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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histologic changes indicative of gastroesophageal reflux disease (GERD) are found on both sides of the squamocolumnar junction (Z-line). In the gastric cardia, inflammation is found as part of GERD in the absence of Helicobacter pylori or other causes of gastritis (carditis). The squamous mucosa is the location most likely to show inflammatory changes, such as neutrophils or eosinophils, close to the Z-line, whereas traditional reactive changes in the squamous mucosa are found only in biopsies taken at least 3 cm above the Z-line. Endoscopic criteria for GERD have a morphologic counterpart in capillary congestion and hemorrhage into the papillae, which have largely been ignored by pathologists as secondary to biopsy trauma. A biopsy protocol that maximizes the chances of detecting changes of GERD is suggested. The traditional definition of Barrett's esophagus as requiring 3 cm of glandular mucosa extending into the esophagus is no longer tenable. However, even the concept of short-segment Barrett's esophagus, in which less than 3 cm of intestinalized mucosa is present, often as tongues, is being challenged because random biopsies immediately distal to the Z-line may also show intestinal metaplasia when Barrett's esophagus is unsuspected endoscopically. Moreover, it is difficult or impossible to determine whether these changes indicate the earliest lesion of Barrett's esophagus or intestinal metaplasia in native cardiac mucosa. It is suggested that Barrett's esophagus be redefined as intestinal metaplasia in the lower esophagus. It is presently unclear whether patients with such minimal Barrett's epithelium are at increased risk for adenocarcinoma or require surveillance. Successful therapy for GERD results in healing of disease in squamous mucosa and may result in regression of Barrett's epithelium. In the stomach it may be associated with temporary regression of H. pylori and associated inflammation, migration of H. pylori into the oxyntic mucosa, hypertrophy and hyperplasia of parietal cells, and a variant of fundic gland polyps. Some patients may be at risk for accelerated atrophic gastritis if inflammation is present before therapy.
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PMID:The biopsy diagnosis of gastroesophageal reflux disease, "carditis," and Barrett's esophagus, and sequelae of therapy. 869 47

The effects of ethanol upon the gastrointestinal tract (mouth, pharynx, esophagus, stomach, duodenum, Oddi's sphincter, small bowel, colon and rectum) were reviewed. Several studies showed that the incidence of cancer in the mouth and pharynx is increased in alcoholics as a consequence of ethanol effects and probably those of other compounds found in liquors. The gastroesophageal reflux disease may be induced by alcohol since it reduces the pressure in the lower and the upper esophageal sphincter, as well as the extent of primary peristalsis. Several studies showed a strong correlation between esophageal cancer and alcohol abuse. The risk for developing this kind of tumour is significantly increased when alcohol abuse and smoking coexist. Alcoholism predisposes patients to Mallory-Weiss syndrome as well as to bleeding of esophageal varices Ethanol may affect gastric secretion, motility, and permeability. Some drugs acting upon the gastric alcohol-dehydrogenase are able to affect gastric absorption of ethanol. Eradication of Helicobacter pylori increases the activity of alcohol-dehydrogenase in the pyloric antrum. The effects of alcohol upon the gastric mucosa include caustic damage, retrograde diffusion of H+, and cytoprotection. This agent may cause an acute gastritis but it is probably not involved in chronic gastritis. Whether alcohol is a risk factor for ulcer or not is unknown. Some studies found an increased incidence of gastric cancer associated with consumption of beer, wine and vodka. Some authors reported a decreased pressure in Oddi's sphincter while others found it increased in association with the consumption of ethanol. The acute and the chronic consumption of alcohol may affect the structure of small bowel as well as the absorption of nutrients. Several studies reported a significant correlation between colorectal cancer and the chronic consumption of ethanol.
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PMID:[Ethanol and the gastrointestinal tract]. 872 88

