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Your search term(s) "Barretts Esophagus" returned 46 results.
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Ablation of Barrett’s Esophagus with Laser and Photodynamic Therapy. IN: Sampliner, R.; Sharma, P., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 196-205.
This textbook chapter focuses on the use of laser and photodynamic therapy for patients with Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. The authors report on a recent randomized trial that demonstrated that photodynamic therapy (PDT) can significantly reduce the risks of cancer development in these patients, compared with watchful waiting. PDT can be particularly useful for the elimination of the metaplastic mucosa of the esophagus in these patients because of the ability of endoscopists to treat large segments of the mucosa with a single application of light and drug. The authors caution that any treatment decisions should be made in light of patient issues, physician considerations, and the physical characteristics of the patient’s Barrett’s esophagus. The authors review the use of thermal lasers as a preventative treatment in Barrett’s esophagus, the role of lasers in the treatment of high-grade dysplasia (HGD) and adenocarcinoma, the principles of and equipment used for PDT, and the indications for PDT, along with expected results of this treatment modality. 1 figure. 3 tables. 51 references.
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Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. 300 p.
This textbook focuses on Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus, emphasizing the latest evidence and information about the topical issues in Barrett’s esophagus research and the latest approaches to patient management. The book offers 27 chapters: a definition and diagnosis of Barrett’s esophagus; the epidemiology and prevalence of Barrett’s esophagus; the epidemiology of esophageal adenocarcinoma; the pathogenesis of Barrett’s esophagus; the role of acid and bile in Barrett’s esophagus; esophageal motility abnormalities in Barrett’s esophagus; mucosal defense in Barrett’s esophagus; the role of Helicobacter pylori in Barrett’s esophagus; molecular biology of Barrett’s esophagus; histology of Barrett’s esophagus: metaplasia and dysplasia; screening for Barrett’s esophagus: targeting high-risk patients; surveillance of Barrett’s esophagus; the cost-effectiveness of screening and surveillance to decrease mortality from esophageal adenocarcinoma; chromoendoscopy in Barrett’s esophagus; surface imaging in Barrett’s esophagus: the role of high-resolution endoscopy, magnifying endoscopy, and related techniques; spectroscopy; optical coherence tomography, confocal imaging, and others; the medical management of Barrett’s esophagus; thermal endoscopic therapy of Barrett’s esophagus; ablation of Barrett’s esophagus with laser and photodynamic therapy; endoscopic resection; the role of endoscopic ultrasound in Barrett’s esophagus and esophageal adenocarcinoma; surgical therapy of Barrett’s esophagus and cancer; chemoprevention for Barrett’s esophagus; management of high-grade intraepithelial neoplasia in Barrett’s esophagus; esophageal and gastroesophageal junction adenocarcinoma; and the options for palliation of esophageal adenocarcinoma. Each chapter is illustrated with black-and-white drawings, photographs, and figures; a section of full-color plates is included. Each chapter concludes with a list of references; a subject index concludes the text.
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Chemoprevention for Barrett’s Esophagus. IN: Sampliner, R.; Sharma, P., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 236-252.
This textbook chapter describes the use of chemoprevention for Barrett’s esophagus, the premalignant lesion for esophageal adenocarcinoma (EAC). The authors review the epidemiology of gastroesophageal reflux disease (GERD) and Barrett’s esophagus, prevention of EAC, the role of diet and lifestyle, pharmacological treatment, the role of Helicobacter pylori, surgery, endoscopic screening and surveillance, and endoscopic ablation therapies. They discuss chemoprevention in detail, defining chemoprevention as a specific medical treatment of carcinogenesis that stops the process in the early phases before an advanced cancer develops. Topics include the development of chemopreventive agents, chemoprevention cost-effectiveness, agents used for chemoprevention in Barrett’s esophagus, nonsteroidal anti-inflammatory drugs (NSAIDs), the timing and cost-effectiveness of aspirin chemoprevention in Barrett’s esophagus, proton pump inhibitors (PPIs), other potential chemopreventive agents for use in Barrett’s esophagus, and the ASPECT Study, a phase IIIb study of aspirin and esomeprazole chemoprevention in Barrett’s metaplasia. The authors conclude that chemoprevention may be an effective approach to reduce mortality from EAC, a challenging situation that has proven resistant to both existing endoscopic strategies and anti-reflux surgery. 2 figures. 4 tables. 92 references.
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Chromoendoscopy in Barrett’s Esophagus. IN: Sampliner, R.; Sharma, P., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 139-148.
This textbook chapter focuses on the use of chromoendoscopy, also called tissue staining, as a diagnostic test for Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. The author notes that chromoscopy, as it is used endoscopically, is an imaging technique used to identify either specific epithelia or to enhance the surface characteristics of the mucosa, allowing for the recognition of epithelial changes such as dysplasia. The author reviews the use of chromoscopy, the different types of stains that may be used, the contribution of chromoscopy to the accuracy of endoscopic results, clinical recommendations for screening patients with chronic gastroesophageal reflux disease (GERD) for Barrett’s esophagus, the use of chromoendoscopy for detecting Barrett’s esophagus, and the use of chromoendoscopy for surveillance of Barrett’s esophagus. The author concludes that both vital staining and contrast staining appear to be potentially useful in screening for Barrett’s esophagus and in the subsequent surveillance of the lesion for the development of neoplasia. Appended to this chapter is the section of full-color plates for the whole textbook. 2 tables. 32 references.
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Cost-Effectiveness of Screening and Surveillance to Decrease Mortality from Esophageal Adenocarcinoma. IN: Sharma, P.; Sampliner, R., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 124-138.
This textbook chapter focuses on the cost-effectiveness of screening and surveillance of patients who have been diagnosed with Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. The authors first present the results of a systematic review of the literature to identify studies of the economic impact of screening and surveillance to decrease mortality from esophageal adenocarcinoma. They then discuss the criteria by which economic analysis of health care interventions should be conducted. Finally, they critically examine the retrieved studies to determine whether consensus is achieved regarding the implementation of screening and surveillance strategies, and they identify key areas to which the models are sensitive to provide potential hypotheses to guide future clinical research. One section focuses on the problems with screening and surveillance in this patient population, including prevalence versus incidence, the lack of reliable markers for progression to cancer, and inadequate therapy. The authors stress that cost-effective analysis (CEA) is not designed to dictate how providers treat individual patients, but rather to highlight the key elements of the management process that influence effectiveness for patients on average, and elements that must be considered from a societal perspective to appropriately allocate resources. CEA on this topic has shown that gastroesophageal reflux disease (GERD) symptoms are insensitive and nonspecific for the presence of Barrett’s esophagus; Barrett’s esophagus is an inadequate marker for the development of esophageal adenocarcinoma. Interventions that reduce the incidence of cancer will be more cost-effective than strategies that rely on detection of cancer. Proposed treatment for Barrett’s esophagus should not negatively affect patients’ quality of life. 1 figure. 4 tables. 49 references.
