[Complications of gastroesophageal reflux disease. 2. Endoscopic diagnosis of Barrett esophagus--can Barrett esophagus be diagnosed by endoscopic observation alone?].
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Barrett Esophagus↗
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Rationale for surgical therapy of Barrett esophagus.
Barrett esophagus has malignant potential and seems to be an acquired abnormality. It is associated with chronic gastroesophageal reflux disease and represents its severest form. The literature comparing medical treatment with antireflux surgery was reviewed. Questions regarding the advantages of surgery, who should undergo surgery, whether surgery can change the course of Barrett esophagus, the change in cancer risk, who needs surveillance, and cost-effectiveness were addressed. The incidence of developing Barrett cancer was 1 in 145 patient-years in reviewing 2032 patient-years of medical therapy compared with 1 in 294 patient-years in reviewing 4122 patient-years after surgery. Median follow-up time in the 2 groups was 2.7 years in the medically treated patients and 4.0 years in the surgically treated patients. Surveillance of Barrett esophagus is required irrespective of treatment. Laparoscopic antireflux surgery was found to be cost-effective after 7 years. Although these data do not prove that surgery is superior to medical treatment in the prevention of cancer related to Barrett esophagus, we found a tendency for surgery to be better than medical therapy to prevent the development and progression of Barrett carcinoma.
Barrett Esophagus↗
Clinicopathologic and molecular analysis of high-grade dysplasia and early adenocarcinoma in short- versus long-segment Barrett esophagus.
Barrett esophagus, especially dysplastic Barrett mucosa, has been regarded as a preneoplastic lesion for esophageal adenocarcinoma. However, the etiology and pathogenesis of dysplasia and early adenocarcinoma in short- (SSBE) and long- (LSBE) segment Barrett esophagus have not been studied in detail. The aims of this study were to clarify clinicopathologic and genetic differences between high-grade dysplasia (HGD) and early adenocarcinoma in SSBE versus LSBE. We analyzed the clinicopathologic features from 47 patients (19 SSBE [<3 cm] and 28 LSBE [> or =3 cm]) with esophagectomy for HGD/T1 adenocarcinoma. Allelic losses on chromosomes 3p (FIHT), 5q (APC), 9p (p16), and 17p (p53) were compared in 12 HGD and 9 T1 tumors from 19 cases of SSBE and in 23 HGD and 15 T1 tumors from 28 cases of LSBE. Patients with SSBE were more likely to be smokers than were patients with LSBE (94.7% v 57.1%; P =.004). HGD or T1 tumors arising from SSBE were less likely to show adjoining nondysplastic Barrett mucosa than those from LSBE (73.6% v 100%; P =.02). LSBE more frequently showed a circumferential pattern of Barrett mucosa than did SSBE (96.4% v 47.3%; P =.0002). Chromosomal allelic losses on 3p, 5q, 9p, and 17p were detected in 19% (4 of 21), 43% (15 of 35), 40% (14 of 35), and 48% (16 of 33) of HGD, respectively, and 26% (5 of 19), 35% (8 of 23), 35% (8 of 23), and 57% (13 of 23) of T1 tumor, respectively. There were no significant differences in allelic loss of 3p, 5q, 9p, or 17p in HGD or T1 tumors from SSBE versus LSBE. These results suggest that both HGD and early adenocarcinoma in SSBE and LSBE may occur through similar genetic alterations, whereas there are some clinicopathologic differences between SSBE and LSBE. HUM PATHOL
Aged↗
Biomarkers in Barrett esophagus.
Barrett esophagus is a premalignant condition that may progress to adenocarcinoma. The risk of developing cancer has been estimated to be approximately 1 in 250 patient-years of observation; however, there appear to be subsets of patients at much higher risk. Risk stratification has previously been determined by histological identification of dysplasia. Several new biomarkers are being tested to help clinicians better determine the risk of cancer development. Although none of these biomarkers has been proven in a prospective study to predict the onset of cancer, they have been correlated with cancer development. Most of these are factors that have been associated with cancer development in other organs. These include assessment of cell proliferation, expression of cyclooxygenase 2, growth factors and oncogenes, secretory factors, cell cycle proteins, adhesion molecules, and aneuploidy and other genetic abnormalities. In addition to their role as potential cancer biomarkers, these factors have increasingly been reported as surrogate markers to monitor the effectiveness of conservative treatments for Barrett esophagus. In this article, biological markers are reviewed for their relevance in Barrett esophagus. Although most biological markers need to be evaluated further and, for most, prospective follow-up studies are lacking, at present abnormal ploidy status, P16 and P53 gene abnormalities, or allelic losses are the most extensively documented.