Feeding problems, anorexia and vomiting are common in infants and children with chronic renal failure (CRF), and play a major role in the growth failure often found in this condition. However, the gastroenterological and nutritional aspects of CRF in children have received little attention, hence therapeutic interventions are usually empirical and often ineffective. Gastritis, duodenitis and peptic ulcer are often found in adults with CRF on regular haemodialysis and following renal transplantation. Despite persistent hypergastrinaemia, gastric acid secretion is decreased rather than increased in most of these patients, and active peptic disease appears to be promoted by the removal of the acid output inhibition (neutralisation of gastric acid by ammonia) that follows active treatment. Helicobacter pylori, on the other hand, does not seem to play a significant role in the pathogenesis of peptic disease in CRF. Gastro-oesophageal reflux has been found in about 70% of infants and children with CRF suffering from vomiting and feeding problems, and thus appears to be a major problem in these patients. In a number of symptomatic patients with CRF, gastric dysrhythmias and delayed gastric emptying have also been found; hence there appears to be a complex disorder of gastrointestinal motility in CRF. Serum levels of several polypeptide hormones involved in the modulation of gastrointestinal motility [e.g. gastrin, cholecystokinin (CCK), neurotensin] and the regulation of hunger and satiety (e.g. glucagon, CCK) are significantly raised as a consequence of renal insufficiency, and can be reverted to normal by renal transplantation. Furthermore, several other humoral abnormalities (e.g. hypercalcaemia, hypokalaemia, acidosis, etc.) are not uncommon in CRF. By directly affecting the smooth muscle of the gut or stimulating particular areas within the central nervous system, all these humoral alterations may well play a major role in the gastrointestinal dysmotility, anorexia, nausea and vomiting in patients with CRF. Specific pharmacological and nutritional interventions should thus be considered for the treatment of vomiting and feeding problems in CRF.
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PMID:Gastrointestinal function in chronic renal failure. 874 22

Helicobacter pylori is a microaerophilic, motile bacterium, especially adapted to life in the human stomach. The presence of H. pylori in the stomach is strongly associated with chronic gastritis and ulcer disease and is a risk factor for gastric cancers. The microorganism may be transmitted orally and has been detected in dental plaque, saliva, and feces, but the hypothesis that oral microflora may be a permanent reservoir of H. pylori is still controversial. A review of the literature suggests that the recovery of H. pylori in the mouth is probably intermittent, associated with gastroesophageal reflux but not with specific oral disease. Nonetheless, the PCR identification of oral H. pylori may become helpful, particularly in cases of gastritis or ulcer relapse after antimicrobial therapy. Eradication of oral H. pylori by local medication or periodontal procedures would rely on the precise identification of its ecological niche. Within family groups, prophylactic methods should be practiced to avoid oral carriage of H. pylori. The risk of iatrogenic transmission during dental care, however, is already circumscribed by standard professional hygiene procedures.
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PMID:Oral carriage of Helicobacter pylori: a review. 902 44

Efficacy of one-week triple antimicrobial therapy (bismuth, tinidazole, amoxicillin) as compared to the same drug combination given for 4 weeks was assessed in children with Helicobacter pylori (H. pylori) gastritis and non-ulcer dyspepsia. Twenty-six patients (group A) and 30 (group B) had one-week and four-week schedule, respectively. Eradication (absence of organism at endoscopy at least 1 month after ending treatment) was achieved in 84.6% of group A (22) and 83.3% of group B (25), with marked reduction of histological gastritis score in both groups. Among patients with eradicated H. pylori, symptoms improved significantly in 14 and 16 patients of group A and B, respectively, but were still present in 17 (8 group A, 9 group B). The latter showed gastroparesis and abnormal gastro-oesophageal reflux at a subsequent diagnostic work-up and improved with prokinetic therapy. In 3 patients of group A and 3 of group B, symptoms improved despite persistence of bacterium into the stomach. Finally, in 3 cases (1 group A, 2 group B) both symptoms and H. pylori infection were unchanged. At 6 month follow-up, symptoms were present in 7 patients (3 group A, 4 group B): 6 of them (3 group A, 3 group B) showed H. pylori gastritis at endoscopy. We conclude that in children with dyspepsia and H. pylori gastritis one-week triple antimicrobial schedule is effective in eradicating bacterium; however, detection of H. pylori gastritis in dyspeptic children does not invariably indicate a pathogenic role of the organism in these patients.
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PMID:Helicobacter pylori gastritis and non-ulcer dyspepsia in childhood. Efficacy of one-week triple antimicrobial therapy in eradicating the organism. 903 84

