethylene vinyl alcohol copolymer). The preliminary results of these studies showed that the implantation method was feasible and safe; however, the only multicenter trial related to outcome that has been published has included just 1 year of follow-up. Here, we review the treatment of GERD: medical, surgical, and endoscopic. In addition, we provide an algorithm based on symptoms and response to treatment for management of these patients.
 ...
PMID:Management of gastroesophageal reflux disease: medications, surgery, or endoscopic therapy? (Current status and trends). 1602 48

Nocturnal gastro-oesphageal reflux is an under-appreciated clinical challenge. This condition may cause symptoms such as nocturnal heartburn, or it may be asymptomatic. In addition, patients may experience sleep disturbances that can potentially lead to complications such as erosive oesophagitis and Barrett's oesophagus, and may be a risk factor for development of oesophageal adenocarcinoma. Delayed-release proton-pump inhibitors (PPIs) have traditionally been effective in treating both daytime and night-time reflux symptoms, but are limited in control of nocturnal acidity by their pharmacodynamic characteristics. This narrative review addresses the prevalence, impact and pharmacologic approaches used to control nocturnal acidity. Methods to optimize nocturnal acid control include careful attention to dosing schedule, using higher doses of PPIs, adding an histamine H2-receptor antagonist at bedtime to once or twice daily delayed-release PPI, or using immediate-release omeprazole (Zegerid powder for oral suspension; Santarus, Inc., San Diego, CA, USA). This new formulation appears to provide sustained control of intragastric pH at steady state, and when dosed at bedtime, and may be effective in improving control of nocturnal pH and treating night-time GERD.
 ...
PMID:Review article: putting immediate-release proton-pump inhibitors into clinical practice--improving nocturnal acid control and avoiding the possible complications of excessive acid exposure. 1630 35

Gastroesophageal reflux disease (GERD) is a chronic disease affecting up to 40% of people in the Western world. Risk factors associated with GERD include age and lifestyle habits, although the clinically relevant contribution of many of these factors is unclear. In GERD, refluxed gastric acid damages the oesophageal mucosa, generally when the pH falls below 4. GERD patients present a variety of symptoms, most commonly heartburn and regurgitation. Oesophageal complications associated with GERD include erosions, ulcers, peptic strictures, and Barrett's oesophagus which is implicated in the development of oesophageal adenocarcinoma. Diagnosis of GERD is problematic due to the range of symptoms which may be presented to the physician and symptom severity is frequently unrelated to disease severity. While endoscopic monitoring may be used to assess the presence and severity of GERD, a lack of visible damage does not necessarily indicate an absence of GERD. Techniques used to diagnose GERD include addition of an acid solution into the oesophagus in order to replicate symptoms (Bernstein test) or 24-hour intra-oesophageal pH monitoring. Proton pump inhibitors are effective in the treatment of GERD, acting to reduce the acidity of the gastric juice and hence reduce oesophageal damage and symptoms associated with GERD. Symptoms most indicative of GERD are those associated with erosive oesophagitis, including heartburn and acid regurgitation. Less common GERD-associated symptoms include chest pain, a range of ear, nose and throat conditions, and asthma. In contrast to perceptions of the disease as 'merely' heartburn, the impact on patients' quality of life can be profound. Increasing awareness of GERD by health care professionals has led to improved diagnosis and a greater appreciation of the need for maintenance therapy.
 ...
PMID:Gastroesophageal reflux disease: clinical features. 1634 49

Gastro-oesophageal reflux disease (GERD) covers a broad range of signs and symptoms arising from the orad movement of gastric contents into the oesophagus, oropharynx, larynx or airway. Most commonly, contact with and damage to the oesophageal epithelium by acidic refluxate causes micro or macroscopic defects leading to the symptom of heartburn. However, GERD can also give rise to extra-oesophageal manifestations such as pharyngitis, laryngitis, asthma and other disorders, identifiable as acid-mediated events by a favorable response to acid suppression. Only one-third of individuals with heartburn have endoscopic evidence of erosive oesophagitis; the remainder have endoscopy-negative or non-erosive reflux disease (NERD). Improved investigative technologies are increasing our understanding of the pathophysiology of NERD. For example, although a number of microscopic abnormalities have been identified, oesophageal damage in NERD has been shown to be characterized by the presence of 'dilated intercellular spaces' within oesophageal stratified squamous epithelium. Dilated intercellular spaces that reflect damage to the intercellular junctions enable levels of acidity that would be considered innocuous when present in the oesophageal lumen to initiate pathological responses within oesophageal nociceptors when present within the intercellular spaces. This effectively gives rise to the symptom of heartburn. Excessive acidity within the intercellular spaces in NERD also presages its evolution to erosive disease, the latter through inflammation-mediated disruption of the antireflux and luminal clearance mechanisms. Support for this scenario is evident by the ability of effective acid control with proton pump inhibitors both to control symptoms, and lead to resolution of dilated intercellular spaces in patients with both erosive and non-erosive disease. This article examines these concepts and how they shape our current understanding of GERD.
 ...
PMID:Current understanding of the mechanisms of gastro-oesophageal reflux disease. 1686 42


<< Previous 1 2 3 4 Next >>