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Esophagus Stent -- Mesh

Gastroesophageal Reflux Disease (GERD, Acid Reflux)

Acid-Alkaline Balance by Karl Loren

Dr. Weston Price -- On Acid -- Alkaline Balance

Endoscopy & Gastroscopy

Abnormal Propulsion of Food

Mass Near The Esophagus -- Cancer?  Benign?

Esophagus Stent -- Mesh

Advice From Friends -- Esophagus Cancer

Treatments and Protocols BEYOND The Traditional

Esophagus Cancer Mortality

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One possible treatment for a narrowing, or closing, of the esophagus is the stent, or mesh that can be inserted.

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The esophagus is a relatively simple tubular structure connecting the throat to the stomach. The major functions of the stomach are to transport ingested food from the oropharynx to the stomach and to prevent regurgitation of food and gastric contents from the stomach back up into the esophagus. At the same time it allows air to be vented out of the stomach thus relieving abdominal bloating. On occasion, a narrowed area will occur in the esophagus resulting in an interruption in the normal swallowing mechanism. This may result in dysphagia or difficulty swallowing. Passage of food or liquid may be impaired through the esophagus with a sensation of a fullness in the chest, pressure-like sensation, shortness of breath and inability to swallow food, liquids or saliva. In many cases this is transient in nature and may only last a short time but on occasion may be prolonged requiring emergent intervention. This narrowing of the esophagus can be caused by many different conditions. The most common of which is a benign stricture. This is the result of peptic esophagitis or gastroesophageal reflux disease and can occur at any age but is more common after the age of 40. The fundamental abnormality is excessive acid reflux from the stomach up into the esophagus resulting in an inflammatory reaction in the lower esophagus that leads to scarring after repeated injury and healing. Eventually, scar tissue is formed and a benign stricture develops which is in the form of a concentric ring that narrows the opening of the esophagus. A hiatal hernia is often present in association with the reflux. This concentric lower esophageal ring sometimes called a Schatzki's ring often occurs at the junction between the esophagus and the stomach and sometimes can be present for years. When diagnosed, it can be easily treated by passage of a dilator through the area to break open the scar tissue and relieve the narrowed area. Other causes of benign esophageal strictures may be congenital in nature such as a membranous diaphragm or web that can occur anywhere in the esophagus but frequently occurs in the upper portion. This is also treated by dilation either through an endoscope or by passage of Bougie dilator. Other conditions leading to benign strictures include corrosive injury to the esophagus from ingestion of a toxic substance (i.e. cleaning solutions, radiation injury to the esophagus, post surgical strictures, or achalasia, which is a gradual thickening of the musculature at the lower end of the esophagus). Other conditions could cause dysphagia (difficulty swallowing), even though no stricture is present. In that case, various neurological conditions, vascular abnormalities, diverticulum, spastic motility disorders, or skeletal muscle disorders like muscular dystrophy and myasthenia gravis are possibilities. In addition to the above, a malignant condition may develop causing a stricture or narrowing of the esophagus. There are about 11,000 new cases of cancer of the esophagus diagnosed yearly and is correlated with smoking or excessive alcohol ingestion, particularly in young adulthood. It is more frequent in men than women and also more frequent in blacks than whites. Esophageal cancer can develop anywhere along the esophagus but is more frequent in the lower portion. A condition called Barrett's esophagus may occur in the lower esophagus due to chronic gastroesophageal reflux disease. This condition is diagnosed by esophageal biopsy and is reflected by a change in the cellular structure of the lower esophagus. Patients who have this condition are at higher risk for developing adenocarcinoma of the lower esophagus and must be screened by performing upper endoscopy on a regular basis. Treatment of a benign esophageal stricture consists of esophageal dilation. This is most commonly done at the time of an upper endoscopy. The upper endoscopy is where a video endoscope is placed through the mouth into the esophagus while the patient is under an IV sedation. The esophagus is then examined and if a benign stricture is present it can be dilated in various ways. A balloon dilator passed through the endoscope is often inflated within the confines of the stricture, thus opening the area and relieving the patient's symptoms. Other types of dilators may also be passed although not through the endoscope. These are called Mallony or savory dilators in increasing sizes in order to break open the stricture. In either case, the patients are sedated and should not feel anything during the procedure. The risks of a dilation include potential bleeding, infection or a tear. If a tear is deep enough, on rare occasion, it might require surgical repair. Treatment of a malignant stricture of the esophagus is available but can often be disappointing. If the malignancy is determined to be small and localized without any spread beyond the esophagus then a surgical repair is often opted for and may, on rare occasion cure the cancer. If the tumor is not curable, then often, palliative treatments are employed which include chemotherapy, radiation therapy, esophageal dilation, laser treatments, injections, tumor probes or placement of an esophageal stent (wire mesh tube) to keep the esophagus open. In any situation the patient must work closely with his or her physician to decide what is the best approach for that individual since it varies from patient to patient.