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Definition and Diagnosis of Barrett’s Esophagus. IN: Sharma, P.; Sampliner, R., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 1-7.
This chapter about definition and diagnosis is from a textbook that focuses on Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. This introductory chapter stresses that diagnosis of Barrett’s esophagus is vital to identify the subpopulation of patients with gastroesophageal reflux disease (GERD) who are at increased risk for esophageal cancer. About 10 to 15 percent of patients with chronic GERD are diagnosed with Barrett’s esophagus. These patients will benefit from regular surveillance to identify progression to dysplasia before development of adenocarcinoma. The authors review the endoscopic recognition of Barrett’s esophagus, classification systems, the histologic diagnosis of Barrett’s esophagus, molecular markers for the diagnosis of intestinal metaplasia, and future developments in this area. The authors note that the diagnosis of Barrett’s esophagus is based on a combination of endoscopic and histologic criteria. The single most important histologic finding is the presence of goblet cells, which confirms the presence of intestinal metaplasia. 45 references.
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Emerging Techniques: Optical Coherence Tomography, Confocal Imaging, and Others. IN: Sharma, P.; Sampliner, R., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 169-179.
This textbook chapter focuses on the emerging use of optical coherence tomography, confocal imaging, and other techniques for screening and surveillance in patients who have been diagnosed with Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. The authors note that recent advances support optical imaging of the esophagus with unprecedented resolution and tissue penetration that extend beyond the capabilities of conventional white-light endoscopy. The main impetus driving these developments is to provide better surveillance of the esophagus for neoplastic changes. The first section considers optical coherence tomography (OCT), including its principle of operation, the linear scanning mode, radial scanning, and the use of OCT in clinical settings. The next section describes confocal imaging, including its principle of operation, distal scanning, proximal scanning, dual axes architecture, and future advancements. Additional techniques described include endocytoscopy and fluorescence imaging. One table summarizes the performance parameters of these emerging techniques, comparing the strengths and limitations of each method. The parameters include transverse and axial resolution, field of view, tissue penetration depth, frame rate, and contrast mechanism. 4 figures. 2 tables. 30 references.
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Emerging Techniques: Spectroscopy. IN: Sampliner, R.; Sharma, P., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 156-168.
This textbook chapter focuses on the emerging use of spectroscopy for screening and surveillance in patients who have been diagnosed with Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. The authors describe the basis of spectroscopy as objectively quantifying the color and brightness of light and to use this information to detect changes within the mucosa that cannot be seen with the eye. Spectroscopic analysis can extract information that is outside the visible range, including measurement of nuclear size, morphology, and density. The authors discuss the limitations of standard endoscopy and histopathology; the use of optical biopsy for detecting dysplasia; the interaction between light and tissue; the types of spectroscopy used, including point-probe spectroscopy, trimodal spectroscopy, Raman spectroscopy, and fluorescence imaging; technical components of spectroscopy, including light sources, optical fibers, detection devices, and endoscopes for fluorescence imaging; and the clinical results that can be obtained with each of the types of spectroscopy under discussion. The authors conclude that although each of the techniques discussed shows great potential, the ideal test would involve a combination of techniques to create a comprehensive picture of the biochemical and morphologic state of tissue. In addition, development of software for performing data analysis in real time at endoscopy is needed. 2 figures. 3 tables. 29 references.
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Endoscopic Resection. IN: Sharma, P.; Sampliner, R., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 206-221.
This textbook chapter focuses on use of endoscopic resection therapy to treat patients with Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. The authors review the background and history of endoscopic resection (ER) and summarize some of the techniques used, including strip biopsy, the suck-and-cut technique, the plastic cap procedure, ER with a ligation device, and other resection techniques being developed. The chapter considers the complications associated with ER and the results of ER treatment in patients with early Barrett’s neoplasia. The authors conclude that, in experienced hands, ER is a safe method of resecting premalignant lesions and early carcinomas in Barrett’s esophagus. The advantages of ER include the opportunity for histological processing of the resected section, which provides information about the depth of invasion of the individual layers of the gastrointestinal tract wall. 2 figures. 1 table. 40 references.
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Epidemiology and Prevalence of Barrett’s Esophagus. IN: Sampliner, R.; Sharma, P., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 8-18.
This chapter about epidemiology and prevalence is from a textbook that focuses on Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. The author briefly reviews the historical understanding of Barrett’s esophagus and defines the condition. The author considers the prevalence of long segment Barrett’s esophagus, prevalence at endoscopy, the prevalence of Barrett’s esophagus in people with symptoms of gastroesophageal reflux, age factors, Barrett’s esophagus in children, gender differences in prevalence, the severity and duration of reflux symptoms and their impact on findings of Barrett’s esophagus, Barrett’s esophagus in patients who do not have symptoms of reflux, race and geographic differences, the population prevalence of Barrett’s esophagus, genetic and familial aspects, and lifestyle factors. A final section of the chapter briefly considers short segment Barrett’s esophagus. 2 figures. 3 tables. 73 references.
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Esophageal Adenocarcinoma: Epidemiology and Association with Barrett’s Esophagus. IN: Sharma, P.; Sampliner, R., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 19-26.
This chapter about the epidemiology of esophageal cancer is from a textbook that focuses on Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. The author considers the epidemiology of esophageal adenocarcinoma, notably its association with Barrett’s esophagus. Topics include incidence; tumor classification; age, sex, race, and socioeconomic factors; the role of heredity; Barrett’s esophagus and gastroesophageal reflux; body mass; tobacco smoking; alcohol drinking; the role of Helicobacter pylori (H. pylori); dietary factors; drugs used to relax the lower esophageal sphincter (LES) and their role in causing reflux; and the problems associated with nonsteroidal anti-inflammatory drugs. The author offers possible explanations for the increasing incidence of esophageal cancer, reports the survival rates and prognosis for patients with esophageal cancer, and considers the role of endoscopic screening or surveillance. Although gastroesophageal reflux is the strongest risk factor for esophageal cancer, it is uncertain whether this factor can explain the increasing incidence of the tumor. The author concludes that gastroesophageal reflux, use of medications that might cause such reflux, obesity, and decreasing occurrence of infection with H. pylori might all be factors that contribute to the increasing incidence of adenocarcinoma of the esophagus. 72 references.
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Esophageal and Gastroesophageal Junction Adenocarcinoma. IN: Schiff, E.; Sharma, P., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 266-276.
This chapter, from a textbook about Barrett’s esophagus, discusses esophageal and gastroesophageal junction (GEJ) adenocarcinoma. Topics include problems in localizing structures at the gastroesophageal junction, problems in defining cancer of the gastric cardia, intestinal metaplasia as a risk factor for cancer of the GEJ, criteria for identifying cancers of the GEJ, clinical features, diagnosis and staging, treatment strategies, and patient management recommendations. The author summarizes the treatment approach as follows: after the diagnosis has been established by barium swallow and endoscopy, the next step involves a decision regarding the patient’s fitness to undergo surgery. If surgery is not an option, primary therapy will include chemoradiation or enrollment in a clinical trial. If the patient is fit enough to undergo surgery, the next step is tumor staging with computerized tomography (CT) and endoscopic ultrasound (EUS) and then surgery for patients with T1 or T2 tumors. A recommended patient care algorithm is provided for the diagnosis and treatment of patients with adenocarcinoma of the GEJ. 3 figures. 3 tables. 87 references.