Barrett Esophagus↗
Barrett esophagus.
Barrett esophagus continues to intrigue investigators and clinicians alike as the new millennium begins. A large number of publications in the past year have discussed issues of epidemiology, prevalence, detection, and treatment of Barrett esophagus. Chronic symptoms of gastroesophageal reflux were identified as a strong risk for esophageal adenocarcinoma. The relative frequency of short and long Barrett and cardia intestinal metaplasia in patients who undergo upper endoscopy have been better defined. Biomarkers in patients with Barrett may eventually be helpful in identifying those at high risk for the development of neoplasia. High-dose proton pump inhibition to the point of near elimination of esophageal acid exposure remains disappointing in its impact on the surface area of Barrett. Finally, the developments in endoscopic therapy for patients with Barrett esophagus continue to be promising.
Journal Article↗
Pathogenesis of gastroesophageal reflux and Barrett esophagus.
Barrett esophagus is a metaplastic condition that affects the lower esophagus and is a complication of gastroesophageal reflux disease (GERD). Under normal circumstances, the reflux of gastric contents into the esophagus is prevented by a complex barrier at the esophagogastric junction. Dysfunction of the lower esophageal sphincter and the presence of a hiatal hernia lead to failure of this barrier. Esophageal mucosal damage results from the chronic exposure of the esophageal mucosa to gastroduodenal contents and the lack of an effective mucosal defense. This article is an overview of the dysfunction of the esophagogastric junction that leads to GERD. The role of the contents of the reflux and that of Helicobacter pylori infection in the pathogenesis of Barrett esophagus are also summarized.
Animals↗
How to make a Barrett esophagus: pathophysiology of columnar metaplasia of the esophagus.
Barrett esophagus is defined as a specialized intestinal replacing the squamous epithelium of the esophageal mucosa in response to gastroesophageal reflux. Barrett metaplasia is a healing process that develops to protect the esophagus from further damage. Although mechanisms by which Barrett metaplasia evolves toward dysplasia and adenocarcinoma have been extensively studied, the process by which squamous epithelium is replaced by specialized intestinal metaplasia is poorly understood. Barrett esophagus develops when defense mechanisms in the esophageal mucosa (luminal secretion of mucus, bicarbonate, growth factors, etc.) are overwhelmed by an ongoing cycle of mucosal injury and repair. Hydrogen ion, pepsin, trypsin, and bile acids are considered harmful agents that synergistically invade the esophageal mucosa. Areas of destroyed squamous epithelium are then progressively reepithelized by a columnar epithelium that may originate from multipotent stem cells located within the basal layer of the normal esophageal mucosa or in the ducts of submucosal glands.
Barrett Esophagus↗
Barrett esophagus.
Barrett esophagus is the term describing the presence of an abnormal columnar epithelium in a portion of the esophagus. We have treated 19 patients within the past three years, representing almost 20% of all our esophageal experience; This one pathologic entity has presented as several different clinical pictures: benign stricture, peptic ulceration of the esophagus, intractable esophagitis, and malignancy. One half the patients were under 50 years old, and most were male. The benign lesions have responded well to surgical therapy. There has been an unusually high incidence of malignancy-26.3%. The reasons for the infrequent diagnosis of Barrett esophagus are confusion with "short esophagus" and failure to biopsy the proper site.
Adult↗
Mucosal ablation therapy of barrett esophagus.
Barrett esophagus is defined by the metaplasia of existing squamous mucosa into a specialized intestinal-type mucosa. The importance of this metaplasia is the association of this condition with the development of adenocarcinoma of the esophagus. Elimination of the metaplastic mucosa may decrease the cancer risk. Currently, several forms of therapy have evolved with the goal of replacing the specialized mucosa with normal squamous mucosa. These proposed treatments include photodynamic therapy and thermal techniques. The effectiveness of photodynamic therapy varies depending on the pharmaceutical photosensitizer used and the wavelength of light applied to activate the drug. Thermal techniques include multipolar coagulation, argon plasma coagulation, KTP:YAG laser therapy, Nd:YAG laser therapy, and argon laser therapy. Finally, mucosal resection has been attempted through the endoscope to remove large areas of the Barrett mucosa. All of these ablative strategies attempt to destroy the metaplastic mucosa and promote the regrowth of squamous epithelium. These therapies have demonstrated the ability to "reverse" the metaplasia to varying degrees, but a decrease in cancer risk has not been demonstrated conclusively with any of these treatment methods.