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Esophageal cancer and Barrett's esophagus

How to approach surveillance, treatment, and palliation

Wael Shahin, MBBS; Joseph A. Murray, MD

VOL 105 / NO 7 / JUNE 1999 / POSTGRADUATE MEDICINE

CME learning objectives

• To review the clinical presentation of and risk factors for esophageal cancer
• To learn the most effective combinations of methods to diagnose and treat esophageal cancer
• To identify early signs and appropriate surveillance of Barrett's esophagus

This is the second of three articles on esophageal diseases

This page is best viewed with a browser that supports tables

Preview: Despite the technologic advances of modern medicine, esophageal cancer remains a deadly and challenging disease. Treatment success depends on identifying cancer early in its course or preventing Barrett's esophagus from progressing to cancer. However, this goal is hampered by the fact that disease is often advanced by the time symptoms appear. In this article, the authors discuss squamous cell carcinoma, adenocarcinoma, and its precursor lesion, Barrett's esophagus. They describe factors that increase patients' risk and steps to take if one of the conditions is detected.

Esophageal cancer is devastating for the patient and family. The prognosis is poor, and dysphagia, regurgitation, and pain can profoundly diminish the patient's quality of life. However, survival rates are improving. About 35 years ago, only 1% of African American patients and 4% of white patients survived 5 years after diagnosis, compared with 9% of African Americans and 13% of whites today (1). Esophageal cancer is almost three times more common among African American men than white men, and it is three times more common among men than women. In 1998, the esophagus was one of the 10 leading sites causing cancer death among men (1). The American Cancer Society estimates that 11,900 patients died of the disease and 12,300 new cases occurred in 1998 (1). In addition to primary disease, the esophagus is occasionally the site of secondary metastasis or direct extension of tumors of the hilum of the lung.

Several uncommon primary tumors of the esophagus may present with gradual onset of dysphagia or may be found incidentally during investigation of other problems further down the gastrointestinal tract. These rare tumors are not discussed in this article but are summarized in table 1. This article addresses the two major esophageal neoplasms, squamous cell carcinoma and adenocarcinoma, and the precursor lesion for adenocarcinoma, Barrett's esophagus.

Clinical presentation

Patients with esophageal cancer usually present with progressive dysphagia on consumption of solid food. Dysphagia may progress rapidly to include semisolids and then liquids, and some patients even have difficulty swallowing saliva by the time they see a physician. Often, patients have significantly modified their diet before they seek medical attention.

Additional symptoms include odynophagia, constant chest or back pain, regurgitation, anorexia, and often, profound weight loss (2). However, in some cases, patients are overweight at presentation, and obesity is a risk factor for esophageal adenocarcinoma. General muscle wasting and malnutrition are more common in patients with squamous cell carcinoma. Rarely, patients being evaluated for heartburn are found to have an early-stage tumor arising from Barrett's esophagus.

Physical examination rarely reveals direct evidence of esophageal cancer but may disclose manifestations of disease extension, such as liver enlargement from metastasis, supraclavicular lymph node enlargement, hoarseness due to recurrent laryngeal nerve damage, or signs of bronchopulmonary involvement caused by pleural effusion or esophagotracheal fistula.

Squamous cell carcinoma

Worldwide, squamous cell carcinoma is more prevalent than adenocarcinoma of the esophagus. In a US study conducted from 1973 through 1982 (3), the annual incidence rate per 100,000 people was 2.6 for squamous cell carcinoma, compared with 0.4 for adenocarcinoma, and occurrence varied by race and sex (table 2). For example, recent studies (4,5) found that squamous cell cancer was the predominant type in African Americans with esophageal cancer (in 92%), whereas adenocarcinoma was much less common.

