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Barrett s esophagus

O GERD can be divided into three distinct categories erosive esophagitis, non-erosive reflux disease, and Barrett s esophagus. [Pg.257]

These symptoms may be indicative of complications of GERD such as Barrett s esophagus, esophageal strictures, or esophageal cancer. [Pg.260]

More specific diagnostic tests may be warranted in patients not responding to empiric (prescription) therapy, those with complicated or alarm symptoms (e.g., weight loss or dysphagia), or those with long-standing symptoms who are at risk for Barrett s esophagus. [Pg.261]

Upper gastrointestinal endoscopy is the preferred diagnostic test for assessing the mucosa for esophagitis and Barrett s esophagus.1 It enables visualization and biopsy of the esophageal mucosa. Endoscopy should be considered upon initial presentation in any patient who presents with complicated symptoms and those at risk for Barrett s esophagus.1... [Pg.261]

The PPIs are superior to H2RAs in patients with moderate to severe GERD. This includes not only patients with erosive esophagitis or complicated symptoms (Barrett s esophagus or strictures), but also those with non-erosive reflux disease who have moderate to severe symptoms. Symptomatic relief is seen in approximately 83% of patients and healing rates at 8 weeks as judged by endoscopy are 78%.1... [Pg.263]

Many patients with GERD relapse if medication is withdrawn, and long-term maintenance treatment is required in such patients.1 Candidates for maintenance therapy include patients whose symptoms return once therapy is discontinued or decreased, patients with complications such as Barrett s esophagus or strictures, and perhaps patients with atypical symptoms. [Pg.264]

Most infants have physiologic reflux with no clinical consequence.26 Complications, although rare, include distal esophagitis, failure to thrive, esophageal strictures, and Barrett s esophagus.27... [Pg.265]

FIGURE 15.4 Computer record of a two-dimensional capillary electrophoresis analysis of a protein homogenate prepared from ahiopsy obtained from the fundus of a Barrett s esophagus patient. The data were generated hy performing 1 s transfers between capillaries and a 9 s second-dimension separation. The first-dimension separation employed the same buffer as the CSE separation in Fig. 15.1 and the second-dimension separation employed the same buffer as the MECC separation in Fig. 15.1. [Pg.355]

This sample is a biopsy taken from the fundus of a patient with Barrett s esophagus under informed consent. The biopsy was fixed in 70% ethanol within 15 s of sampling and was homogenized within 5 min. It is possible to obtain the sample, process it, and complete the electrophoresis within 1 h. The biopsy is roughly 3 mm long, 1 mm wide and 500 pm deep. Its total protein content is 150 pg. This homogenate is prepared in 400 pL of solution and can be used for dozens of analyses. [Pg.358]

Barium radiography is less expensive than endoscopy but lacks the sensitivity and specificity needed to accurately determine the presence of mucosal injury or to distinguish Barrett s esophagus from esophagitis. Twenty-four-hour ambulatory pH monitoring is useful in patients who continue to have symptoms without evidence of esophageal damage, patients who are refractory to standard treatment, and patients who... [Pg.277]

Esophagus (biopsies from human Barrett s esophagus metaplastic tissue)... [Pg.53]

A number of observations (Table 3.6) indicate that tumours arise in an apoptosis-resistant pre-malignant cell population. Barrett s esophagus (BE) is a pre-malignant lesion of the distal esophagus in which squamous epithelial cells... [Pg.56]

P. C. Konturek, A. Nikiforuk, J. Kania, M. Raithel, E. G. Hahn and S. Muhldorfer, Activation of NFkappaB represents the central event in the neoplastic progression associated with Barrett s esophagus a possible link to the inflammation and over-expression of COX-2, PPARgamma and growth factors. Dig. Dis. Sci., 2004, 49(7-8), 1075. [Pg.64]

K. Dvorakova, C. M. Payne, L. Ramsey, H. Bernstein, H. Holubec, M. Chavarria, C. Bernstein, R. E. Sampliner, C. Riley, A. Prasad and H. Garewal, Apoptosis resistance in Barrett s esophagus ex vivo bioassay of live stressed tissues. Am. J. Gastroenterol, 2005, 100(2), 424. [Pg.65]

J. Dominguez, B. Dvorak, H. Bernstein, C. Bernstein, A. Prasad, R. Pass, H. Cui and H. Garewal, Increased expression and secretion of interleukin-6 in patients with Barrett s esophagus, Clin. Cancer Res., 2004,10(6), 2020. [Pg.65]

M. Menges, M. Muller and M. Zeitz, Increased acid and bile reflux in Barrett s esophagus compared to reflux esophagitis, and effect of proton pump inhibitor therapy. Am. J. Gastroenterol., 2001, 96(2), 331. [Pg.68]

H. J. Stein, W. K. Kauer, H. Feussner and J. R. Siewert, Bile reflux in benign and malignant Barrett s esophagus effect of medical acid suppression and nissen fundoplication, J. Gastrointest. Surg., 1998, 2(4), 333. [Pg.68]

Type I tumor Adenocarcinoma of the distal esophagus, which usually arises from an area with specialized intestinal metaplasia of the esophagus (i.e., Barrett s esophagus) and which may infiltrate the esophagogastric junction from above. [Pg.223]

Wilson KT, Fu S, Ramanujam KS, et al. Increased expression of inducible nitric oxide synthase and cyclooxygenase-2 in Barrett s esophagus and associated adenocarcinomas. Cancer Res 1998 58 2929-2934. [Pg.405]

Proton pump inhibitors are the most effective agents for the treatment of nonerosive and erosive reflux disease, esophageal complications of reflux disease (peptic stricture or Barrett s esophagus), and extraesophageal manifestations of reflux disease. Once-daily dosing provides effective symptom relief and tissue healing in 85-90% of patients up to 15% of patients require twice-daily dosing. [Pg.1314]

Bian, Y.-S., Osterheld, M.-C., Bosman, F. T., Benhattar, J., and Fontolliet, C. 2001. p53 gene mutation and protein accumulation during neoplastic progression in Barrett s esophagus. Mod. Pathol. 74 397-403. [Pg.308]

Walch, A., Specht, K., Bink, K., Zitzelsberger, H., Braselmann, H., Bauer, M., Aubele, M., Stein, H., Siewert, J. R., Hofler, H., and Wemer, M. 2001. Her-2/new gene amplification, elevated mRNA expression, and protein overexpression in the metaplasia-dysplasia-adenocarcinoma sequence of Barrett s esophagus. Lab. Invest. 57 791-2001. [Pg.347]

Lanas A Potent gastric acid inhibition in the management of Barrett s esophagus. Drugs. 2005 65(suppl 1) 75-82. [Pg.399]


See other pages where Barrett s esophagus is mentioned: [Pg.257]    [Pg.258]    [Pg.258]    [Pg.258]    [Pg.260]    [Pg.261]    [Pg.263]    [Pg.263]    [Pg.361]    [Pg.276]    [Pg.282]    [Pg.284]    [Pg.50]    [Pg.54]    [Pg.55]    [Pg.62]    [Pg.69]    [Pg.215]    [Pg.216]    [Pg.344]    [Pg.61]    [Pg.85]   
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