Disease relevance of Esophagitis

• METHODS: Patients with esophagitis and/or chronic GERD were enrolled; 155 patients were randomized to ARS and 155 to long-term omeprazole therapy [1].
• Children presented with symptoms suggestive of gastroesophageal reflux and esophagitis: vomiting, abdominal pain, odynophagia, dysphagia, and heartburn [2].
• Omeprazole heals esophagitis and relieves dysphagia more efficaciously than H2RA while decreasing costs to patients [3].
• METHODS: The case population consisted of all patients with erosive esophagitis (International Classification of Diseases code 530.1) or esophageal stricture (ICD code 530.3) who were discharged from hospitals of the Department of Veteran Affairs between 1981 and 1994 [4].
• Nutcracker esophagus and nonspecific contraction abnormalities were found in 7 patients, and gastroesophageal reflux with esophagitis and a low lower esophageal sphincter resting pressure was found in 1; only 3 patients had normal esophageal motility [5].

Psychiatry related information on Esophagitis

• Ranitidine therapy for esophagitis in children with developmental disabilities [6].

High impact information on Esophagitis

• Recommendations to reduce the risk of esophagitis include swallowing alendronate with 180 to 240 ml (6 to 8 oz) of water on arising in the morning, remaining upright for at least 30 minutes after swallowing the tablet and until the first food of the day has been ingested, and discontinuing the drug promptly if esophageal symptoms develop [7].
• Participants were then stratified according to their initial grade of esophagitis and randomly assigned to 12 months of treatment with one of the following: cisapride (10 mg three times a day), ranitidine (150 mg three times a day), omeprazole (20 mg per day), ranitidine plus cisapride (10 mg three times a day), or omeprazole plus cisapride [8].
• Doxycycline-induced esophagitis [9].
• Esophagitis related to cromolyn [10].
• Eotaxin-3 and a uniquely conserved gene-expression profile in eosinophilic esophagitis [11].

Chemical compound and disease context of Esophagitis

• We now report an original model of experimental esophagitis induced by exposure of mice to respiratory allergen [12].
• Esophagitis healing with ranitidine [13].
• Sucralfate was tested in a rabbit model for its ability to prevent experimental esophagitis [14].
• METHODS: Thirty-four dysphagic patients with peptic stricture and erosive esophagitis were dilated and randomized to omeprazole 20 mg every day versus H2RA (ranitidine 150 mg twice daily or famotidine 20 mg twice daily) [3].
• CONCLUSIONS: Fluconazole and itraconazole are provided with good long-term therapeutic efficacy in the treatment of Candida esophagitis in patients with AIDS [15].

Biological context of Esophagitis

• The animals were killed 16 weeks after operation or injection, the entire esophageal mucosa was harvested, and mutation frequency was determined through standard Big Blue Mutagenesis Assay. RESULTS: Gross esophagitis was evident in all operated animals [16].
• Their average number per high-power field was low in benign squamous epithelium away from tumors (average 0.8/high-power field) but much higher in biopsies with the other categories of histology, especially those with active esophagitis and infection (6.3/high-power field) [17].
• Similarly, EFS-induced but not ACh-induced muscle contraction decreased in esophagitis and after incubation in PGE2 and PAF C-16 [18].
• Compared with controls, repeated acid perfusion induced erosive esophagitis and significant esophageal shortening, associated with enhanced LM responses to carbachol, a significantly depolarized resting membrane potential, and abnormal spike patterns [19].
• As previously shown, refluxers with esophagitis also had more frequent acid gastroesophageal reflux and prolonged gastric emptying [20].

Anatomical context of Esophagitis

• The patients with erosive esophagitis also had significantly diminished lower esophageal sphincter pressures and increased frequency and duration of gastroesophageal reflux episodes [21].
• A 71-year-old woman experienced severe, acute esophagitis and severe stricture of the esophagus due to oral alendronate therapy [22].
• Also alendronate is far more damaging at acidic than at neutral pH, suggesting its association with esophagitis requires gastric acid for expression [23].
• Our objectives were to determine whether esophageal IELs express the recently described cytotoxic T-cell (CTLs) markers, TIA-1 and granzyme-B, and whether the number of CTLs correlates with well-defined endoscopic, clinical, and histological features of esophagitis [24].
• Routinely processed hematoxylin and eosin (H&E)-stained slides of esophageal mucosal biopsies from 14 patients with both active esophagitis and multinucleated epithelial giant cells were evaluated for a variety of inflammatory and epithelial features [25].

Gene context of Esophagitis

• There was also no significant increase in COX-2 expression in patients with esophagitis or in those who used nonsteroidal anti-inflammatory drugs [26].
• It is noteworthy, however, that the CDX2 mRNA expression was initiated at the stage of esophagitis, when neither CDX1 nor intestine-specific genes had emerged yet [27].
• All operated mice (6 ApcMin/+, 12 WT, and 4 Trp53-/-) had esophagitis, with squamous hyperplasia and early focal ulceration [28].
• Intratracheal IL-13 induces eosinophilic esophagitis by an IL-5, eotaxin-1, and STAT6-dependent mechanism [29].
• We investigated the roles of prostaglandin (PG) E2 and cyclooxygenase (COX) isoenzymes in the mucosal defense of the esophagus, using subtype-selective EP agonists and antagonists as well as various COX inhibitors, in an acute rat esophagitis model [30].

Analytical, diagnostic and therapeutic context of Esophagitis

• Sixty-two consecutive patients were studied who had chronic upper abdominal pain or nausea where endoscopy had shown no evidence of peptic ulceration, esophagitis, or malignancy; 47 had essential dyspepsia, and 15 had dyspepsia plus gastroesophageal reflux [31].
• To determine the value of bethanechol in the treatment of erosive esophagitis, a double-blind study was undertaken in which 28 patients were randomized to either bethanechol and antacid, or placebo and antacid [32].
• Two doses of omeprazole versus placebo in symptomatic erosive esophagitis: the U.S. Multicenter Study [33].
• CONCLUSIONS: Nissen fundoplication alleviated symptoms of gastroesophageal reflux and cured esophagitis in great majority of cases [34].
• Patients whose esophagitis healed or improved after sucralfate tended to have lower serum PG-I levels than those with treatment failure (104 +/- 35 ng/mL vs 125 +/- 45 ng/mL), whereas the opposite occurred in patients treated with cimetidine (132 +/- 58 ng/mL in responders vs 78 +/- 27 ng/mL in nonresponders, p = 0.048) [35].

References