The most important risk factors for squamous cell cancer are a history of prolonged use of tobacco or alcohol, a history of ingestion of a caustic substance, nutritional deficiencies, or chronic esophagitis. There is tremendous variation in the incidence of esophageal cancer in certain parts of the world, particularly Africa and Asia, which some experts believe is explained by exposure to environmental factors (eg, nitrates, petroleum oil derivatives), especially in the setting of poor nutrition. For example, squamous cell esophageal cancer is a common cause of death in Linxian province in north-central China, but the disease is quite rare in another part of China only a few hundred miles away (2). The rare familial condition of palmoplantar keratoderma (tylosis) carries a very high risk of squamous cell esophageal cancer and may help reveal a genetic basis for more common cancers (6).

Adenocarcinoma

The incidence of adenocarcinoma of the esophagus, including the esophagogastric junction, has been increasing rapidly among US men since the 1970s (figure 1: not shown). According to one study (7), increases ranged from 4% to 10% per year, compared with a relatively stable incidence of squamous cell carcinoma (and a slight decrease in adenocarcinoma of the distal stomach) in the same period. Another study (4) found that in the 1970s, adenocarcinoma accounted for 16% of all esophageal cancer in white men in the United States. By the mid-1980s, it increased to 33% and by 1990 approached 50%. In 1995, adenocarcinoma surpassed squamous cell cancer as the leading cause of esophageal cancer in white men. Thus, within two decades, esophageal and gastric cardia adenocarcinoma has risen from a rare tumor to one of the top 15 cancers among white men.

As in squamous cell carcinoma, the incidence of adenocarcinoma varies by race and sex (table 2). Studies (4,5) found that in white patients, adenocarcinoma was more common (found in 66% of cases) than squamous cell carcinoma (found in 32% of cases). Although both types of esophageal cancer are more common in men, the difference is more pronounced in adenocarcinoma (table 2), in which the male-female ratio is 7:1 in white patients and 10:1 in African American patients (3).

In addition to a strong association between adenocarcinoma and Barrett's esophagus (discussed later), the risk of adenocarcinoma is increased with obesity, smoking, heartburn, and middle age (8). Risk decreases with intake of raw fruits and vegetables (especially green and dark yellow vegetables, vegetables in the cabbage family, soy products, and legumes) and dietary fiber. On the other hand, there are no significant associations with total caloric or fat intake, number of meals per day, or consumption of coffee or tea (9).

Diagnostic approach

Diagnosis of esophageal cancer is usually straightforward but often involves more than one method of evaluation. Surveillance programs provide the only real hope of detecting esophageal cancer at a readily treatable stage. When found during one of these programs, cancer may be limited entirely to the esophageal mucosa. The TNM system is used in staging esophageal cancer, and the major determinants of long-term survival are the depth of local invasion, spread to distant lymph nodes, and presence of metastatic disease. All imaging methods are geared to assess these factors.

Radiography
Barium-swallow testing reveals any obstructing lesion (figures 2 and 3: not shown). On radiography, esophageal cancer appears as an intraluminal mass or an irregular, eccentric stricture with a shelf-like presentation. Occasionally, the radiographic appearance may mimic achalasia, which emphasizes the need for careful endoscopic evaluation before making a definitive diagnosis in any patient with possible achalasia (figure 4: not shown).

Endoscopy
Endoscopy is recommended in addition to radiography in all patients with esophageal dysphagia, because radiographic methods may not detect subtle cancers. Endoscopy allows direct visual inspection of the esophagus and the opportunity to take biopsy specimens for histopathologic and cytopathologic evaluation (figure 5: not shown). In many cases, a lesion that is not apparent on endoscopy is found by cytologic methods (in the case of squamous cell carcinoma) or biopsy (in the case of adenocarcinoma occurring in Barrett's esophagus).

Imaging techniques
Computed tomography (CT) and endoscopic ultrasound may be considered complementary methods for staging esophageal cancer before therapy. In general, CT is done first, because it is more readily available than endoscopic ultrasound and a finding of distant metastasis would obviate further evaluation. CT is the standard tool for regional and distant staging of esophageal cancer. It may detect a thickened esophagus, enlarged lymph nodes, and involvement of the mediastinum, lung, or liver. The finding of bulky mediastinal lymph node involvement is a poor prognostic sign. CT lacks the sensitivity of endoscopic ultrasound for staging local disease and detecting smaller lymph node metastasis, especially celiac axis involvement.