A prospective study was performed in 190 control subjects and in 236 patients with different degrees of endoscopic esophagitis in order to determine the prevalence of Helicobacter pylori infection at duodenal gastric and esophageal mucosa and its correlation with histological findings. All patients with pathologic gastroesophageal reflux had 24-h pH monitoring studies confirming the presence of acid reflux into the esophagus. Besides the endoscopic findings, biopsies were taken from the duodenal bulb, gastric antrum, gastric fundus and distal esophagus or at the specialized columnar epithelium in patients with Barrett's esophagus. Patients with pathological gastroesophageal reflux were divided into three groups: 55 with absence of endoscopic esophagitis (gastroesophageal reflux), 81 patients with erosive esophagitis and 100 patients with Barrett's esophagus. There was no H. pylori infection present at duodenal or esophageal mucosa or at the specialized columnar epithelium of the distal esophagus in any case. The prevalence of H. pylori infection at gastric antrum was similar in controls and in any group of patients with reflux disease (20-25% of H. pylori infection). No differences in age and sex distribution were seen. H. pylori infection at gastric fundus was very low (less than 5%). The presence of HP infections was correlated with the finding of chronic active superficial or athrophic gastritis while, in the absence of H. pylori infection, gastric mucosa was normal. In the presence of intestinal metaplasia, no H. pylori infection occurred. Based on these findings, it seems that there is no significant evidence for an important pathogenic role for H. pylori infection in the development of pathologic chronic gastroesophageal reflux, erosive esophagitis or Barrett's esophagus, and the presence of antral gastritis in patients with Barrett's esophagus is closely related to the presence of H. pylori infection, and probably not related to an increased duodenogastric reflux.
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PMID:Prevalence of Helicobacter pylori infection in 190 control subjects and in 236 patients with gastroesophageal reflux, erosive esophagitis or Barrett's esophagus. 907 72

The discovery of Helicobacter pylori has opened new opportunities in the management of gastrointestinal disorders, with the cure of chronic ulcer disease now being possible for the first time. The 1994 United States National Institutes of Health Consensus Conference recommended that patients with duodenal or gastric ulcers unrelated to the use of non-steroidal anti-inflammatory drugs (NSAID) should be given eradication therapy. These guidelines were refined at a conference held recently in Maastricht. The updated guidelines strongly recommend treatment in patients with duodenal or gastric ulcer disease, low-grade mucosa-associated lymphoid tissue (MALT) gastric lymphoma, gastritis with severe macro- or microscopic changes and after resection of early gastric cancer. Despite a lack of hard scientific evidence, the guidelines also suggest that eradication treatment is advisable in patients with unequivocally diagnosed functional dyspepsia, a family history of gastric cancer, long-term treatment with proton-pump inhibitors for gastro-oesophageal reflux disease (GORD), planned or existing NSAID treatment, after gastric surgery for ulcer or cancer, or if the patient wants to be treated. Many different therapeutic regimens have been used previously, but at present the best treatment is proton-pump inhibitor-based triple therapy, comprising a proton-pump inhibitor plus two drugs out of clarithromycin, a nitroimidazole and amoxycillin. One-week low-dose triple therapy cures 85-95% of infected patients.
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PMID:Management of Helicobacter pylori-related disorders. 2249 2