Antacids↗
Frequent c-myc amplification in high-grade dysplasia and adenocarcinoma in Barrett esophagus.
Barrett esophagus (BE) is a condition in which the normal squamous epithelium of the esophagus is replaced by a metaplastic columnar epithelium. BE is a premalignant lesion that represents the initial step in a metaplasia-dysplasia-carcinoma sequence. In the present study, amplification of the proto-oncogene c-myc was determined by means of differential polymerase chain reaction analysis of metaplastic specialized epithelium, low-grade dysplasia, high-grade dysplasia, and invasive adenocarcinoma obtained by microscopic dissection of 43 esophagectomy specimens. Amplification of c-myc was found in none of 29 specialized epithelial specimens, none of 23 low-grade dysplasia specimens, 6 of 24 high-grade dysplasia specimens, and 17 of 39 adenocarcinoma specimens. Our data indicate that amplification of c-myc is a late event in the metaplasia-dysplasia-carcinoma sequence in BE. Furthermore, determination of c-myc amplification may help identify high-risk patients who would benefit from intensified endoscopic surveillance or from immediate treatment.
Adenocarcinoma↗
Prospective evaluation of the prevalence of gastric Helicobacter pylori infection in patients with GERD, Barrett's esophagus, Barrett's dysplasia, and Barrett's adenocarcinoma.
OBJECTIVE: This study was undertaken to prospectively determine the prevalence of gastric H. pylori infection in Barrett's esophagus and Barrett's complicated by dysplasia or adenocarcinoma. METHODS: The prevalence of H. pylori was determined in Barrett's esophagus patients compared to a control population of patients with gastroesophageal reflux disease (GERD) only. All patients had a minimum of 10 gastric surveillance biopsies obtained. H. pylori colonization was determined upon the basis of hematoxylin and eosin and use of a modified Giemsa and or Steiner's silver stain of all gastric biopsy specimens. RESULTS: Two hundred and eighty-nine Barrett's patients and 217 GERD control patients were included in the study. H. pylori was found in 95/289 (32.9%) of the Barrett's patients, compared with 96/217 (44.2%) of the GERD controls (NS). Forty-seven of the Barrett's patients had low-grade dysplasia/indefinite dysplasia, 14 high-grade dysplasia, and 20 Barrett's adenocarcinoma. When Barrett's was subgrouped according to absence of dysplasia, and presence of low-grade dysplasia, high-grade dysplasia, or adenocarcinoma, H. pylori prevalence was found to be significantly less for patients with Barrett's high-grade dysplasia (14.3%) and adenocarcinoma (15.0%) versus patients with GERD alone (44.2%), Barrett's alone (35.1%), or Barrett's with low-grade dysplasia (36.2%) (p = 0.016). This difference could not be explained by differences between Barrett's esophagus patients infected with H. pylori and those who were not with respect to gender, smoking history, alcohol consumption, use of proton pump inhibitor, or length of Barrett's mucosa. CONCLUSIONS: Barrett's high-grade dysplasia and adenocarcinoma are significantly more prevalent in patients who are not infected with H. pylori. H. pylori appears to have a protective effect against the development of Barrett's adenocarcinoma.
Adenocarcinoma↗
[Barrett esophagus].
Barrett's oesophagus is a complication of chronic gastrooesophageal reflux disease and occurs in eight percent of patients with reflux symptoms. The diagnosis is made by endoscopy with biopsy. Dysplasia and early adenocarcinoma may involve only very small irregular areas of the oesophageal mucosal surface. Biopsies should therefore be taken from each quadrant at 1-2 cm intervals. The prevalence of dysplasia is about five to 16 percent, while the prevalence rate of oesophageal adenocarcinoma ranges from nought to ten percent and the incidence is one case per 87 patients years. No consensus concerning the treatment strategy for patients with metaplasia and low grade dysplasia has been achieved, because there is no conclusive proof as yet that screening programmes reduce the mortality from adenocarcinoma. Patients with high grade dysplasia should be controlled with endoscopy and biopsies every sixth month. Flow cytometry seems to be able to identify a subset of patients with an increased risk of oesophageal adenocarcinoma.
Adenocarcinoma↗
The incidence of adenocarcinoma and squamous cell carcinoma of the esophagus: Barrett's esophagus makes a difference.