Endoscopic ultrasound consists of insertion of an ultrasound probe into the esophagus and stomach. This method reveals exquisitely fine details of the esophageal wall and closely adjacent structures (figure 6: not shown). At present, endoscopic ultrasound provides the most accurate estimation of the cancer's depth of penetration, the length of esophagus affected, and the extent of lymph node involvement (10,11). Fine-needle aspiration biopsy of suspicious lymph nodes may be useful in differentiating metastatic from nonmetastatic disease.

Newer methods of imaging (eg, positron emission tomography, immunohistochemical analysis of lymph node samples to detect micrometastasis) may increase the accuracy of staging in the future but for now are neither proven nor widely available.

Therapeutic approach

Treatment options for esophageal cancer are determined by the stage of the disease at presentation. When cancer is found early (ie, stage 1), 5-year survival rates approach 90% (12). However, such early detection usually occurs in patients participating in a surveillance program, and few are fortunate enough to be in this situation.

Because of the rising incidence of esophageal adenocarcinoma, especially in otherwise healthy young men, and the dismal results historically reported in patients who have the disease, efforts have been made to use more aggressive therapy in the hope of improving long-term survival. Concurrent with these efforts have been technologic developments in endoscopic palliation, which have enhanced the ability to improve patients' quality of life, primarily by relieving dysphagia.

In general, therapy can be divided into methods used for cancer that is restricted to the esophagus and those used when the disease has spread distantly.

Methods for local disease
When cancer is limited to the esophagus, the traditional approach has been surgical resection. In some cases, radiation therapy may be used alone, or combination therapy consisting of systemic chemotherapy along with surgery or radiation may be appropriate. Chemotherapy alone has not been found to be helpful in esophageal cancer. A new option being tried in disease limited to the mucosa is ablation of neoplastic tissue with endoscopic techniques.

Surgery: When the patient is a viable candidate for surgery, that is the option of choice in esophageal cancer shown by CT and endoscopic ultrasound to be limited to a local area. Local involvement of regional lymph nodes, if they are not bulky, is not necessarily a contraindication to surgery. The aim of surgery is to remove the lesion along with any lymph nodes draining from the area.

Transthoracic resection allows more complete dissection of para-aortic lymph nodes, but the transhiatal approach may be less invasive. Regardless of the approach, success depends on the surgeon's skill and experience. Perioperative morbidity can be substantial, but postoperative mortality is usually low when the operation is performed by a practiced expert.

Radiation therapy: Radiation alone is a useful measure for relieving the dysphagia of esophageal cancer. Occasionally, patients have a prolonged disease-free interval after external-beam irradiation. Intraluminal radiation therapy (brachytherapy) is rarely used, because it is less effective and inconvenient for the patient and operator.

Combination therapy: This approach is often beneficial, because esophageal cancer has both a high rate of distant metastasis and a significant risk of local complications (11,13). Preoperative chemotherapy and radiation may have an important role in decreasing the risk of distant metastasis, and they may provide a cancer-free radial margin during surgery (14,15). Preoperative chemoradiation is helpful in decreasing tumor size and thereby facilitating surgery (16). Nutritional-support strategies should be utilized in patients during the period of preadjuvant chemoradiation. In patients who have localized disease and are not candidates for surgery, chemoradiation alone may be useful.

Endoscopic therapy: The advent of newer techniques to ablate neoplastic tissue has created opportunities for treating very early stage esophageal cancer by endoscopic means. Long-term success with this therapy is not yet established, so its use is restricted to patients who have a medical condition that precludes resection and to those who refuse the operation. With modern techniques of preoperative evaluation and supportive care, even the very elderly can usually tolerate esophagectomy.

The following methods have been used to remove esophageal tumors, and a combination of them may be applied to ensure the most complete excision of malignant tissue possible:

• Endoscopic mucosal resection. The area is usually raised on a cushion of injected saline to allow the endoscopist to cut in the plane between the submucosa and the underlying muscle layer. The mucosa is removed using a wire snare.
• Nd:YAG laser. Under direct visualization, the laser beam is aimed at the tumor until it heats and vaporizes malignant tissue. The method is effective but carries high morbidity and risk of perforation.
• Photodynamic therapy. A chemical photosensitizer is administered, which becomes more concentrated in tumor tissue than normal tissue. The surface of the tumor is then illuminated with light of a specific wavelength. Oxygen free radicals are produced, which destroy malignant tissue and its blood supply (17).

Methods for advanced disease
When esophageal cancer is advanced, attempts should be made to improve the patient's quality of life. The following palliative endoscopic techniques may have beneficial effects. The choice of method is largely dependent on the facilities and expertise available.