To investigate the prevalence and the significance of Helicobacter pylori duodenal colonization, endoscopic duodenal biopsies were performed in 168 children with chronic abdominal pain, gastroesophageal reflux, gastrointestinal bleeding, and malabsorption syndrome. Helicobacter pylori infection was detected in 68 children (40.4%): in 31 of them H. pylori was present in the gastric antrum, and in 37 in the duodenum also. Duodenitis was observed in 25 children with duodenal H. pylori; gastric metaplasia in 3. Scanning electron microscopy revealed the presence of the micro-organism in 3/13 cases; the bacteria were located in the intercellular spaces and alterations of the epithelial surface were found. In conclusion, H. pylori gastritis in children is often associated with duodenal colonization which can cause duodenitis, and also without gastric metaplasia, which indicates a possible role of the micro-organism in the pathogenesis of the lesions.
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PMID:Helicobacter pylori duodenal colonization in children. 917 19

The publication of the National Institutes of Health Consensus Development Conference guidelines on management of Helicobacter pylori infection in 1994 set a precedence. At present, at least eight European countries have produced national guidelines, and, more recently, the European Helicobacter pylori Study Group also outlined guidelines based on the strength of available evidence. It is generally agreed that H. pylori should be eradicated in peptic ulcer disease. In nonsteroidal anti-inflammatory drug (NSAID)-related ulcers, most countries that considered the issue suggested discontinuing NSAIDs when possible and eradicating H. pylori. The prophylactic eradication of H. pylori was not recommended. A number of panels felt that there was not enough evidence available to recommend eradication of H. pylori in functional dyspepsia, whereas other groups felt that nonulcer dyspepsia, particularly after investigation and with severe or recurrent symptoms, was an indication for eradication therapy. Other conditions (i.e., gastroesophageal reflux disease [GERD] and mucosa-associated lymphoid tissue [MALT] lymphoma) have emerged in this short time as possible indications for H. pylori eradication. There is no evidence that H. pylori infection has a role in the pathogenesis of GERD, but there is evidence suggesting that patients with H. pylori infection who require long-term acid suppression may be at risk of developing atrophic gastritis. The European Helicobacter pylori Study Group has suggested that eradication therapy should be offered to infected family members of patients with gastric cancer. It also recommended that eradication therapy was "strongly recommended" on the basis of "supportive" evidence in gastritis with severe abnormalities and after early resection of early gastric cancer. An "uncertain" recommendation with "equivocal" evidence was given for asymptomatic subjects, extra-alimentary tract disease, the prevention of gastric cancer in the absence of risk factors, and in pediatric patients with recurrent abdominal pain. Despite considerable advances, further research studies are needed to provide definite direction for the treatment of many conditions.
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PMID:Who should be treated for Helicobacter pylori infection? A review of consensus conferences and guidelines. 939 69

In order to gain further knowledge about the clinical and endoscopic features of chronic gastritis (CG) associated with Helicobacter pylori (H py) we retrospectively analyzed 81 pediatric cases. All were biopsy-proven. The cases were divided in two groups: Group (1988-1992) included 21 cases. These represented the early stage of clinical recognition of the disease. Group 2(1993-1995) comprised 60 cases and represents the stage in which the disease was mandatory. Mean number of cases/year was 4.2 and 20 for group 1 and 2, respectively. Recurrent abdominal pain (RAP) was the most frequent clinical symptom (74/81; 91%), followed by upper digestive tract hemorrhage (UDTG) (34/81; 41.9%). The combination gastroesophageal reflux (GER) and esophagitis (E) was found in 52/81 (64.2%) of the children. Endoscopically, granularity of the mucosa was more frequently found in cases with RAP (47/74), GER (28/36) and E, while a smooth mucosa predominated in patients with UDTH (23/34). Our findings strongly suggest that symptomatic CG with H py in children expresses peculiar clinical and endoscopic features. Since RAP was present in 91% of the cases it appears adequate to include this disease in the differential diagnosis of it. These clinical manifestations have not been previously linked to CG with H py. Better understanding of the clinical and endoscopic spectrum of CG with H py results in adequate treatments and possibly prevention of gastric (and esophageal) diseases found in adults.
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PMID:[Clinico-endoscopic spectrum of gastritis associated with Helicobacter pylori in pediatrics]. 941 43


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