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)

The incidence of esophageal adenocarcinoma in the United States is rising at an epidemic rate. Although the cause for this rapid rise is unclear, it is well established that nearly all cases of esophageal adenocarcinoma arise from a premalignant lesion of the esophagus, known as Barrett's esophagus. Although Barrett's esophagus is recognized as a precursor lesion, the etiology, prevalence, and malignant risk of this lesion remain unclear. The relatively short, two-decade time frame for the rise in esophageal adenocarcinoma incidence and the increase across populations is a strong argument for environmental factors as etiological agents, perhaps interacting with genetically determined characteristics that define personal susceptibility. Because of the strong link between Barrett's esophagus and esophageal adenocarcinoma and the link between Barrett's esophagus and gastroesophageal reflux disease, risk factors for gastroesophageal reflux disease have been the prime suspects offered as possible explanations for the rise in esophageal adenocarcinoma. A plethora of hypotheses have been advanced, implicating tobacco and alcohol consumption, changes in obesity and diet, and the changing pattern in use of medications that affect the upper gastrointestinal tract. The following text will review what is currently known about the epidemiology of Barrett's metaplasia, its risk for malignant transformation, and the proposed theories of etiogenesis.
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PMID:Etiology of Barrett's metaplasia and esophageal adenocarcinoma. 952 45

Barrett's oesophagus is the eponym applied to the columnar epithelium-lined lower oesophagus which is acquired as a complication of chronic gastro-oesophageal reflux (GER). Various complications seen in the Barrett's oesophagus, such as peptic ulcer, stricture, adenocarcinoma are named as Barrett's ulcer, Barrett's stricture-and Barrett's carcinoma, respectively. It is now generally accepted that Barrett's oesophagus is an acquired condition resulting from chronic repetitive GER. The frequency of Barrett's oesophagus seems to be higher in Caucasian than in Oriental or Negro populations. There is a tendency towards increasing prevalence rates all over the world, including Taiwan, due to the Westernization of diet, rapid growth in the elderly population, obesity etc. Almost 6% of the patients who manifest heartburn in GI clinics in Taiwan now suffer from GER, which is almost similar to the 7% reported by Nabel, (USA) in 1976. During the last 30 years, the incidence of esophageal adenocarcinoma has increased rapidly. Patients with Barrett's oesophagus have an increased risk of developing oesophageal adenocarcinoma and should be kept under surveillance. Regular follow-up, at least twice a year or preferably, every 2-3 months, for those patients with SCE using endoscopic surveillance and biopsy for those with severe dysphasia (oesophageal columnar intraepithelial neoplasia) in the surrounding area to detect Barrett's oesophagus cancer, is very important.
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PMID:Review: Barrett's oesophagus in Taiwan. 919 7

A series of 98 laparoscopic fundoplications, included 7 cases (7.1%) of recurrent gastro-oesophageal reflux. Six of these cases occurred within 12 months of surgery. Four were successfully treated by a second laparoscopic procedure. The mean interval between the initial and corrective operations was 10 months. Factors related to failure were: technical errors, operative inexperience, obesity and the size of the hiatus hernia (when crural closure was not performed). Laparoscopic re-operation to was relatively easy and without mortality but had an increased risk of pleural effusions. The mean length of hospital stay for re-operations was identical to that of initial operations (4 days). No further recurrences were noted after a mean follow-up of one year (280-475 days). We conclude that early failures following laparoscopic fundoplication can be effectively dealt with laparoscopic surgery.
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PMID:[Laparoscopic correction of recurrent gastro-esophageal reflux following laparoscopic fundoplication (4 cases)]. 940 61