• Dilatation of stricture caused by the lesion is simple, fast, and inexpensive. However, risk of perforation is high and effects are short-lived.
• Insertion of a rigid stent is effective and inexpensive, but placement is difficult and the perforation rate is high. A self-expanding wire-mesh stent is wide, thin-walled, effective, and easier to place, but it is more expensive, easily occluded by a growing tumor, and subject to food impaction.
• Direction of the Nd:YAG laser beam to heat and vaporize tumor tissue and reopen the lumen is effective and relatively safe.
• Photodynamic therapy, with adjustment of the dose of laser light to correspond to the depth of necrosis, carries less risk of perforation than does use of the Nd:YAG laser.
• Injection of dehydrated ethanol or chemotherapeutic agents directly into the tumor through a sclerotherapy needle may have beneficial effects on tumor size and luminal occlusion (17).
• Radiation therapy relieves dysphagia in about half of patients.

Barrett's esophagus

Barrett's esophagus is the most important predisposing factor for adenocarcinoma of the esophagus. Once considered a rare congenital disorder, it is now recognized to be a relatively common acquired condition, or special form of healing, that develops as a consequence of gastroesophageal reflux disease (18). Barrett's esophagus is the first step in a metaplasia-dysplasia-carcinoma sequence, and patients with the condition have a 30- to 125-fold increased risk for adenocarcinoma of the esophagus (19). The esophagus is easily accessible for inspection, biopsy, and follow-up with endoscopy, so the condition is an ideal model for study of the pathogenesis of esophageal carcinoma (4).

In Barrett's esophagus, squamous cell epithelium of the distal esophagus is replaced by a specialized columnar cell epithelium, which resembles mucosa of the small intestine with its goblet cells but lacks the well-defined brush border (20). A villiform pattern may be noted.

The condition occurs predominantly in white men and has a diagnosed prevalence of about 1 per 400 people. However, it remains undiagnosed in most patients (21), partly because of decreased sensitivity of the columnar epithelium to acid but more likely because of prolonged self-treatment of frequent heartburn.

Development
For Barrett's esophagus to develop, injury of the esophageal squamous cell epithelium and an abnormal esophageal environment during the period of repair are required. The initiating luminal environment contains acid (possibly bile acids or other elements). Exposure to the acid is more prolonged in patients with Barrett's esophagus than in patients with reflux but no Barrett's mucosa. The prolonged exposure appears to be due to the combination of a mechanically defective lower esophageal sphincter, inefficient esophageal clearance, gastric acid hypersecretion, and the presence of hiatal hernia. Duo-denogastric reflux of bile acids may also be involved (19).

Rarer causes of development of Barrett's esophagus are chronic exposure of the esophagus to cytotoxic agents (eg, antineoplastic drugs), which injure the esophageal squamous mucosa, and long-term chemotherapy, which creates an abnormal environment in which esophageal mucosa is replaced by more resistant columnar epithelium (22).

Diagnostic approach
Barrett's esophagus should be suspected in high-risk patients with a long history of reflux symptoms. Dysphagia and loss of weight are usually manifestations of advanced neoplastic disease. White middle-aged men should receive particular consideration, because they have the highest likelihood of adenocarcinoma complicating Barrett's esophagus. Biopsy and endoscopy are the "gold standards" in diagnosis and follow-up of Barrett's mucosa.

Biopsy: Even before onset of dysphagia and the appearance of endoscopically visible lesions, biopsy can detect invasive adenocarcinoma of the esophagus (22). It can reveal specialized, abnormal-looking epithelium above the gastroesophageal junction (ie, the site of transition from stratified squamous cell epithelium of the esophagus to columnar cell epithelium of the cardia of the stomach).

So-called long-segment Barrett's esophagus extends at least 3 cm into the tubular esophagus, versus short-segment Barrett's esophagus, which is defined as a measurable "tongue" of Barrett's-type epithelium 2 cm or less above the gastroesophageal junction. Because Barrett's esophagus and hiatal hernia often coexist, short-segment Barrett's esophagus may be overdiagnosed endoscopically. Therefore, biopsy should be performed above the gastroesophageal junction to confirm endoscopic findings. The risk for malignancy is high with long-segment Barrett's esophagus but has not been established for short-segment disease (23).