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Esophageal Motility Abnormalities in Barrett’s Esophagus. IN: Sampliner, R.; Sharma, P., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 49-59.
This textbook chapter reviews esophageal motility abnormalities in patients with Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. The authors note there is very little information available about motility abnormalities in Barrett’s esophagus separate from those associated with severe esophagitis. They discuss the roles of abnormalities of the anti-reflux barrier, esophageal clearance, and gastric function in the pathogenesis of acid-induced mucosal damage of the esophagus. They emphasize the motility abnormalities associated with hiatal hernia, noting the strong association of this condition with Barrett’s esophagus. Specific topics include the diaphragmatic sphincter and hiatal hernia, the mechanical properties of the relaxed esophagogastric junction (EGJ), hiatal hernia and esophageal clearance, peristaltic dysfunction, gastric emptying and duodenogastroesophageal reflux (DGER), and the therapy used for motor abnormalities in Barrett’s esophagus. The authors conclude that although neither medical nor surgical therapy corrects the peristaltic defect associated with Barrett’s esophagus, anti-reflux therapy can create an effective anti-reflux barrier. 4 figures. 66 references.
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Histology of Barrett’s Esophagus: Metaplasia and Dysplasia. IN: Sampliner, R.; Sharma, P., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 92-100.
This textbook chapter focuses on the histology, including metaplasia and dysplasia, of Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. The authors note that Barrett’s esophagus is characterized by an alteration of the esophageal mucosa that is visible without a microscope and a corresponding histologic abnormality. They discuss the normal anatomy and histology of the esophagus, the histology of Barrett’s esophagus, intestinal metaplasia of the esophagogastric junction (EGJ), low-grade and high-grade dysplasia related to Barrett’s esophagus, a diagnosis of indefinite-for-dysplasia, and the use of surrogate biomarkers for assessing the risk of esophageal adenocarcinoma. Histologically, two morphologic characteristics—architecture and cytology—are used to identify dysplastic glandular in routine stained sections. More complex glandular architecture usually accompanies more severe cytologic alterations. The authors conclude by reviewing several adjunctive techniques that have been proposed as having a possible role in the screening or surveillance of patients with Barrett’s esophagus. 3 figures. 66 references.
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Management of High-Grade Intraepithelial Neoplasia in Barrett’s Esophagus. IN: Sharma, P.; Sampliner, R., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 253-265.
This textbook chapter focuses on the management of high-grade intraepithelial neoplasia in Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. The authors note that malignant degeneration of Barrett’s esophagus is thought to be a multistep process in which intestinal metaplasia progresses through low-grade and high-grade dysplasia into intramucosal and invasive carcinoma. Endoscopic surveillance is used to identify patients with early and curable cancers. In patients with high-grade intraepithelial neoplasia (HGIN), management options include endoscopic follow-up, application of endoscopic treatment modalities such as endoscopic mucosal resection (EMR), photodynamic therapy (PDT), and surgical resection. The authors cover the controversies regarding making the histological diagnosis in these patients and discuss the importance of endoscopic imaging for making the clinical diagnosis of HGIN. The authors describe the advantages and disadvantages of the different management options available, providing practical advice for the optimal use of each. Treatments discussed include endoscopic ablation therapy, EMR, and surgical resection. The authors conclude by emphasizing that, regardless of the choice of treatment approach, patients with HGIN in Barrett’s esophagus should be managed by a multidisciplinary team that includes gastroenterologists, pathologists, and surgeons. 3 tables. 60 references.
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Medical Management of Barrett’s Esophagus. IN: Sampliner, R.; Sharma, P., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 180-187.
This textbook chapter focuses on the medical management of patients who have been diagnosed with Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. The author stresses that endoscopy is required for the adequate assessment of the condition of the esophageal mucosa in an individual patient, in particular to evaluate for the presence of erosive esophagitis and Barrett’s esophagus. After diagnosis of Barrett’s esophagus, further medical management mostly consists of drug therapy, and endoscopic surveillance and treatment if needed. The authors discuss the prevalence and severity of symptoms and esophagitis, proton pump inhibitor (PPI) therapy, H2-receptor antagonists and prokinetics, prevention of symptomatic relapse, regression of Barrett’s epithelium, profound acid suppressive therapy, and the use of aspirin and cyclooxygenase-2 inhibitors. Drug treatment aims at symptom control, healing of esophagitis, and possible prevention of progression of Barrett’s esophagus to dysplasia and adenocarcinoma. The authors conclude that most patients with Barrett’s esophagus will need maintenance treatment with a PPI, primarily to improve symptoms of acid reflux and for healing and prevention of recurrence of esophagitis. Many of these patients have severe acid reflux, even if their symptoms are relatively mild. 1 table. 49 references.
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Molecular Biology of Barrett’s Esophagus. IN: Sharma, P.; Sampliner, R., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 82-91.
This textbook chapter focuses on the molecular biology of Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. The authors review recent advances in molecular biology that support efforts to characterize the specific molecular events that happen during the evolution of esophageal cancer. The identification of molecular biomarkers would offer an improved screening tool, compared with the present strategies that miss most patients with esophageal adenocarcinoma who are unaware they have Barrett’s esophagus and therefore are not being screened. Molecular biomarkers may serve as targets at which to direct therapeutic agents and to measure effectiveness. Topics covered include genetic instability, the cell cycle, the clinical implications of understanding the molecular biology of Barrett’s esophagus, oncogenes, the role of growth factors and growth factor receptors, signal transducer pathways, tumor suppressor genes, apoptosis, telomeres and telomerase, vascular endothelial growth factors (VEGFs), cadherins and catenins, and matrix metaloproteinases. The authors conclude that although the routine clinical use of these biomarkers and targeted molecular therapies is not yet recommended, it is reasonable to assume that diagnostic and therapeutic strategies based on molecular composition will lead to clinical advances and improved outcomes for patients with adenocarcinoma in Barrett’s esophagus. 1 figure. 73 references.
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Mucosal Defense in Barrett’s Esophagus. IN: Sharma, P.; Sampliner, R., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 60-72.
This textbook chapter considers the role of mucosal defense systems in Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. The author further explains Barrett’s esophagus as the presence of a metaplastic specialized columnar epithelium (SCE), or lining, or the distal esophagus. This develops in the esophagus of about 10 percent of people with reflux esophagitis, replacing the native stratified squamous epithelium (SSE) that was damaged by exposure to refluxed acid-pepsin. The author notes that although SCE has a high rate of cell turnover that increases the risk of esophageal cancer, in more than 90 percent of patients with Barrett’s esophagus the SCE remains stable for life. Some of these patients are even symptom-free, possibly due in part to SCE’s ability to resist acid. The author proposes that SCE could be seen as a successful adaptation for esophageal protection against more severe reflux injury. The author presents a working model of mucosal defense in Barrett’s esophagus that emphasizes those features of SCE that make it uniquely suited for survival in a reflux setting. 6 figures. 1 table. 85 references.