To explore the potential contributions of gastroesophageal reflux disease, as opposed to Helicobacter pylori infection, to the development of gastric carditis, we evaluated gastric carditis (using the criteria of the updated Sydney system for the classification of gastritis), clinical and morphologic features of esophagitis, and H. pylori infection (evaluation of Steiner stains) in biopsy specimens from the gastroesophageal squamocolumnar junction. We correlated clinical, endoscopic, and histologic features in an unselected group of 116 patients. Some degree of carditis was found in 107 (92%) of the patients. The mean age of the patients increased with increasing severity of carditis (P < .05). The various groups of patients with different degrees of carditis did not differ significantly in sex ratio, ethnic background, presence of obesity, percentage having symptoms of gastroesophageal reflux disease (such as heartburn, regurgitation, dysphagia, or odynophagia), endoscopic evidence of esophagitis and columnar epithelium in the distal esophagus, or histologic evidence of active esophagitis. The presence, however, of active gastritis and H. pylori infection in the distal stomach and/or in the cardia was significantly associated with carditis. In patients without carditis, H. pylori was not detected in any cardiac or distal gastric biopsy specimen. In contrast, H. pylori was demonstrated in gastric tissue samples (either from the cardia or distally) of patients with carditis, with the prevalence rate increasing with greater degrees of cardiac inflammation. The H. pylori prevalence rate was 12% in the group with mild carditis, 40% in those with moderate carditis, and 57% in patients with marked carditis (P = .0001). In summary, carditis is commonly found in patients with symptoms related to upper gastrointestinal diseases. From analysis of our study cohort, we concluded that carditis was significantly associated with H. pylori infection and active gastritis but not with symptoms or signs of gastroesophageal reflux disease. These findings suggest that carditis with histologic features similar to those of gastritis in the distal stomach was a sequel of H. pylori infection and represented a part of an H. pylori--associated gastric inflammation.
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PMID:Gastroesophageal reflux disease versus Helicobacter pylori infection as the cause of gastric carditis. 979 21

The authors studied the relationship of endoscopic esophagitis and gastroesophageal flap valve (GEFV) in patients with symptomatic gastroesophageal reflux (GER). On endoscopy, the GEFV was graded as I to IV in 138 patients with acid regurgitation and heartburn relieved by antacids, and in 54 control subjects without symptoms suggestive of GER. Grade of GEFV was correlated with the grade of esophagitis, response to medical treatment, duration of symptoms, obesity, smoking, sex, and age of the patient. Abnormal GEFV (grades III and IV) was more frequent in patients with symptomatic GER, both with and without esophagitis, compared with control subjects (p = 0.000001. p = 0.03). Abnormal GEFV was significantly more common in patients with GER with esophagitis compared with those without (p < 0.00001). There was no significant difference in the distribution of normal and abnormal GEFV in patients with grade I esophagitis. However, grade 2 and grade 3 esophagitis were associated more commonly with an abnormal GEFV (p < 0.00001, p < 0.02 respectively). Hiatal hernia is always associated with an abnormal GEFV. Abnormal GEFV correlated significantly with age (more frequent when older than 40 years). Sex, duration of symptoms (>3 years), response to medical therapy, smoking, and obesity (body mass index > 30 kg/m2) did not correlate significantly with abnormal GEFV. We conclude that endoscopic esophagitis is usually associated with abnormal GEFV. It is more frequent in grades 2 and 3 but not grade 1 esophagitis. It is also encountered more commonly after the age of 40 years.
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PMID:Endoscopic esophagitis and gastroesophageal flap valve. 1019 2

Obesity, or the presence of a body mass index exceeding 30 kg/m2, has assumed epidemic proportions in the United States. More than a cosmetic issue, obesity is associated with many comorbidities that contribute to multiple organ dysfunction, illness, and shortened life span. This review covers new and emerging information on the relationship of obesity to common and debilitating hepatic and gastrointestinal disorders, including nonalcoholic steatohepatitis, gastroesophageal reflux, gallstones, and increased risk of colon cancer. Understanding the role of obesity in these disorders should lead to new insights into the pathogenesis of common liver and gastrointestinal diseases and to new treatment strategies for the practicing gastroenterologist.
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PMID:Obesity: effects on the liver and gastrointestinal system. 1058 86

We have developed mathematical models to estimate the risk of perioperative adverse events in patients with pre-existing conditions undergoing day-case surgery. We studied 17,638 consecutive day-case surgical patients in a prospective study. Preoperative, intraoperative and postoperative data were collected. Risk modelling was performed with backward stepwise multiple logistic regression and validated on a separate subset of our patients. Eighteen pre-existing conditions were entered into the model. We adjusted for age, sex, and duration and type of surgery. Seven associations between pre-existing medical conditions and perioperative adverse events were statistically significant. Hypertension predicted the occurrence of any intraoperative event and intraoperative cardiovascular events. Obesity predicted intraoperative and postoperative respiratory events, and smoking and asthma predicted postoperative respiratory events. Gastro-oesophageal reflux predicted intubation-related events. The presented models of risk estimation were validated internally and provided a useful tool for accurate risk estimation.
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PMID:Pre-existing medical conditions as predictors of adverse events in day-case surgery. 1061 41