Further confounding the diagnostic picture is the fact that between 20% and 40% of people without disease have specialized epithelium at a normal-appearing gastroesophageal junction (ie, so-called intestinal metaplasia) (24). This condition is of unknown significance, but it is not associated with a sufficiently high risk of malignant change to justify the label of Barrett's esophagus.

Endoscopy: Use of magnification endoscopy and dyes (eg, Lugol's iodine) is very helpful in detecting early lesions in high-risk patients and in delineating Barrett's mucosa and tumor margins before surgery (10). An early endoscopic sign of Barrett's esophagus is reddish mucosa encroaching into the tubular esophagus (figure 7: not shown).

Use of laser spectroscopic probes: This technique is helpful in detecting areas of dysplasia and early cancer, as shown by their different pattern of laser-induced fluorescence (25).

High-resolution endoscopic ultrasonography: This promising new method has successfully identified Barrett's mucosa with a sensitivity of 100% and specificity of 86%; however, it could not recognize dysplasia (26).

Radiography: Barium studies are insensitive in detecting uncomplicated Barrett's esophagus (11). However, the presence of a large hiatal hernia or stricture increases the likelihood of coexistent Barrett's esophagus.

Follow-up and treatment
Over the last 10 to 15 years, the number of patients having adenocarcinoma of the esophagus has increased rapidly. These patients (mostly men), in contrast to those with squamous cell carcinoma, are younger (between ages 35 and 60) and quite fit, so they can tolerate aggressive combined-modality therapy. Considering the clear relationship between Barrett's esophagus and increased risk of adenocarcinoma, surveillance of Barrett's esophagus and early diagnosis of cancer are high-priority goals (27).

Barrett's esophagus without dysplasia: Suggested follow-up in patients with these findings is a second endoscopic evaluation with four-quadrant biopsy every 2 cm in the mucosa that has Barrett's-esophagus appearance. If no dysplasia is found, repetition of the procedure every 2 to 3 years is the most cost-effective strategy. This protocol may be discontinued when the patient's general health declines to a point that surveillance is no longer worthwhile or he or she would not withstand surgery.

Treatment of reflux should be undertaken to heal inflammation and control symptoms. Most often, medical therapy using a proton pump inhibitor is chosen. Antireflux surgery may be considered, but it does not seem to reduce the risk of subsequent cancer. Therefore, surgery should be followed by endoscopic surveillance.

Barrett's esophagus with low-grade dysplasia: Differentiation of low-grade dysplasia from the reactive atypia seen in inflammation may be difficult. Hence, a 12-week course of intensive acid-suppression therapy is important, followed by meticulous endoscopic and histologic examination of the Barrett's epithelium. If dysplasia persists, antireflux therapy should be continued, with endoscopic surveillance and multiple biopsies every 6 months.

Barrett's esophagus with high-grade dysplasia: Whenever histopathologic findings of Barrett's esophagus with high-grade dysplasia are found, a second pathologist should review the slides. If he or she confirms the diagnosis, the possibility of coexistent cancer must be considered. More than 30% of patients presenting for the first time with high-grade dysplasia are found to have adenocarcinoma in the resection specimen (14).

Esophagectomy is the only curative treatment of Barrett's esophagus with high-grade dysplasia, and it should be the first choice in patients who are medically fit. A significant portion of these patients have invasive cancer at the time of surgery. In those in whom high-grade dysplasia is found as part of an endoscopic surveillance program, postoperative survival at 5 years is 90% (17).

Conservative options can be offered to patients who have coexisting medical conditions that prohibit surgery and to patients who decline surgery. One such method is meticulous endoscopic surveillance with aggressive biopsy procedures every 3 months, then every 6 months if no changes are observed (16). This option depends on the endoscopist's ability to distinguish high-grade dysplasia from early adenocarcinoma in biopsy specimens.

Ablation of Barrett's esophagus with laser and photodynamic therapy has been tried experimentally. Ablation removes both Barrett's mucosa and dysplasia in a high proportion of patients (28,29); however, both conditions can recur. Occasionally, Barrett's mucosa underlies newly formed squamous mucosa, so less-accessible cancerous lesions may be a concern. Use of ablation technique is currently reserved for research protocols.

Summary

Esophageal cancer is an increasingly common problem with poor survival rates in patients who present with symptoms. The underlying cause for the progressive rise in the incidence of this cancer remains to be determined. Reducing mortality requires either early identification of patients or prevention of progression from Barrett's esophagus to cancer. Significant questions remain regarding the cost-effectiveness of endoscopic and nonendoscopic methods of surveillance.