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Options for Palliation of Esophageal Adenocarcinoma. IN: Sampliner, R.; Sharma, P., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 277-288.
This chapter, which reviews the options for palliation of esophageal adenocarcinoma, is from a textbook about Barrett’s esophagus, the premalignant lesion for cancer of the esophagus. The authors note that despite advances in the diagnosis and treatment of esophageal cancer, up to 50 percent of patients have incurable disease at presentation, resulting in the need for palliative care. The goal of palliative therapy in patients with unresectable carcinoma is to ameliorate symptoms and treat complications, thereby improving their quality of life. The authors review the many modalities available for palliation of esophageal cancer, including surgical tumor resection, radiation therapy and chemotherapy, tissue ablation, esophageal dilation, photodynamic therapy, laser therapy, and esophageal stents. The authors conclude that surgical resection should be considered in the fit patient without evidence of metastatic disease. For those with poor performance status or metastatic disease, endoscopic measures may be most appropriate. They note that, because of improved design, materials, and deployment systems, self-expendable metal stents (SEMS) have become an attractive alternative to palliate esophageal carcinoma. 1 figure. 4 tables. 71 references.
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Pathogenesis of Barrett’s Esophagus. IN: Sampliner, R.; Sharma, P., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 27-37.
This textbook chapter focuses on the pathogenesis of Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. The authors note that although reflux of gastric contents into the esophagus certainly plays an important role in the development of Barrett’s esophagus, inflammatory, environmental, and genetic factors are also likely involved. Topics covered include the cell of origin, the role of the refluxate, inflammation in Barrett’s esophagus, the role of inherited factors, and host, dietary, and lifestyle factors. The authors conclude that the microenvironment created by the combination of these various factors around the cell of origin produces the selective pressure required for the generation and development of clones of cells that give rise to the metaplastic tissue. 2 figures. 92 references.
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Role of Acid and Bile in Barrett’s Esophagus. IN: Sharma, P.; Sampliner, R., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 38-48.
This textbook chapter focuses on the role of acid and bile in Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. The author notes that Barrett’s esophagus is a metaplastic process in which the normal squamous epithelium of the lower esophagus is replaced by specialized columnar epithelium, or lining cells. This condition develops in about 10 percent of patients who have gastroesophageal reflux disease (GERD). The author reviews Barrett’s esophagus as an acquired condition, the importance of acid and pepsin, the importance of bile and duodenogastroesophageal reflux (DGER), methods for measuring DGER, human studies assessing the role of simultaneous acid and DGER, human studies assessing the role of DGER alone, and the clinical implications of these research findings. The author concludes that possibly all patients with Barrett’s esophagus, regardless of symptoms, should undergo serial pH testing to titrate the adequacy of therapy with proton pump inhibitors (PPIs). However, this approach can be time-consuming and too expensive and may interfere with the important endoscopic surveillance recommended for these patients. Further study is suggested to clarify these issues. A brief final section considers the use of anti-reflux surgery, particularly in younger patients who are facing long-term medical therapy. 6 figures. 1 table. 39 references.
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Role of Endoscopic Ultrasound in Barrett’s Esophagus and Esophageal Adenocarcinoma. IN: Sampliner, R.; Sharma, P., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 213-221.
This textbook chapter focuses on the role of endoscopic ultrasound in patients with Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. The authors describe how endoscopic ultrasound (EUS) incorporates flexible endoscopy and high-frequency ultrasound to capture images into and through the luminal digestive tract. This enables the endosonographer to evaluate the wall layer pattern of the esophagus and to detect the presence of regional and celiac lymph nodes. The authors describe how EUS can be used for staging esophageal cancer and in the evaluation and management of Barrett’s esophagus-associated dysplasia. Other topics include the use of EUS in patients who have cancer with stenosis, restaging after neoadjuvant therapy, and the limitations of EUS. The authors conclude that EUS has an important role in the evaluation and management of patients with esophageal carcinoma and in patients with dysplastic Barrett’s esophagus, particularly in the detection of otherwise unrecognizable invasive carcinoma and the decision-making process regarding which patients should undergo surgery. 6 figures. 1 table. 41 references.
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Role of Helicobacter Pylori in Barrett’s Esophagus. IN: Sampliner, R.; Sharma, P., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 73-81.
This textbook chapter focuses on the role of Helicobacter pylori (H. pylori) in Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. The authors stress the complexity of the interrelationships between H. pylori and gastroesophageal reflux disease (GERD) and its complications, including Barrett’s esophagus and esophageal cancer. They stress that there is no definitive evidence that H. pylori infection is either causative or protective, although studies have demonstrated the possibility of both. This chapter considers nonerosive reflux disease, erosive reflux disease, and Barrett’s esophagus as distinct entities, focusing on pathophysiology, epidemiology, esophagogastric motor function, and clinical intervention trials. The authors conclude that even though there is some epidemiological data indicating that a subset of H. pylori-infected patients may experience a reduced risk of Barrett’s carcinoma, it is premature to assign H. pylori a protective role against the development of esophageal adenocarcinoma. 1 figure. 4 tables. 68 references.
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Screening and Surveillance of Barrett's Esophagus. Gastroenterology and Hepatology. 2(2): 91-93. September 2006.
This article answers clinical care questions on the screening and surveillance of patient’s with Barrett’s esophagus (BE). Topics include the lack of standard practice guidelines, the usefulness of screening and surveillance for Barrett’s esophagus, the differences between screening and surveillance, the problems associated with screening the vast numbers of adults with chronic gastroesophageal reflux disease (GERD) symptoms, practical guidelines for screening, the indirect evidence regarding the benefit of screening and surveillance, risk factors associated with endoscopy (used for screening), experimental technologies being developed for screening and surveillance, prognostic factors for predicting which patients with chronic GERD are likely to progress to BE, and cost and insurance concerns. The authors conclude that screening and surveillance can be beneficial, but there has been no proof in the form of a randomized controlled trial. Most gastroenterologists will recommend regular endoscopic surveillance for anyone presenting with Barrett’s esophagus. Patient selection for screening is a more complicated issue. 6 references.
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Screening for Barrett’s Esophagus: Targeting High-Risk Patients. IN: Sampliner, R.; Sharma, P., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing, Inc. 2006. pp 101-106.
