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)

Intrinsic asthma, defined as asthma which is not from allergy to pneumo-allergens, of cause unknown, may show several etiologies. Allergics, remembering that there in some subjects there may be small amounts of IgE on the mastocytes, with specific RAST IgE negative, skin tests only weakly positive, but with a positive provocation test to pneumo-allergens. Food allergy, isolated and associated, may also contribute a not-negligible cause. Non-allergics, responding to the frequent triggering factors: Gastro-oesophageal reflux; Neuro-endocrine origin; Infections; Physical origin (exercise). In our study, we quote two types of extremely severe asthma, linked to intolerance to aspirin and metabisulfites with others that are associated.
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PMID:[Must the concept of intrinsic asthma be supported?]. 307 65

The authors reviewed 64 jejunostomies performed in 57 patients. Data were collected regarding complications and performance of the catheters. Patient diagnoses were grouped as follows: cystic fibrosis (25), neurological impairment (14), and miscellaneous other (25). Indications were malnutrition (43), inability to feed (17), and gastroesophageal reflux (4). Complications were compared between these groups. The age range was 7 days to 23 years. There were 251 tube changes over 142 years of cumulative site patency, for an average of 1.8 tube changes per year and an average life of 2.2 +/- 2.4 years per site. The longest duration was 11.7 years. Four tube changes resulted in intraperitoneal insertion (6.2% of changes). The overall complication rate was 37.5%. The major and minor complication rates were 21.9% each. Some patients had more than one complication. Stratification of complications by diagnosis showed that the highest incidence was among the neurologically impaired children (64%), followed by those with cystic fibrosis (32%) and then others (28%). Sixty-four percent of major and 54% of minor complications occurred within the first 6 months. The mortality rate was 4.7%. Infections requiring intravenous antibiotics occurred in 9.4% of the sites, at an average site age of 8.7 +/- 7.7 months. Tube dislodgment requiring surgical replacement occurred in 9.4% of the patients. Our mortality and complication rates compare favorably to those of previously reported series. Surgical jejunostomy is a reliable long-term solution to feeding but is associated with a significant risk of complications, especially in neurologically impaired children. The risk is greatest in the first 6 months after insertion, then decreases as the site "matures."
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PMID:Complications of long-term jejunostomy in children. 878 4

Cancer of the distal stomach, both of the intestinal and diffuse type, is strongly associated with Helicobacter pylori colonization. This bacterium causes chronic active inflammation of the gastric mucosa in the majority of colonized subjects. In a considerable number of them, this will eventually lead to a loss of gastric glands, and thus the establishment of atrophic gastritis, which is associated with the development of intestinal metaplasia and dysplasia. Development of atrophy and metaplasia of the gastric mucosa are thus strongly associated with H. pylori infection, instead of a direct and inevitable consequence of ageing. Approximately 40-50% of infected subjects develop these conditions, but they are rare in non-infected subjects. The presence of these consecutive disorders leads to a 5-90-fold increased risk for cancer of the distal stomach, in particular of the intestinal type. This sequence explains the increased risk for gastric cancer in H. pylori-infected subjects, as has been shown in various cross-sectional and longitudinal studies. In a combined analysis of three longitudinal studies, a significant trend was observed towards an increased odds ratio with longer intervals between (retrospective) serological diagnosis of H. pylori infection and observation of gastric cancer, this risk being more than eight-fold increased if the interval had been at least 15 years. This is thought to reflect development of atrophic gastritis and intestinal metaplasia with loss of H. pylori colonization in the years prior to development of cancer. Atrophic gastritis and gastric cancer thus appear closely associated with the presence of H. pylori, yet not all infected subjects will eventually develop atrophy and only a small minority develop gastric cancer. Factors that influence the risks for atrophy and cancer in the presence of infection may be related to the time that infection occurred and to characteristics of the bacterial strain and the host. Evidence for the role of these factors is now increasing. Recognition of the causal role of H. pylori in the induction of gastric cancer theoretically presents tools for cancer prevention. The efficacy of screening and bacterial eradication for prevention of distal gastric cancer is being studied in a number of large-scale intervention studies in different populations. It is hoped that these studies will also provide answers to the potential preventive role of H. pylori colonization in the development of gastro-oesophageal reflux disease and associated conditions, in particular development of cancer of the proximal stomach. Infection with H. pylori plays an important role in the aetiology of atrophic gastritis and gastric cancer. Studies suggest an eight-fold increased risk for both conditions in the presence of infection. Factors that influence the risk for both conditions in the presence of infection are the age at which infection occurred and the presence of cagA as a marker for more pathogenetic H. pylori strains. The efficacy and side-effects of intervention for the prevention of distal gastric cancer has yet to be established.
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PMID:Review article: exploring the link between Helicobacter pylori and gastric cancer. 1020 81