For local esophageal cancer, the traditional approach has been surgical resection. Radiation therapy is sometimes used alone, but chemotherapy alone is not helpful. Combination therapy consisting of chemotherapy along with surgery or radiation may be the best choice. A new option being tried in disease limited to the mucosa is ablation of neoplastic tissue with endoscopic techniques.

Treatment of advanced-stage esophageal cancer is limited and may be hampered by the presence of micrometastatic disease. Morbidity and quality-of-life issues need to be considered and discussed with patients, given the current short survival time of most patients with esophageal cancer.

References

1. American Cancer Society. Cancer information page. American Cancer Society Web site. Available at http://www.cancer.org. Accessed March 23, 1999
2. Yang CS, Sun Y, Yang QU, et al. Vitamin A and other deficiencies in Linxian, a high esophageal cancer incidence area in northern China. J Natl Cancer Inst 1984;73(6):1449-53
3. Yang PC, Davis S. Incidence of cancer of the esophagus in the US by histology types. Cancer 1988;61(3):612-7
4. Chalasani N, Wo JM, Waring JP. Racial differences in the histology, location, and risk factors of esophageal cancer. J Clin Gastroenterol 1998;26(1):11-3
5. Sharma P, Morales TG, Bhattacharyya A, et al. Dysplasia in short-segment Barrett's esophagus: a prospective 3-year follow-up. Am J Gastroenterol 1997;92(11):2012-6
6. Ellis A, Field JK, Field EA, et al. Tylosis associated with carcinoma of the oesophagus and oral leukoplakia in a large Liverpool family: a review of six generations. Eur J Cancer B Oral Oncol 1994;30B(2):102-12
7. Brown LM, Swanson CA, Gridley G, et al. Adenocarcinoma of the esophagus: role of obesity and diet. J Natl Cancer Inst 1995;87(2):104-9
8. Lagergren J, Bergstrom R, Lindgren A, et al. Symptomatic gastroesophageal reflux as a risk factor for esophageal adenocarcinoma. N Engl J Med 1999;340(11):825-31
9. Spechler SJ. Complications of gastroesophageal reflux disease. In: Castell DO, ed. The esophagus. 2d ed. Boston: Little, Brown, 1995:533
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11. Kelsen D. Multimodality therapy for adenocarcinoma of the esophagus. Gastroenterol Clin North Am 1997;26(3):635-45
12. Haddad NG, Fleisher DE. Neoplasms of the esophagus. In: Castell, ed (9), p 269
13. Al-Sarraf M, Pajak T, Herskovic, et al. Progress report of combined chemo-radiotherapy vs radiotherapy alone in patients with esophageal cancer: an intergroup study. (Abstr) Pro Am Soc Clin Oncol 1993;12:19
14. Walsh TN, Noonan N, Hollywood D, et al. A comparison of multimodal therapy and surgery for esophageal adenocarcinoma. N Engl J Med 1996;335(7):300-7
15. Clark GW, Ireland AP, DeMeester TR. Dysplasia in Barrett's esophagus: diagnosis, surveillance and treatment. Dig Dis 1996;14(4):213-27
16. Levine DS, Haggitt RC, Blount PL, et al. An endoscopic biopsy protocol can differentiate high-grade dysplasia from early adenocarcinoma in Barrett's esophagus. Gastroenterology 1993;105(1):40-50
17. Laukka MA, Wang KK. Initial results using low-dose photodynamic therapy in the treatment of Barrett's esophagus. Gastrointest Endosc 1995;42(1):59-63
18. Stein HJ, Siewert JR. Barrett's esophagus: pathogenesis, epidemiology, functional abnormalities, malignant degeneration, and surgical management. Dysphagia 1993;8(3):276-88
19. Peters FT, Sleijfer DT, van Imhoff GW, et al. Is chemotherapy associated with development of Barrett's esophagus? Dig Dis Sci 1993;38(5):923-6
20. Reid BJ, Weinstein WM, Lewin KJ, et al. Endoscopic biopsy can detect high-grade dysplasia or early adenocarcinoma in Barrett's esophagus without grossly recognizable neoplastic lesions. Gastroenterology 1988;94(1):81-90
21. Cameron AJ. Epidemiology of Barrett's esophagus. Gastroenterol Clin Biol 1994;18(1 Pt 2):D3-4
22. Stevens PD, Lightdale CJ, Green PH, et al. Combined magnification endoscopy with chromoendoscopy for the evaluation of Barrett's esophagus. Gastrointest Endosc 1994;40(6):747-9
23. Trier JS. Morphology of the columnar cell-lined (Barrett's) esophagus. In: Spechler SJ, Goyal RK, eds. Barrett's esophagus: pathophysiology, diagnosis, and management. New York: Elsevier, 1985:19-28
24. Spechler SJ, Zeroogian JM, Antonioli DA, et al. Prevalence of metaplasia at the gastro-oesophageal junction. Lancet 1994;344(8936):1533-6
25. Vincent ME, Robbins AH, Spechler SJ, et al. The reticular pattern as a radiographic sign of the Barrett esophagus: an assessment. Radiology 1984;153(2):333-5
26. Hiele M, De Leyn P, Schurmans P, et al. Relation between endoscopic ultrasound findings and outcome of patients with tumors of the esophagus or esophagogastric junction. Gastrointest Endosc 1997;45(5):381-6
27. Ponec RJ, Kimmey MB. Endoscopic therapy of esophageal cancer. Surg Clin North Am 1997;77(5):1197-217
28. Sampliner RE. Ablative therapies for the columnar-lined esophagus. Gastroenterol Clin North Am 1997;26(3):685-94
29. Laukka MA, Wang KK, Cameron AJ, et al. The use of photodynamic therapy in the treatment of Barrett's esophagus. Gastrointest Endosc 1993;39(Mar/Apr):291