This textbook chapter focuses on screening for Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. The author focuses on the identification of high-risk patients, noting that more than 95 percent of patients who undergo surgical resection for esophageal adenocarcinoma have not had Barrett’s esophagus diagnosed before their diagnosis of cancer. Topics include a definition of screening, the prevalence of Barrett’s esophagus, identifying people at high risk for Barrett’s esophagus, how to screen for this disease, and the effectiveness and cost of screening. A final section briefly considers options for future screening methods and approaches. High-risk candidates appropriate for screening include those patients with chronic gastroesophageal reflux disease (GERD) symptoms who are older, male, and Caucasian. The challenges for screening programs include identifying patients with Barrett’s esophagus who have no symptoms, the costs and risks associated with endoscopy, the accuracy of endoscopy and histology, and the lack of predictors to increase the yield of screening. Alternatives to using endoscopy for screening include the use of brush cytology, unsedated endoscopy, and esophageal capsule endoscopy. 4 tables. 47 references.
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Surface Imaging in Barrett’s Esophagus: The Role of High-Resolution Endoscopy, Magnifying Endoscopy, and Related Techniques. IN: Sharma, P.; Sampliner, R., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 149-155.
This textbook chapter focuses on the use of surface imaging and endoscopy for surveillance in patients who have been diagnosed with Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. The authors focus on the role of high-resolution endoscopy, magnifying endoscopy, and related techniques. They note that because malignancy develops in a standard sequence—metaplasia to dysplasia to cancer—the goal of surveillance is to diagnose and treat dysplasia or early cancer and thus prevent the development of advanced cancer, which is associated with a poor prognosis. They discuss high-resolution endoscopy, magnifying endoscopy, techniques that can enhance high-resolution and magnifying endoscopy, acetic acid chromoendoscopy, indigo carmine chromoendoscopy, methylene blue chromoendoscopy, narrow band imaging, and determining which dye or technique to use. Magnifying endoscopy enables the detection of abnormalities of the surface mucosal and vascular pattern, resulting in the distinction of early abnormalities that may accompany neoplastic transformation. Chromoendoscopy with various staining agents may further enhance the surface structure; however, it is labor-intensive and operator-dependent for best results. 24 references.
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Surgical Therapy of Barrett’s Esophagus and Cancer. IN: Sharma, P.; Sampliner, R., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 222-235.
This textbook chapter focuses on use of surgical therapy to treat patients with Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. The authors outline the three goals of treatment for Barrett’s esophagus before it has progressed to high-grade dysplasia (HGD) or cancer: to provide long-term control of reflux symptoms; to provide a durable gastroesophageal barrier to acid and bile; and to promote the regression or reduce the progression of Barrett’s esophagus, thus reducing the risk of adenocarcinoma. The authors discuss the options for symptom control, including medical and surgical therapy; control of reflux, with medical or surgical therapy; medical and surgical options for inducing regression of Barrett’s esophagus; treating HGD, including some of the controversial issues of patient selection and the role of surveillance; and the presentation, diagnosis, staging, neoadjuvant therapy, preoperative assessment, and operative techniques for esophageal cancer. 2 figures. 2 tables. 63 references.
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Surveillance of Barrett’s Esophagus. IN: Sampliner, R.; Sharma, P., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 107-123.
This textbook chapter focuses on surveillance of patients who have been diagnosed with Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. The author reminds readers that the best hope for improved survival of patients with esophageal adenocarcinoma is detection of the cancer at an early and potentially curable stage. Surveillance is defined as a technique applied to individuals who warrant continued ongoing investigation until they either develop a target lesion while in a surveillance program or exit a surveillance program for some other reason, such as declining health. Topics include the increasing incidence of esophageal adenocarcinoma, the mortality associated with esophageal cancer, a definition of surveillance, the rationale for endoscopic surveillance, determining the risk of esophageal adenocarcinoma in a patient, the development of esophageal adenocarcinoma from Barrett’s esophagus, candidates for endoscopic surveillance, available surveillance techniques, recommended surveillance intervals, and the limitations of surveillance. A final section reviews future strategies that could be used to enhance surveillance, including cytology, chromoendoscopy, optical biopsy techniques, risk stratification, and biomarkers of increased risk. 8 figures. 1 table. 98 references.
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Thermal Endoscopic Therapy of Barrett’s Esophagus. IN: Sharma, P.; Sampliner, R., eds. Barrett’s Esophagus and Esophageal Adenocarcinoma. 2nd ed. Williston, VT: Blackwell Publishing Inc. 2006. pp 188-195.
This textbook chapter focuses on the use of thermal endoscopic therapy to treat patients with Barrett’s esophagus, the premalignant lesion for adenocarcinoma of the esophagus. The author defines Barrett’s esophagus as the replacement of squamous esophageal epithelium by intestinal metaplasia (IM) in the distal esophagus. The author briefly reviews the traditional treatment for Barrett’s esophagus, with proton pump inhibitors (PPIs) or surgical therapies, and then introduces the use of thermal endoscopic modalities as an alternative, less invasive treatment option. The author discusses the destruction of nondysplastic Barrett’s esophagus, leading to its replacement of squamous epithelium, in the hope of having a direct impact on the risk of tumor development. Thermal endoscopy can be used to treat Barrett’s esophagus associated with low-grade dysplasia, for the same purpose. A final section discusses the use of thermal endoscopic methods for the treatment of high-grade dysplasia or intramucosal adenocarcinoma in patients who present with a potential indication for surgical resection. The author concludes that no evidence currently exists to support the routine use of thermal therapy for Barrett’s epithelium; however, there are many aspects of these techniques that deserve further research. 2 tables. 47 references.
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Barrett's Esophagus Can and Does Regress After Antireflux Surgery: A Study of Prevalence and Predictive Features. Journal of the American College of Surgeons. 196(5): 706-713. May 2003.
This article reports on a study undertaken to investigate the factors leading to histologic regression of metaplastic and dysplastic Barrett's esophagus (BE). The study sample consisted of 91 consecutive patients with symptomatic BE; pretreatment and posttreatment biopsies were reviewed from 77 patients treated surgically and 14 patients treated with proton pump inhibitors (PPI). Histopathologic regression occurred in 28 of 77 patients (36.4 percent) after antireflux surgery and in 1 of 14 patients (7.1 percent) treated with PPIs alone. After surgery, regression from low-grade dysplastic to nondysplastic BE occurred in 17 of 25 patients (68 percent) and from intestinal metaplasia to no intestinal metaplasia in 11 of 52 patients (21.2 percent). Both types of regression were significantly more common in short than long segment BE. Eight patient progressed, five from intestinal metaplasia alone to low grade dysplasia, and three from low to high-grade dysplasia. All those who progressed had long segment BE. On multivariate analysis, presence of short segment BE and type of treatment were significantly associated with regression; age, gender, surgical procedure, and preoperative lower esophageal sphincter and pH characteristics were not. The authors conclude that this study refutes the widely held assumption that once established, Barrett's esophagus does not change. 4 figures. 4 tables. 15 references.
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Barrett's Esophagus. In: Katzka, D.A. and Metz, D.C., eds. Esophagus and Stomach. Orlando, FL: Mosby, Inc. 2003. p. 39-48.
