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

The role of Helicobacter pylori infection in the control of lower esophageal sphincter (LES) motility, especially the occurrence of transient LES relaxations (TLESRs), was studied in eight H. pylori-positive and eight H. pylori-negative healthy subjects. During endoscopy, biopsy specimens were taken from the cardia, fundus, and antrum for determinations of H. pylori status, gastritis, and proinflammatory cytokine mucosal concentrations. LES motility was monitored during three different 30-min periods: baseline, gastric distension (barostat), and gastric distension with CCK infusion. Gastric distension significantly increased the TLESR rate, whereas CCK increased the rate of distension-induced TLESRs further and reduced resting LES pressure without significant differences between infected and noninfected subjects. H. pylori status did not influence resting LES pressure or gastric compliance. Cytokine mucosal concentrations were increased in infected patients, but no correlation was found with the TLESR rate, which was also independent of inflammation at the cardia, fundus, and antrum. These results suggest that H. pylori-associated inflammation does not affect the motor events involved in the pathogenesis of gastroesophageal reflux.
 ...
PMID:H. pylori and transient lower esophageal sphincter relaxations induced by gastric distension in healthy humans. 1144 14

We systematically reviewed the literature on gastroesophageal reflux disease (GERD) related to Helicobacter pylori therapy, and classified the GERD according to various aspects. Preexisting GERD is active GERD before H. pylori therapy, and a substantial proportion of the GERD patients improve after successful H. pylori therapy. If the GERD does not persist or recur after cessation of acid-suppressive therapy combined with H. pylori therapy, it may have been cured (cured GERD). If it recurs, it may have been masked by acid-suppressive therapy and unmasked with cessation of the therapy (pharmacologically masked and unmasked GERD). Newly developed GERD after successful H. pylori therapy is a kind of unmasked GERD arising after cure of infection (de novo unmasked GERD). The possible mechanism of the improvement of cured GERD is normalized hyperacidity associated with an improved cytokine-somatostatin-gastrin system followed by normalized G-cell activity and parietal cell mass. Preexisting GERD is not a reason to avoid eradication therapy. De novo unmasked GERD develops in a substantial proportion of patients with cured infection. The possible mechanism is increased acid exposure in the esophagus due to gastric acid increase, which is caused by a loss of neutralizing effect by ammonia, normalized cytokine-acid suppression and improvement of corpus atrophy. De novo unmasked GERD is important because GERD is recurrent and may induce adenocarcinoma of the esophagus. However, it is expected that cure of infection lowers gastric cancer incidence. Eradication therapy is recommended irrespective of the possibility that de novo unmasked GERD may have a slight increase of the risk of esophageal adenocarcinoma.
 ...
PMID:Active and inactive gastroesophageal reflux diseases related to Helicobacter pylori therapy. 1295 Jun

The relationship between bronchial asthma (BA) and gastro-esophageal reflux (GER) impose to study by frequency, reciprocally prognosis and therapeutics difficulty. Coexistence of both diseases is suggested by presence of asthmatics symptoms in non-atopic patients, difficult control and resistance of the specific treatment of asthma disease, worsening of respiratory symptoms in circumstances which favored GER. Pathogenetic relationship between BA and GER in children is the result of the associations- digestive particularity and: esophago-bronchial neurogenic mechanism produced by micro-aspiration , genetic or obtained inflammations development by commune Th2 mediators, medications effects. Classical treatments (H2-inhibitors, prokinetics agents, inhibitors of protonic pumps) is associated of the antiasthmatics "controller" therapy and in the future, anti-cytokine and anti-receptor therapy.
 ...
PMID:[Pathogenic basis of treatment in children with bronchial asthma and gastroesophageal reflux]. 1600 11

Esophageal adenocarcinoma is increasing in incidence; it relates to chronic gastroesophageal reflux, it is difficult to cure, and treatment modalities increasingly use chemotherapy and radiation therapy prior to resectional surgery. Nuclear factor-kappa B (NF-kappaB) is a pleiotropic transcription factor that regulates several genes for cytokines and enzymes involved in inflammation and immunity, and we have previously described sequential expression of NF-kappaB from the normal esophagus through Barrett's metaplasia to adenocarcinoma. The aim of this exploratory study was to assess the NF-kappaB status and cytokine profiles pre- and post-chemoradiotherapy for esophageal adenocarcinoma. Fresh biopsy specimens obtained from 20 patients with esophageal adenocarcinoma and normal adjacent squamous epithelium were obtained pre-, during and post-chemoradiotherapy, and NF-kappaB expression was analyzed by electrophoretic mobility shift assay. The cytokine protein content of interleukin-1 beta (IL-1beta) and interleukin-8 (IL-8) of tissue homogenates was measured using the ELISA technique. NF-kappaB was constitutively activated in tumor tissues from esophageal adenocarcinoma but was not detected in adjacent normal esophageal mucosa. Elevated levels of IL-1beta and IL-8 were significantly (P < 0.05) higher in tumor tissues compared to control tissues. Patients with a major or complete pathological response (responders) were associated with absence of activated NF-kappaB from nuclear extracts after treatment. Moreover, IL-1beta and IL-8 levels were significantly (P < 0.05) down-regulated in tumor tissues from patients who demonstrated a complete pathological response. No differences in NF-kappaB, IL-1beta and IL-8 levels were detected pre- and post-treatment in patients who did not have a major or complete pathological response (non-responders). The study suggests that monitoring of molecular and cytokine patterns in patients undergoing this neoadjuvant regimen may help subselect the cohort that derives most benefit from the multimodal approach.
 ...
PMID:Activated nuclear factor-kappa B and cytokine profiles in the esophagus parallel tumor regression following neoadjuvant chemoradiotherapy. 1612 81