Dr Shahin is a research fellow and Dr Murray is associate professor of medicine, division of gastroenterology and hepatology, Mayo Medical School, Rochester, Minnesota. Correspondence: Joseph A. Murray, MD, Department of Gastroenterology and Hepatology, Mayo Clinic, 200 First St SW, Rochester, MN 55905. E-mail: murray.joseph@mayo.edu.

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SUBSCRIBE:  The Wednesday Letter is a free electronic monthly newsletter written and published by Karl Loren.  You can view more than 50 back issues of this publication by clicking here.  The Wednesday Letter subscription list is maintained on a secure server, no name is ever given or sold to anyone, and it is never used except for this Newsletter.  It is automatically published on the Tuesday night just before the first Wednesday of every month.  You can subscribe to this free monthly electronic letter by entering your eMail address and name below.  You will then automatically receive a request for confirmation, sent to whatever address you have entered.  If you do NOT receive this confirmation request, then you will not be subscribed.  There may have been an error with your address and you should resubmit.  The letter is never sent twice to the same address -- so you do not have to worry about a duplicate subscription.  When you receive this confirmation request you must reply to it, or your subscription will not become active.  No one can subscribe your name, and address, without you being notified, and if you get an unwanted notice of subscription you only need to DO NOTHING and the subscription will NOT be active.

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Personal Message:  When you send a personal message to Karl Loren, you will receive a personal reply as per his instructions.  Karl pledges that every personal message will get a personal answer. When you provide your mail address, we will send you free information including our free catalog and a cassette tape lecture by Karl Loren about heart disease, no charge, by mail, even if outside the US.  You can select particular information you would like to receive, along with the free cassette tape and catalog.

You can reach Vibrant Life in many ways, including by mail to Vibrant Life, 2808 N. Naomi St., Burbank, CA 91504.  Within the US and Canada, use the toll free number:  (800) 523-4521, the local number:  (818) 558-1799, the FAX:  (818) 558-7299, eMail to kimberly@oralchelation.com or any one of the hundreds of message forms throughout the 50 web sites.  Vibrant Life normally ships the same day we get an order.  There are message forms on each of the 100,000+ pages on this and other sites where you can communicate with Vibrant Life.  Check out our companion site, at:  http://www.oralchelation.net where Karl's 2000 page book is published.  Karl Loren is the author and webmaster for this BOOK, as well as for another web site about ORAL CHELATION.  His personal philosophical articles are at PHILOSOPHY. 

Copyright © May 20, 2008 6:23 AM by Karl Loren on behalf of Vibrant Life, ALL RIGHTS RESERVED.  Permission is granted for non-commercial downloading, copying, distribution or redistribution on two conditions:  One, that some form of copyright notice is included in every copy distributed or copied, showing the copyright belonging to Vibrant Life, Burbank, CA, at www.oralchelation.com . The second condition is that the material is not to be used for any purpose contrary to the purposes and objectives of this site.  This permission does not extend to materials on this site which are copyrighted by others.