Barrett's esophagus, intestinal metaplasia of the esophagus, is a premalignant condition of the esophagus leading to esophageal adenocarcinoma (cancer of the esophagus). This condition has been identified in up to 20 percent of patients undergoing endoscopy for gastroesophageal reflux symptoms and is estimated to occur in at least 700,000 adults in the United States. This chapter on Barrett's esophagus is from a textbook on the esophagus and stomach in which the authors focus on differential diagnosis, pitfalls, and evidence-based management approaches. The chapter covers epidemiology, risk factors and pathophysiology, diagnosis, esophageal adenocarcinoma from Barrett's, surveillance strategies, treatment (medical therapy, anti-reflux surgery, and endoscopic therapy), and chemoprevention. The chapter begins with a chapter outline, includes extensive tables and illustrations, and concludes with a list of recommended readings. 5 figures. 1 table. 15 references.
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Screening and Surveillance for Barrett Esophagus in High-Risk Groups: A Cost-Utility Analysis. Annals of Internal Medicine. 138(3): 176-186. February 4, 2003.
Once in a lifetime screening for Barrett esophagus has been proposed for patients with gastroesophageal reflux disease (GERD), but there is little evidence of its cost-effectiveness. This article reports on a study that designed a model to determine the cost effectiveness of screening high risk groups for Barrett esophagus and for providing surveillance to patients with Barrett esophagus; the model also compared the results with the cost-effectiveness of no screening or surveillance. Results determined that screening with surveillance limited to patients with Barrett esophagus with dysplasia required $10, 440 per quality adjust life year (QALY) saved compared to no screening or surveillance. The incremental cost-effectiveness ratio of surveillance every 5 years in patients with Barrett esophagus without dysplasia compared to those with dysplasia was $596,000 per QALY saved. The authors conclude that screening 50 year old men with symptoms of GERD to detect adenocarcinoma associated with Barrett esophagus is probably cost-effective. However, subsequent surveillance of patients with Barrett esophagus but no dysplasia, even at 5 year intervals, is an expensive practice. 2 figures. 4 tables. 63 references.
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Barrett's Esophagus. Gastroenterology. 122(6): 1569-1591. 2002.
This article reviews the current thinking regarding Barrett's esophagus, an acquired condition resulting from severe esophageal mucosal injury. It still remains unclear why some patients with gastroesophageal reflux disease (GERD, the return of gastric acid from the stomach back to the esophagus) develop Barrett's esophagus whereas others do not. Despite a relatively simple definition of the condition, diagnostic inconsistencies remain a problem, especially in distinguishing short segment Barrett's esophagus from intestinal metaplasia of the gastric cardia. Barrett's esophagus would be of little importance were it not for its well-recognized association with adenocarcinoma (cancer) of the esophagus. The incidence of esophageal cancer continues to increase and the 5 year survival rate for this cancer remains dismal. Current strategies for improved survival in patients with esophageal cancer focus on cancer detection at an early and potentially curable stage. This can be accomplished either by screening more patients for Barrett's esophagus or with endoscopic surveillance of patients with known Barrett's esophagus. Current screening and surveillance strategies are inherently expensive and inefficient. New techniques to improve the efficiency of cancer surveillance are evolving rapidly and hold the promise to change clinical practice in the future. Treatment options include aggressive acid suppression, anti-reflux surgery, chemoprevention, and ablation therapy, but there is still no clear consensus on the optimal treatment for these patients. 4 figure. 4 tables. 226 references.
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Barrett's Esophagus: A Role for High-Resolution Magnification Chromoendoscopy?. Journal of Gastroenterology and Hepatology. 17 (6): 633-635. June 2002.
Barrett's esophagus features the replacement of normal squamous cells lining the esophagus with dysplasia (abnormal tissue cells). This article considers the role of high resolution magnification chromoendoscopy in Barrett's esophagus. Currently recommended conventional endoscopic diagnostic techniques tend to underdiagnose Barrett's esophagus. The author considers problems with surveillance endoscopy, the controversy regarding length of Barrett's esophagus and the resulting risk levels, the histological changes that pose a cancer risk, and the use of chromendoscopy and high magnification endoscopy in Barrett's esophagus. The author concludes that current data in support of chromoscopy for the identification of Barrett's dysplastic change are scanty. The technique of combined high magnification endoscopy with chromoscopic enhancement requires further large prospective studies before its validity in routine clinical practice can be accepted. 21 references.
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Prevalence of Barrett's Esophagus in Asymptomatic Individuals. Gastroenterology. 123(2): 461-467. August 2002.
The incidence of esophageal adenocarcinoma (cancer) in the western world has been linked to chronic heartburn, regurgitation, and the development of the premalignant epithelium of Barrett's esophagus (BE). However, up to 40 percent of esophageal adenocarcinomas occur in patients without prior reflux symptoms. This article reports on a study in which the authors prospectively screened for the presence of BE in asymptomatic subjects older than 50 years of age undergoing screening sigmoidoscopy for colorectal cancer. Of 408 potential study candidates, 110 subjects were screened; 9 were women. The mean age was 61 years, plus or minus 9.3 years; most of the population (73 percent) was Caucasian. Intestinal metaplasia (IM) extending above the esophagogastric junction (EGJ) was detected in 27 subjects (25 percent); 8 patients (7 percent) had long segment BE and 19 (17 percent) had short segment BE. Patients with BE were no more likely to be obese, consumers of tobacco or alcohol, report a family history of gastroesophageal reflux disease (GERD), show association with toxic exposure, or use antacids more than once a month, compared with those without BE. BE was detected in 25 percent of asymptomatic male veterans older than 50 years of age undergoing screening sigmoidoscopy for colorectal cancer. 1 figure. 3 tables. 30 references.
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Prevention and Treatment of Dysplasia in Gastroesophageal Reflux Disease: The Results and the Challenges Ahead. Journal of Gastroenterology and Hepatology. 17 (Supplement): S113-S124. February 2002.
This article discusses dysplasia (abnormal tissue growth) in gastroesophageal reflux disease (GERD) that arises in a setting of Barrett's esophagus. The author notes that since the last World Congress of Gastroenterology there has been an explosion of interest in Barrett's esophagus. The goal of interventions designed to prevent, detect, or treat GERD associated Dysplasia is to attenuate or eliminate the risk of progression to cancer. To do so, the subset of GERD patients with Barrett's esophagus must first be identified. Barrett's esophagus may affect over 1 percent of the North American population, but many more millions than that have chronic GERD. This review article focuses on the advances in treatment and on the challenges ahead for those individuals with known Barrett's esophagus. However, it is sobering to note at the outset that the current best efforts may have limited impact on morbidity and mortality from Barrett's related cancer in the population. For example, in a recent systematic review of published surgical cohort studies, the authors found that only 5 percent of patients reported to have undergone resection of esophageal adenocarcinoma (cancer) were known to have a prior diagnosis of Barrett's and were thus potentially eligible for surveillance. The best case scenario begins with cost-effective and health-effective strategies being developed to screen GERD patients to identify all who have Barrett's esophagus. 3 tables. 61 references.