Idiopathic pulmonary fibrosis (IPF) is a chronic fibrosing lung disease limited to the lungs and associated with the histologic appearance of usual interstitial pneumonia (UIP) on surgical lung biopsy. The estimated prevalence in the United States is between 35,000 and 55,000 cases,and evidence suggests that the prevalence is increasing for IPF. Risk factors associated with pulmonary fibrosis include smoking, environmental exposures, gastroesophageal reflux dis-ease, commonly prescribed drugs, diabetes mellitus, infectious agents, and genetic factors. The diagnosis requires a careful history and physical examination, characteristic physiological and radiological studies, and, in some cases, a surgical lung biopsy. The natural history of IPF is not known, but evidence supports the concept of a continuum of idiopathic interstitial pneumonias that may overlap in time. Most patients with IPF succumb to respiratory failure, cardiovascular disease, lung cancer, pulmonary embolism, infection, and other health problems. The median survival time for patients with IPF is less than 3 yr. Factors that predict poor outcome include older age, male gender, severe dyspnea, history of cigarette smoking, severe loss of lung function, appearance and severity of fibrosis on radiological studies, lack of response to therapy,and prominent fibroblastic foci on histopathologic evaluation. Conventional therapy (corticosteroids, azathioprine, cyclophosphamide) provides only marginal benefit. Lung transplantation should be considered for patients with IPF refractory to medical therapy. In light of the poor prognosis and lack of response to available anti-inflammatory therapy, alternative approaches to therapy are being pursued. Emerging strategies to treat patients with IPF include agents that inhibit epithelial injury or enhance repair, anti-cytokine approaches, agents that inhibit fibroblast proliferation or induce fibroblast apoptosis, and other novel approaches.
 ...
PMID:Pulmonary fibrosis. 1613 Feb 30

We report the development and spontaneous resolution of annular erythematous skin lesions consistent with sarcoid dermatitis in a child with DiGeorge syndrome (DGS) carrying the 22q11.2 microdeletion. The skin lesion developed after she was treated with isoniazid (INH) following exposure to active tuberculosis (TB). After resolution of the skin lesions, this child developed sterile hyperplastic osteomyelitis consistent with SAPHO (synovitis, acne, pustulosis, hyperostosis, and osteitis) osteomyelitis in her right mandible triggered by an odontogenic infection. This child had congenital heart disease, dysmorphic facies, recurrent sinopulmonary infection, gastroesophageal reflux disease, scoliosis, reactive periostitis, and developmental delay. She had a low CD4 and CD8 T cell count with a normal 4/8 ratio, but normal cell proliferation and T cell cytokine production in response to mitogens. When she was presented with sterile osteomyelitis of right mandible, she revealed polyclonal hypergammaglobulinemia with elevated erythrocyte sedimentation rate (ESR)/angiotensin converting enzyme (ACE) levels, but negative CRP. Autoimmune and sarcoidosis workup was negative. Inflammatory parameters gradually normalized following resolution of odontogenic infection and with the use of non-steroidal anti-inflammatory drugs (NSAIDs). The broad clinical spectrum of DGS is further expanded with the development of autoimmune and inflammatory complications later in life. This case suggests that patients with the DGS can present with unusual sterile inflammatory lesions triggered by environmental factors, further broadening the clinical spectrum of this syndrome.
 ...
PMID:SAPHO osteomyelitis and sarcoid dermatitis in a patient with DiGeorge syndrome. 1649 84

The production of cytokines (MIG, IFN-gamma, TNF-alpha, IL-4, IL-5, and IL-10) was studied in 39 individuals, including 28 with chagasic esophagopathy and 11 nonchagasic patients with gastroesophageal reflux disease. A sandwich enzyme immunoassay employing monoclonal antibody pairs specific for each cytokine was used. IFN-gamma and MIG production was significantly higher in patients with megaesophagus compared to control. Furthermore, in the absence of stimulation TNF-alpha levels were lower in the chagasic group than in the control group. In addition, significantly lower TNF-alpha levels were observed for the advanced form of the disease compared to the nonadvanced form. These results support the hypothesis that, although patients with advanced phase of megaesophagus present low number of CD4+ T lymphocytes, PBMC from this patients are able to respond up specific antigen stimulation.
 ...
PMID:Evaluation of cytokines (MIG, IFN-gamma, TNF-alpha, IL-4, IL-5, and IL-10) during the different evolutive phases of chagasic esophagopathy. 1651 26