Barrett's metaplasia develops in 6% to 14% of individuals with gastroesophageal reflux. Barrett's adenocarcinomas are increasing in epidemic proportions for, as yet unknown, reasons; approximately 0.5% to 1% of patients with Barrett's metaplasia develop adenocarcinoma. Heartburn duration and frequency (but not severity), male gender, and white race are major risk factors for developing cancer. Obesity and smoking are weak risk factors. Survival is determined by depth of tumor invasion (stage). Once invasion of the muscularis propria occurs, most patients have developed widespread metastasis, even when clinical staging studies are negative. No currently available therapy results in prolonged survival once metastases develop. Thus, the more widespread use of effective surveillance strategies is the only currently available means for reducing the morbidity and mortality associated with Barrett's adenocarcinoma.
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PMID:Barrett's esophagus. Reducing the risk of progression to adenocarcinoma. 1069 10

Increased esophageal acid exposure in gastroesophageal reflux disease has several potential causes, some related primarily to physiological dysfunction of the LES and others related to anatomic distortion of the gastroesophageal junction as occurs with hiatus hernia. One attractive feature of implicating hiatal hernias in the pathogenesis of reflux disease is that, like reflux disease, axial hernias become more common with age and obesity. However, the importance of hiatus hernia is obscured by imprecise definition and an all-or-none conceptualization that has led to wide variation in estimates of prevalence among normal or diseased populations. There are at least three potentially significant radiographic features of a hiatus hernia: axial length during distention, axial length at rest, and competence of the diaphragmatic hiatus. Although any or all of these features may be abnormal in a particular instance of hiatus hernia, each is of different functional significance. Grouping all abnormalities of the gastroesophageal junction as "hiatus hernia" without detailing the specifics of each case defies logic. Mechanistically, the gastroesophageal junction must protect against reflux both in static and dynamic conditions. During abrupt increases in intra-abdominal pressure, the crural diaphragm normally serves as a "second sphincter," and this mechanism is substantially impaired in individuals with a gaping hiatus. Large, non-reducing hernias also impair the process of esophageal emptying, thereby prolonging acid clearance time following a reflux event (especially while in the supine posture). These anatomically-determined functional impairments of the gastroesophageal junction lead to increased esophageal acid exposure. Thus, although hiatus hernia may or may not be an initiating factor at the inception of reflux disease, it clearly can act as a sustaining factor accounting for the frequently observed chronicity of the disease.
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PMID:The role of hiatus hernia in GERD. 1078 May 71

In a Swedish nationwide case-control study, gastroesophageal reflux and obesity were identified as strong and independent risk factors for esophageal adenocarcinoma. A moderately strong association was found with adenocarcinoma of the gastric cardia. No significant association was found with squamous cell carcinoma of the esophagus. With increasing duration and severity of reflux symptoms and with increasing body mass index (BMI) the risk increased in a dose-dependent manner. When combined, reflux symptoms and obesity entailed greatly increased risk estimates, with relative risks exceeding 100 compared with persons with neither reflux symptoms nor obesity. However, because adenocarcinoma of the esophagus and gastric cardia are rarities, the absolute risk of developing these tumors was still not high. Our calculations revealed that even in the group with the highest risk, endoscopic surveillance is not readily recommended. Possible reasons for the increasing incidence of adenocarcinoma of the esophagus include 1) a suspected increase in the prevalence of reflux disease; 2) the increasing prevalence of obesity reported in western populations; and 3) the widespread use of medications that relax the lower esophageal sphincter and might cause reflux. All of these hypotheses suffer from inconsistencies that need to be solved before any firm conclusions can be drawn concerning the reasons for the increasing incidence of esophageal adenocarcinoma.
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PMID:[Increased incidence of adenocarcinoma of the esophagus and cardia. Reflux and obesity are strong and independent risk factors according to the SECC study]. 1082 53


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