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Barrett Esophagus. Danbury, CT: National Organization for Rare Disorders, Inc. 2001. 5 p.
Barrett syndrome is a rare disorder caused by chronic inflammation and ulceration of the esophagus. Symptoms develop due to reflux of stomach acid into the esophagus and may include heartburn and recurring pain behind the sternum. Late symptoms may include a narrowing of the esophagus and difficulty swallowing. This fact sheet describes the symptoms, causes, affected population, and standard and investigational therapies. Disorders with similar symptoms, including achalasia, gastroesophageal reflux, and hiatal hernia are briefly discussed. The fact sheet lists 3 resources for more information. 14 references.
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Barrett's Esophagus and Adenocarcinoma. In: Freston, J.W. Diseases of the Gastroesophageal Mucosa: The Acid-Related. Totowa, NJ: The Humana Press, Inc. 2001. p.167-175.
Barrett's esophagus is a change in the esophageal epithelium (lining), recognized on endoscopy, which is confirmed at biopsy to contain intestinal metaplasia (growth of tissue). This chapter on Barrett's esophagus and adenocarcinoma (cancer) is from a text that emphasizes the diagnosis and treatment of gastric mucosal diseases. Topics include a definition of Barrett's esophagus and its classification (short segment and long segment), when to look for Barrett's esophagus, diagnostic strategies, a definition of dysplasia, surveillance and monitoring of patients with Barrett's esophagus, and therapeutic options. The authors conclude by noting that Barrett's esophagus is the precursor lesion of adenocarcinoma of the esophagus, so surveillance endoscopy is warranted. Surveillance endoscopy intervals are based on the presence and grade of dysplasia. Early endoscopy allows for early intervention and improved outcome. Therapy for Barrett's esophagus entails complete symptomatic relief of GERD with proton pump inhibitor (PPI) therapy or fundoplication. 3 figures. 1 table. 25 references.
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Barrett's Oesophagus, Dysplasia and Pharmacologic Acid Suppression. Alimentary Pharmacology and Therapeutics. 15(3): 269-276. March 2001.
Barrett's esophagus, a significant complication of gastroesophageal reflux disease (GERD), is the single most important risk factor for esophageal adenocarcinoma (cancer of the esophagus). This article reviews Barrett's esophagus, dysplasia (alteration in size, shape and organization of cells), and pharmacologic acid suppression (drug therapy). The authors stress that the strong association between Barrett's esophagus and chronic GERD suggests that abnormal esophageal acid exposure plays an important role in this condition. The progression of Barrett's esophagus from specialized intestinal metaplasia (cells out of place) to dysplasia (misshapen cells) and finally invasive carcinoma is incompletely understood, but increased and disordered proliferation is a key cellular event. In research experiments, cell proliferation is increased after exposure to short pulses of acid, while proliferation in reduced in Barrett's esophagus specimens taken from patients with esophageal acid exposure normalized by antisecretory therapy (patients whose gastric acid levels are controlled by drugs). In long term clinical studies, consistent and profound intra esophageal acid suppression with proton pump inhibitors (PPI) decreases cell proliferation and increases differentiation in Barrett's esophagus, but the clinical importance of such favorable effects on these surrogate markers is not clear. In clinical practice, PPIs relieve symptoms and induce partial regression to squamous epithelium, but abnormal esophageal acid exposure and the risk for dysplasia or adenocarcinoma persist in many patients. The authors conclude that the ability of PPIs to suppress acid profoundly and consistently may be critical in the long term management of Barrett's esophagus. 1 figure. 1 table. 34 references.
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Potential Role for Photodynamic Therapy in the Management of Upper Gastrointestinal Disease. Alimentary Pharmacology and Therapeutics. 15(3): 311-321. March 2001.
Photodynamic therapy involves the activation of an exogenously (outside the body) administered, or an endogenously (inside the body) generated, photosensitizer with light to produce localized tissue destruction. Photodynamic therapy is an attractive, predominantly endoscopic technique used for the palliation of advanced upper gastrointestinal cancer and the eradication of early neoplastic (new growth, benign or malignant) and pre neoplastic lesions. The nature of the biological response allowing safe healing and the exploitation of tissue threshold effects mean that adjacent tissue damage can be minimized. This review article used a database of 368 papers. The nature of the photosensitizer is critical to the depth of tissue damage and the risk of adjacent tissue damage and stricture formation. The generation of protoporpyrin IX following administration of 5 aminolaevulinic acid has proved useful for the treatment of high grade dysplasia in Barrett's esophagus. Studies have shown that photodynamic therapy is a safe and effective method for the ablation (removal or destruction) of low grade dysplasia. The treatment of more advanced lesions requires exogenously administered photosensitizers. However, recent data indicate that the neoplastic potential remains in some patients and continued followup is necessary. The authors conclude that photodynamic therapy can be used to eradicate early neoplasia and palliative advanced cancer, but caution is required before a definitive cure can be claimed. 2 figures. 1 table. 79 references. Digestive System Diseases. Barretts Esophagus. Neoplasms. Therapy.
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Barrett's Esophagus. Practical Gastroenterology. 24(5): 15-16, 18, 25-27, 30, 32, 35. May 2000.
Barrett's esophagus is defined as the presence of specialized intestinal metaplasia (SIM) within the tubular esophagus. This article considers the pathogenesis, histologic and endoscopic diagnosis, demographics and epidemiology, treatment, and risk of dysplasia and andenocarcinoma (cancer) associated with Barrett's esophagus; the author also considers surveillance issues and developing areas of concerns for physicians following Barrett's patients. Goblet cells represent the singular histologic finding that defines SIM. Endoscopically, specific landmarks must be identified to correctly diagnose long segments Barrett's esophagus(LSBE), short segments Barrett's esophagus (SSBE), and SIM of the esophagogastric junction (EGJ), the connection between the esophagus and the stomach) and cardia. Each entity has a different prognosis. The endoscopic landmarks include the EGJ, the squamocolumnar junction (SCJ), and the diaphragmatic hiatus (DH). With Barrett's esophagus, SIM is noted in the area between the EGJ and SCJ. Most LSBE and SSBE patients are white males whose mean ages range between 55 and 65 years. Heartburn duration is greatest for LSBE patients, although heartburn severity may be greater in SSBE patients. LSBE is characterized by severe, proximal esophageal acid reflux while less severe, distal acid reflux is noted in SSBE. The combined prevalence of SSBE and EGJ SIM is 7 to 8 times greater than LSBE, although the prevalence of dysplasia and cancer is 3 to 4 times greater in LSBE. Medical therapy or anti reflux surgery has not been shown to reverse Barrett's esophagus and long term surveillance at 2 to 3 year intervals is most appropriate in LSBE. Presently, high grade dysplasia is treated with esophagectomy (removal of part of the esophagus) or mucosal ablation for high risk patients (who cannot tolerate surgery). Future diagnostic options include chromoendoscopy (using methylene blue, lugol's, or toluidine staining), laser induced fluorescence, and balloon cytology. Flow cytometry and p53 biomarkers may help differentiate which patients have a propensity to develop cancer. The author concludes that photodynamic therapy, argon plasma coagulation, heat probes, cryotherapy, and ultrasound are the techniques under contention for the future of ablative therapy for Barrett's esophagus. 9 figures. 2 tables. 11 references.
