Barrett's esophagus: prevalence and size of hiatal hernia

OBJECTIVE: Barrett's esophagus is caused by gastroesophageal reflux and predisposes to adenocarcinoma. Hiatal hernia may cause reflux. The prevalence and size of hernias in patients with Barrett's esophagus was investigated. METHODS: Axial hernia length and the width of the diaphragmatic hiatus were measured prospectively at endoscopy. RESULTS: A 2-cm or longer hernia was found in 96% of 46 patients with Barrett's esophagus, in 42% of 103 controls (p < 0.001), and in 72% of 18 patients with short segment Barrett's esophagus (p < 0.05 vs controls). A hernia was found in 71% of 31 controls with esophagitis and in 29% of 72 controls without esophagitis (p < 0.001). Of 54 controls with neither esophagitis or reflux symptoms, 20% had a hernia. Mean hernia length was 3.95 cm in Barrett's esophagus, and 2.81 cm in controls (p < 0.005). Mean hiatus width was 3.52 cm in patients with Barrett's esophagus and hernia, and 2.24 cm in controls with hernia. Hernia length was similar in patients with and without esophagitis, and in short segment Barrett's esophagus. CONCLUSIONS: Most patients with Barrett's esophagus have hiatal hernia; their hernias are longer and the hiatal openings wider than in controls with or without esophagitis. Hiatal hernia likely contributes to the development of Barrett's esophagus.     

食管裂孔疝的诊治

食管裂孔疝（HH）是临床上常见的消化系统疾病,发病率随年龄增加而增加,诊断方法多种多样,目前主要有胸部X线片、CT影像检查、内镜、高分辨率食管测压等,HH的诊断及分型通过以上检查可以更好的明确。根据患者的病情及临床分型选择不同的治疗方式,临床症状轻微的滑动型食管裂孔疝仍以保守治疗为主,其他分型首选外科治疗。目前腹腔镜治疗已替代传统开放性手术成为外科治疗的首选,疝修补及胃底折叠术作为标准术式,但具体术式的选择及补片的应用应结合病情及术者的经验遵循个体化治疗原则。对于术后并发症应尽早评估、积极预防、及时处理。     

A predictive model for length of Barrett's esophagus with hiatal hernia length and duration of esophageal acid exposure

BACKGROUND: A significant correlation between the duration and height of esophageal acid exposure and the length of Barrett's mucosa has been demonstrated. The aims of this study were to determine if there is a correlation between hiatal hernia length and Barrett's esophagus length, and to develop a predictive model for Barrett's esophagus length by using hiatal hernia length and duration of esophageal acid exposure. METHODS: Consecutive patients with Barrett's esophagus diagnosed endoscopically were enrolled in the study. Barrett's esophagus was defined by the presence of intestinal metaplasia in biopsy specimens obtained from salmon-colored mucosa extending into the esophagus. Barrett's mucosa 3 cm or greater in length was considered long-segment Barrett's esophagus; and less than 3 cm long was considered short-segment Barrett's esophagus. Hiatal hernia was considered present if the esophagogastric junction was displaced 1 cm or more proximal to the diaphragmatic hiatus. RESULTS: Twenty-four men (mean age 66.1 +/-2.4 [SE]) with Barrett's esophagus were included in this study. Mean Barrett's length was 4.1 +/-0.7 cm. The Pearson correlation coefficient between hiatal hernia length and Barrett's esophagus length was 0.62 (p < 0.01). Similarly, there was a significant correlation between esophageal acid exposure and Barrett's length (r = 0.62; p < 0.01). Multiple linear regression analysis revealed that hiatal hernia length and duration of esophageal acid exposure were associated significantly with length of Barrett's mucosa (R(2) = 0.54; p < 0.001). A regression equation was developed expressing mean Barrett's length (cm) = 0.79 + (0.68) hernia length (cm) + (0.075) duration of esophageal acid exposure (% time pH < 4). CONCLUSIONS: The length of Barrett's mucosa correlated with the length of hiatal hernia. A predictive model for Barrett's length by using hiatal hernia length and duration of esophageal acid exposure was developed. This suggested that these two pathophysiologic factors are good predictors of the length of Barrett's mucosa.     