BACKGROUND: Adenocarcinoma limited to the esophagus (ACE) arises in Barrett's esophagus (BE). The incidence of ACE is therefore restricted to this BE subpopulation, whose size is unknown and which is for 95% unidentified. AIMS: To determine the age- and gender-specific incidence rates of ACE, limited to the BE subpopulation, within a defined geographical area and to compare them with those of squamous cell carcinoma of the esophagus (SCC), which can affect the entire population. METHODS: The age- and gender-specific incidence rates for ACE and adenocarcinoma of the cardia (AGC) were calculated after an expert panel classified 87% of all cases of adenocarcinoma of the esophagus reported to the Danish Cancer Registry over a 6-yr period as ACE or AGC. RESULTS: The age-specific incidence rates of ACE for males rose from 0.09/10(5) (30-34 yr) to 14.14/10(5) (80-84 yr), falling to 7.2/10(5) (85+ yr), for females from 0.19/10(5) (45-49 yr) to 2.79/10(5) (80-84 yr), falling to 2.43/10(5) (85+ yr) and yielding a gender ratio of 5.9:1; AGC demonstrated a similar pattern and a gender ratio of 4.26:1. However, the incidence rates of SCC continued rising after the age of 80 yr, with a gender ratio of 2.46:1. CONCLUSIONS: The continuing rise in the SCC incidence rates in the elderly demonstrated that the unexpected decline and fall in the incidence rates of ACE over the age of 80 yr did not result from underdiagnosis but were most probably caused by a declining prevalence rate of BE, restricting the elderly BE subpopulation at risk of developing ACE.
Adenocarcinoma↗
The spectrum of columnar-lined esophagus--Barrett's esophagus.
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Adenocarcinoma↗
Incomplete intestinal metaplasia in the diagnosis of columnar lined esophagus (Barrett's esophagus).
To investigate the distribution and specificity of intestinal metaplasia (IM) in columnar lined esophagus (CLE), the authors reviewed biopsies of the hiatal hernia pouch (HHP) and esophagus from 17 patients with CLE (84 biopsies) and 10 controls (25 biopsies). The proximal margin of the gastric folds was used as an endoscopic landmark, corresponding to the gastroesophageal muscular junction (GEMJ). No biopsies obtained above the GEMJ in control patients showed columnar mucosa. No goblet cell metaplasia was seen in 21 biopsies of the HHP from patients with CLE or in 13 corresponding biopsies from controls. In contrast, alcian blue (AB) stains showed diffuse acid mucins in 3 of 21 biopsies of the HHP from patients with CLE and in 10 of 13 corresponding biopsies from controls, demonstrating that goblet cell metaplasia clearly distinguishes biopsies of CLE from the HHP (P less than 0.01), whereas small amounts of diffuse acid mucin on AB stains do not. IM evidenced by goblet cell metaplasia was frequently seen in biopsies only 2-3 cm above the GEMJ, and CLE was limited to that area in three patients, suggesting that the distal esophagus cannot be dismissed as a site for metaplastic and possibly premalignant mucosa. Adenocarcinoma was diagnosed during the course of the study in one patient with only 5 cm of columnar mucosa above the GEMJ.
Adult↗
Celiac disease and intestinal metaplasia of the esophagus (Barrett's esophagus).
Previous studies on celiac patients demonstrated that exposure to gliadin alters the motility of the upper gastrointestinal tract, leading to increased acid reflux. No literature is available regarding the possible presence of specialized intestinal metaplasia of the esophagus as a consequence of chronic reflux in adult celiac patients. Our purpose was to evaluate endoscopically and histologically the esophagi of a group of untreated celiac patients. We studied 60 celiac patients, 13 men and 47 women (mean age, 40 +/- 14 [SD] years; range, 18-80 years), at their first endoscopy (following a normal diet). The distal esophagus was evaluated and multiple biopsies were taken. Hematoxylin-eosin and alcian blue stainings were performed. A group of nonceliac, age- and sex-matched patients was used as a control. We found intestinal metaplasia in the distal esophagus of 16 of 60 (26.6%) celiacs (mean age, 45 +/- 13 years; range, 27-75 years), in comparison with a control-group prevalence of 10.9% (OR, 3.9; 95% CI, 1.4-11.2%). Among the celiac group with metaplasia, only one patient had reflux-like symptoms. None had esophagitis. In conclusion, we observed an increased prevalence of esophageal metaplasia in patients with celiac disease. This finding could be the result of motor abnormalities leading to chronic acid reflux, combined with a mucosa which is sensitive to gliadin.
Adult↗
Cyclooxygenase-2 in Barrett's esophagus, Barrett's adenocarcinomas, and esophageal SCC: ready for clinical trials.
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Adenocarcinoma↗
[Barrett esophagus and Barrett cancer].
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Adenocarcinoma↗