Obesity is a risk factor for being diagnosed with asthma, but there is conflicting evidence on whether obesity is a risk factor for lung function abnormalities characteristic of asthma. We studied a cohort of 488 subjects, 47% of whom were obese. Obese and non-obese subjects with asthma had similar airflow limitation and bronchodilator responsiveness, but obese participants had increased sleep disturbance and gastroesophageal reflux disease, higher cytokine levels, and a trend towards increased exacerbations when treated with theophylline. Obese and non-obese asthmatics have similar lung function abnormalities, but comorbidities and altered responses to medications may significantly affect asthma control in obese people.
 ...
PMID:Effect of obesity on clinical presentation and response to treatment in asthma. 1693 98

Recent studies have shown that esophageal mucosal inflammatory response is involved in the pathophysiology of gastro-esophageal reflux disease. The aim of the present study was to identify specific gene expression profiles of the esophageal mucosa in a rat model of combined-type chronic reflux esophagitis. Esophagogastroduodenal anastomosis was carried out in male Wistar rats by anastomosing the jejunum to the gastroesophageal junction under diethyl-ether inhalation anesthesia. Esophageal epithelial cells were obtained from esophagi of rats by laser capture microdissection. Preparation of cRNA and target hybridization were performed according to the Affymetrix GeneChip eukaryotic small sample target labeling assay protocol. The gene expression profile was evaluated by the rat toxicology U34 GeneChip. Array data analysis was carried out using Affymetrix GeneChip operating software, ingenuity pathway analysis software, and Gene Springs software. A comparison between esophagitis and sham-operated rats 2 weeks after the operation revealed that 368 probes (36%) were significantly affected, i.e. 185 probes were up-regulated, and 183 probes were down-regulated, both at levels of at least 1.5-fold in the esophagitis rats. Ingenuity signal analysis of 207 affected probes revealed the interleukin-6 signaling pathway as the most significantly affected caronical pathway. In addition, the expression of many genes associated with cytokine and transcription factor was enhanced in the esophagitis rats. This transcriptome approach provided insight into genes and putative genetic pathways thought to be affected by stimulation with gastroduodenal refluxates.
 ...
PMID:Inflammatory response of esophageal epithelium in combined-type esophagitis in rats: a transcriptome analysis. 1701 11

Differentiating eosinophilic esophagitis from gastroesophageal reflux disease is important given their pathogenetic differences and responses to therapy. Eotaxins are a family of chemokines important for activation and recruitment of eosinophils mediated by their receptor, chemokine receptor-3 (CCR-3). Interleukin 5 (IL-5) is a key cytokine involved in many steps of eosinophil production and recruitment. The aim of this study was to compare the messenger RNA expression of the eotaxins, CCR-3, and IL-5 between well-characterized groups of patients with eosinophilic esophagitis, patients with gastroesophageal reflux disease, and healthy individuals. This was a retrospective study using esophageal biopsies from 33 patients with eosinophilic esophagitis, 20 patients with gastroesophageal reflux disease, and 17 healthy controls. Parameters studied included demographic features, presenting symptoms, endoscopic findings, histopathologic features, and messenger RNA levels of eotaxins 1, 2, and 3, CCR-3, and IL-5 by quantitative real-time polymerase chain reaction using formalin-fixed, paraffin-embedded tissue. Patients with eosinophilic esophagitis were predominantly males (M/F=3:1), with a mean age of 15.9 years and a mean eosinophil count of 55 per x400 high-power field. Patients with gastroesophageal reflux disease had a mean age of 31.5 years and a mean eosinophil count of 5.8 per high-power field. Total intraepithelial eosinophil and lymphocyte counts, the presence of superficial eosinophil clusters, microabscesses, and basal cell hyperplasia were all significantly associated with eosinophilic esophagitis as opposed to gastroesophageal reflux disease (P<.0001). The mean expression levels of eotaxin-3 were markedly elevated in patients with eosinophilic esophagitis as compared with the gastroesophageal reflux disease and healthy control groups (731+/-276, 31+/-12, and 1.5+/-0.4 pg/ng beta-actin, respectively; P<.001). Mean expression levels of eotaxins 1 and 2, IL-5, and CCR-3 were also significantly increased in the patients with eosinophilic esophagitis, albeit at lower levels than eotaxin-3. In conclusion, our results highlight the important contribution of eotaxin-3 in the pathogenesis of eosinophilic esophagitis. Determination of eotaxin-3 levels by real-time polymerase chain reaction on paraffinized, formalin-fixed tissue may be a useful test in the differentiation of eosinophilic esophagitis from gastroesophageal reflux disease.
 ...
PMID:Increased expression of eotaxin-3 distinguishes between eosinophilic esophagitis and gastroesophageal reflux disease. 1790 Jun 56


1 2 3 4 5 Next >>