The Expert Panel Report 2. Guidelines for the Diagnosis and Management of Asthma (1) begins its section on controlling factors that precipitate or worsen asthma with the statement: "For successful long-term asthma management, it is essential to identify and reduce exposures to relevant allergens and irritants and to control other factors that have been shown to increase asthma symptoms and/or precipitate asthma exacerbations." The presence of allergy to indoor allergens and certain seasonal fungal spores has been found to be a risk factor for asthma in epidemiologic studies around the world. Generally between 70% and 85% of asthmatic populations studied have been reported to have positive skin-prick tests. Exposure of allergic patients to inhalant allergens increases airway inflammation, airway hyper-responsiveness, asthma symptoms, need for medication, severe attacks, and even death due to asthma. Environmental tobacco smoke exposure has been shown to increase the prevalence of childhood asthma and to increase asthma symptoms and bronchial hyperresponsiveness while reducing pulmonary function in children chronically exposed. Exposure to other indoor irritants, largely products of unvented combustion, has also been found to increase asthma symptoms. Outdoor air pollution increases asthma symptoms; levels of specific pollutants correlate with emergency room visits and hospitalization for asthma. Rhinitis/sinusitis and gastroesophageal reflux are commonly associated with asthma, and treatment of these conditions has been shown to improve asthma. In patients sensitive to aspirin and nonsteroidal anti-inflammatory drugs or metabisulfites, exposure to these agents can precipitate severe attacks of asthma. Viral infections are common causes for exacerbations of asthma. Infections with Mycoplasma pneumoniae and Chlamydia pneumoniae contribute to acute exacerbations and perhaps to long-term morbidity, as well. This chapter will discuss preventive and therapeutic measures that have been found effective in reducing the impact of aggravating or precipitating factors in patients with asthma.
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PMID:Allergen and irritant control: importance and implementation. 1068 68

Infection with Helicobacter pylori is accepted as the primary cause of peptic ulcer disease, and there is evidence to suggest its role in other gastrointestinal disorders. An estimated 20% to 40% of the Canadian population is infected with H pylori; however, clinically relevant disease is present in only approximately 10% to 20% of these individuals. Therefore, it is crucial to identify the diseases for which eradication of H pylori is beneficial to ensure that patients do not receive unnecessary treatment. In patients with ulcers induced by long term treatment with nonsteroidal anti-inflammatory drugs, preliminary results suggest that eradication of H pylori may reduce the risk of peptic ulcer bleeding. Furthermore, a benefit has been observed for the eradication of H pylori before patients commence therapy with a nonsteroidal anti-inflammatory drug. An association between the presence of H pylori and specific dyspeptic symptoms has yet to be established; however, there may be a subset of patients with functional dyspepsia who benefit from the eradication of H pylori. The relationship between gastroesophageal reflux disorder and H pylori infection remains unclear. In Canada, the recommended therapy for the eradication of H pylori is seven days of twice-daily treatment with a proton pump inhibitor, clarithromycin, and amoxicillin or metronidazole. Although the proton pump inhibitors are treated as a class for use in these regimens, there is suggestion that a faster onset of action may lead to a higher rate of eradication.
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PMID:Update on the role of H pylori infection in gastrointestinal disorders. 1133 27

Helicobacter pylori, the most common source of chronic infection worldwide, is a principal aetiological agent of type B gastritis, gastric and duodenal ulcers, and mucosa-associated lymphoid tissue lymphomas; the presence of this pathogen is also associated with gastric carcinoma. Infection with H. pylori is prevalent in patients with gastro-oesophageal reflux disease (GORD) even though it does not appear to play an important role in GORD pathophysiology. However, epidemiological studies have shown that colonization with cagA-positive H. pylori provides significant protection against the development of GORD and its long-term complications. Whereas clinical trial results indicate that the presence of H. pylori has little influence on the effectiveness of antisecretory therapy with a proton pump inhibitor (PPI) in patients with GORD, the meta-analysis of results from long-term studies suggests that risk of GORD relapse may be reduced in the presence of H. pylori infection. Several investigators have raised concerns about increased risk for gastric neoplasia in H. pylori-positive patients treated with PPIs. However, long-term follow-up of such patients indicates neither significant risk of neoplasia nor accelerated development of gastric glandular atrophy. Thus, the excellent safety record of these compounds seems not to be compromised by the presence of H. pylori.
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PMID:Gastro-oesophageal reflux disease and Helicobacter pylori or gastro-oesophageal reflux disease from Helicobacter pylori? 1143 May 5