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Barrett's Esophagus: A Problem Caused by GERD. San Bruno, CA: StayWell Company. 2000. [2 p.].
This brochure describes Barrett's esophagus, a condition in which part of the lining of the esophagus near the stomach has changed. This change is caused by the acid reflux that occurs with gastroesophageal reflux disease (GERD). The changed lining is not cancer, but it can lead to cancer. The brochure reviews the symptoms of GERD, including heartburn, sour tasting fluid in the mouth, frequent burping or belching, and symptoms that get worse after eating, bending over, or lying down. Barrett's esophagus is often found when a test for another problem is done. The brochure describes endoscopy, a test that is often used to diagnose Barrett's esophagus. The brochure explains how readers with Barrett's esophagus or GERD can prevent further damage through lifestyle changes and medications. One sidebar describes GERD and includes an illustration of the anatomy involved. Readers are encouraged to participate in the recommended program of followup and monitoring of their condition, which usually includes an endoscopy every 2 years. The brochure is illustrated with full color drawings. 5 figures.
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Barrett's Esophagus: Treatment with 5-Aminolevulinic Acid Photodynamic Therapy. Gastrointestinal Endoscopy Clinics of North America. 10(3): 421-437. July 2000.
This article discusses the management of patients with metaplastic (cell changes) and in particular dysplastic (cell changes indicative of cancer or precancer) Barrett's esophagus. The lower esophagus is normally lined with squamous mucosa. Under certain conditions of gastroesophageal reflux (the return of the stomach's gastric acid into the esophagus), this is replaced with a metaplastic columnar epithelium, also called Barrett's esophagus. Barrett's esophagus is a risk factor for esophageal cancer. The author stresses that there is an urgent need for minimally invasive methods that eradicate the abnormal mucosa associated with high grade dysplasia, but that do not cause the high rates of morbidity and mortality associated with esphagectomy (removal of part or all of the esophagus). The author proposes the use of 5 aminolevulinic acid (ALA) photodynamic therapy (PDT) as a method for ablation for Barrett's epithelium. The author covers the mechanism of this technique; specificity of tissue localization following ALA administration; dosimetric considerations for this type of PDT; the tissue pharmacokinetics of 5ALA induced protoporphyrin IX accumulation in Barrett's esophagus; the methods of treatment, including photosensitizer administration and light irradiation; and patient selection and management considerations. The author concludes by emphasizing the need for ongoing patient surveillance after these PDT methods, as they may not reverse the biologic progression of the dysplasia (of the cells remaining after the ablation). 6 figures. 39 references.
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Columnar-Lined (Barrett's) Esophagus: Can Progression to Cancer be Prevented?. Postgraduate Medicine. 107(7): 59-65. June 2000.
The risk of adenocarcinoma in patients with columnar lined (Barrett's) esophagus has risen dramatically in recent decades. In this article, the author explains the difficulties in defining the condition and examines current strategies in prevention and management. Barrett's esophagus is an acquired disorder caused by chronic esophageal injury from gastroesophageal reflux (GER) that results in intestinal metaplasia (normal tissue cells converted into another, less differentiated type). Intestinal type metaplasia, marked by goblet cells, carries a significantly increased risk of adenocarcinoma of the esophagus, a malignant lesion that is escalating dramatically in prevalence. Patients with chronic reflux, especially white males, have the highest risk and should probably be screened for the disorder. Reducing reflux either medically (with drug therapy) or surgically may diminish the occurrence or progression of the disease. Surveillance of a patient with known Barrett's esophagus may help to reduce morbidity and mortality by early detection of progression. The author notes that mucosal ablation techniques show promise as emerging therapeutic options. This article can be used for continuing medical education (CME) credits. 1 table. 18 references.
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Final Results from 10 Year Cohort of Patients Undergoing Surveillance for Barrett's Oesophagus: Observational Study. BMJ. 321(7271): 1252-1255. November 18, 2000.
This article reports on a study undertaken to review the benefit of an endoscopic surveillance program for patients with Barrett's esophagus. The study including 409 patients in whom Barrett's esophagus was identified during 1984 to 1994; 143 of these patients were entered into the annual surveillance program. The average period of surveillance was 4.4 years; 55 patients were reassessed in 1994, but only 8 patients remained in the program in 1999. Withdrawal was due to death (not from carcinoma of the esophagus), illness, or frailty. Five of the patients who entered surveillance developed carcinoma of the esophagus. Only one cancer was identified as a result of a surveillance endoscopy; the others were detected during endoscopy to investigate altered symptoms. Of the 266 patients who were not suitable for surveillance, one died from esophageal cancer and 103 from other causes. Surveillance has resulted in 745 endoscopies and about 3000 biopsy specimens. The authors conclude that this current surveillance strategy has limited value, and it may be appropriate to restrict surveillance to patients with additional risk factors such as stricture (narrowing), ulcer, or long segment Barrett's esophagus. 2 tables. 13 references.
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Photodynamic Therapy of Barrett's Esophagus. Gastrointestinal Endoscopy Clinics of North America. 10(3): 409-419. July 2000.
This article discusses the use of photodynamic therapy for patients with Barrett's esophagus. The lower esophagus is normally lined with squamous mucosa. Under certain conditions of gastroesophageal reflux (the return of the stomach's gastric acid into the esophagus), this is replaced with a metaplastic columnar epithelium, also called Barrett's esophagus. Barrett's esophagus is a risk factor for esophageal cancer. Unfortunately, the treatment for Barrett's esophagus (removal of part or all of the esophagus) is complex and dangerous. Photodynamic therapy uses endoscopic therapies to eliminate metaplastic mucosa (cancer or precancer cells) and allow repopulation of the surface of the esophageal lining with normal squamous mucosa. This treatment is designed to decrease the risk of cancer development. The authors discuss acid suppression, photosensitizers in photodynamic therapy, lasers and photodynamic therapy, photoradiation devices, tissues effects of photodynamic therapy, and clinical results. The authors conclude that photodynamic therapy seems able to control high grade dysplasia within Barrett's esophagus about 80 percent of the time. Long term results are not yet available, but the treatment is promising. Given the success with surgical intervention, however, use of photodynamic therapy should be reserved for nonsurgical candidates at the current time. The complications that occur with photodynamic therapy are not trivial and must be weighed against the potential benefits. Cutaneous photosensitivity, chest pain, nausea, and stricture formation all may occur. Improved dosimetry is needed to decrease these problems. 1 table. 27 references.
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