Gastric carcinoma is thought to develop via the actions of inducers and promoters of carcinogenesis. Tryptophan in charred fish or animal meat, ultraviolet rays, and irradiation, which damage genes of normal cells, have long been regarded as inducers of carcinoma, and agents such as alcohol, tobacco, aflatoxin, and nitrosoamine as promoters, with tobacco having both activities. The interaction between these environmental factors, principally diet, and Helicobacter pylori (Hp) is important in the genesis of gastric carcinoma. In this report, the histopathological feature of the Hp gastritis-carcinoma sequence is outlined, and the pathological characteristics of gastroesophageal reflux disease (GERD) and endoscopically negative reflux disease (ENRD) and the risk factors for lower esophageal carcinoma after Hp eradicated status in particular are discussed regarding aspects of cell cycle-associated factors. We conclude that (1) Infection with Hp increases the risk of gastric cancer in two histological phenotypes (i.e., diffuse undifferentiated type and intestinal differentiated type). Excessive cell replication and interrupting the mucus secretion mechanism may result in a large proportion of cells with genetic abnormalities. (2) Genetic alterations in gastric carcinogenesis may differ from those in colonic carcinogenesis. (3) The degree of GERD in Japanese patients is milder than that in patients from Western countries, although the incidence of GERD increases the status after successful eradication of Hp. It is also possible that accumulation of genetic abnormalities increases the number of cardiac and lower esophageal cancers. Investigation of cell cycle factors in GERD including ENRD can be expected to reveal the risk of carcinogenesis.
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PMID:Pathological issues of gastric and lower esophageal cancer: helicobacter pylori infection and its eradication. 1210 62

Helicobacter pylori is uniquely adapted to colonize the human stomach. Infection leads to a range of subclinical and clinical outcomes that depend on properties of the infecting strain, the host, and the environment. Eradication therapy is indicated for infected persons who develop peptic ulcer disease or gastric lymphoma or who are beginning long-term treatment with nonsteroidal anti-inflammatory drugs. However, treatment may worsen gastroesophageal reflux disease and increase the risk of esophageal cancer. H. pylori infections can be diagnosed noninvasively and can be eradicated with approximately 85% success by a variety of multidrug, 7-14-day regimens. Unfortunately, antibiotic resistance is affecting treatment effectiveness in the United States and abroad. A more complete understanding of the variation in H. pylori pathogenesis should lead to clearer recommendations about treatment for infected persons who have neither peptic ulcer disease nor gastric lymphoma.
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PMID:Helicobacter pylori: consensus and controversy. 1211 96

Infection with Helicobacter pylori strains harboring determinants of pathogenicity may lead to a strong inflammatory response in gastric mucosa. In this work, we examined the frequency of the cagA, vacA and iceA genotypes in H. pylori strains isolated from Brazilian patients and correlated these with the clinical manifestations. H. pylori was isolated from 165 patients [30 with non-ulcer dyspepsia cases (NUD); 93 peptic ulcer disease (PUD): 31 gastric ulcers (GU) and 62 duodenal ulcer disease (DU); 18 with erosive gastritis (EG); and 24 gastroesophageal reflux disease (GERD)]. Allelic variants of cagA, vacA and iceA were identified using the polymerase chain reaction. More than one H. pylori strain was detected in 28 cases (17%), and these were excluded from the statistical analysis. We were unable to confirm an association between iceA status and clinical outcome. There was a strong association between the genotype cagA-positive vacA s1 and PUD. However, logistic regression analysis showed that vacA s1 was the only predictive factor for PUD (OR=4.19; 95% CI 1.95-8.98). The presence of the less virulent strain vacA s2 was related to GERD (OR=8.59; 95% CI 2.85-25.91). Our results support the hypothesis that virulent strains may protect against the development of GERD.
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PMID:Clinical relevance of the cagA, vacA and iceA genotypes of Helicobacter pylori in Brazilian clinical isolates. 1273 89

Gastro-oesophageal reflux disease (GORD) and Helicobacter pylori infection are both common in Western countries. A recently published meta-analysis has shown an association between an absence of H. pylori infection and GORD symptoms. Infection with cagA-positive H. pylori strains is a causative factor for the development of duodenal ulcer and is a risk factor for gastric cancer. Data about a protective role of cagA-positive H. pylori strains against more severe reflux oesophagitis are documented in several studies, but questioned by some other studies. There is a need for further studies to clear the definite role of cagA-positive H. pylori strains in severe reflux oesophagitis and their possible effect on the development of Barrett's adenocarcinoma. The role of Helicobacter pylori in gastro-oesophageal reflux disease (GORD) is still discussed controversially. Different factors might be responsible for the remarkably heterogeneous results of previously performed studies (e.g. location, environmental factors and different virulence factors of H. pylori strains). A very recently published meta-analysis has shown a significant association between the absence of H. pylori infection and GORD symptoms, and a positive correlation between anti-H. pylori therapy and the occurrence of both de-novo and rebound/exacerbated GORD. The results of this meta-analysis are questioned by some authors because of single larger trials and geographical variations of the studies analysed. Data on the role of the cytotoxic-associated antigen (cagA)-positive H. pylori strains are contradictory. Several studies have provided evidence supporting the protecting role of cagA-positive H. pylori strains against GORD, but these results were not confirmed by all studies. A multitude of patients suffer from H. pylori infection and GORD, simultaneously. Therefore, further studies are needed to clearly answer the question whether infection with cagA-positive H. pylori strains, which bear a well-documented risk for gastric cancer and gastro-duodenal ulcer, is really helpful against more severe reflux oesophagitis and, in consequence, perhaps protective against Barrett's oesophagus and Barrett's adenocarcinoma.
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PMID:cagA-positive Helicobacter pylori strains and gastro-oesophageal reflux disease: still puzzling? 1520 76


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