Hiatal hernia and the risk of Barrett's esophagus

Background and Aim: Barrett's esophagus has been associated with the presence of hiatal hernia; however, to date no meta‐analysis of the relationship has been performed. We aimed to conduct a systematic review and meta‐analysis, providing a quantitative estimate of the increased risk of Barrett's esophagus associated with hiatal hernia. Methods: A search was conducted through four electronic databases (Medline, PubMed, Embase, and Current Contents Connect) to 4 April 2012, for observational studies of Barrett's esophagus patients. We calculated pooled odds ratios and 95% confidence intervals using a random effects model for the association of hiatal hernia with any length Barrett's esophagus, as well as with short segment Barrett's esophagus and long segment Barrett's esophagus. 33 studies comprising 4390 Barrett's esophagus patients were eligible for the meta‐analysis. Results: Hiatal hernia was associated with an increased risk of Barrett's esophagus of any length (odds ratio 3.94; 95% confidence interval 3.02–5.13). Heterogeneity was present (I² = 82.03%, P < 0.001), and the Egger test for publication bias was significant (P = 0.0005). The short segment Barrett's esophagus subgroup analysis likewise showed an increased risk (odds ratio 2.87; 95% confidence interval 1.75–4.70). The strongest association was between hiatal hernia and long segment Barrett's esophagus (odds ratio 12.67; 95% confidence interval 8.33–19.25). The increased risk was present even after adjusting for reflux and body mass index. Conclusions: The presence of hiatal hernia was associated with an increased risk of Barrett's esophagus, even after adjusting for clinically significant confounders. The strongest association was found between hiatal hernia and long segment Barrett's esophagus.     

Reduction of acid exposure and regression of Barrett's esophagus

The goals of treatment of Barrett's esophagus (BE) include relieving reflux symptoms, healing inflammatory lesions, and preventing esophageal adenocarcinoma. Reduction of acid reflux is believed to prevent progression of BE. A critical question is whether or not regression of BE occurs in response to therapy with proton pump inhibitors. The natural history of BE is altered both by the use of medications (over-the-counter or prescribed) and by endoscopic surveillance with periodic biopsies. Regression occurs when the length and surface area of BE decreases, along with the emergence of islands of squamous epithelium in the BE segment. However, the extent of regression is difficult to assess because intestinal metaplasia may underlie the islands of squamous epithelial regrowth. Sampling by endoscopic biopsy is useful in ruling out progression of BE to dysplasia or adenocarcinoma; however, complete regression of the lesion cannot be definitively proven by this technique. To date, published clinical trials of proton pump inhibitor therapy in patients with BE provide evidence of increases in squamous islands in the BE segment, but do not provide convincing data in support of complete regression of BE. In a review of prospective studies of the treatment of BE with proton pump inhibitors (PPIs) (with or without surgery), only 3 of 123 patients had apparent complete reversal of BE. This article reviews the current understanding of regression in BE following treatment with PPIs.     

Prospective multivariate analysis of factors predictive of complete regression of Barrett's esophagus

OBJECTIVE: Demographic, endoscopic, and histological features of Barrett's esophagus at initial diagnosis were examined for their ability to predict complete endoscopic and histological regression of Barrett's during long-term follow-up. METHODS: Barrett's patients who have been followed up for a minimum of 2 yr and who have had at least two follow-up surveillance examinations were included in the analysis. Complete regression of Barrett's was defined as total disappearance of all tongues and patches of Barrett's epithelium at endoscopy (confirmed with Lugol's iodine) in conjunction with only squamous epithelium on biopsy. Chi2 and stepwise logistic regression analyses were performed on the following clinical, endoscopic, and histological variables with regards to their ability to predict complete Barrett's regression: patient age in years (<65 or > or =65), length in cm of Barrett's (< or =2, >2<6, and > or =6), presence of a hiatal hernia (yes or no), presence of dysplasia at diagnosis (yes or no), and type of long-term medical treatment (histamine antagonists, proton pump inhibitor [PPI], or PPI and cisapride). RESULTS: Ninety-nine patients, all men with a mean age +/- SD in years of 61.6+/-13.1 have been followed prospectively for 24-106 months (mean +/- SD, 48.0+/-19.8). Seven patients have had complete regression of Barrett's. Univariate analysis showed that complete regression of Barrett's was associated only with absence of a hiatal hernia (p = 0.012). Stepwise logistic regression analysis revealed that complete regression was significantly and independently associated again only with absence of a hiatal hernia (p = 0.025). Stepwise logistic regression analysis utilizing only hiatal hernia (yes vs no) and length of Barrett's (<6 cm vs > or =6 cm) as variables revealed that absence of a hiatal hernia (p = 0.0447) and shorter lengths (<6 cm) of Barrett's (p = 0.0418) were significantly and independently predictive of complete Barrett's regression. CONCLUSIONS: The absence of a hiatal hernia was noted to be the most important factor associated with Barrett's regression. Complete regression of Barrett's esophagus occurs in a minority of patients, primarily in those with no hiatal hernia and shorter lengths of Barrett's epithelium.     

Immunohistochemical analysis of short-segment Barrett's esophagus

BACKGROUND AND AIMS: The majority of dysplasias and adenocarcinomas in Barrett's esophagus are closely associated with the specialized columnar epithelium. In this study, we performed an immunohistochemical analysis of columnar metaplasia presenting in short-segment Barrett's esophagus (SSBE). PATIENTS AND METHODS: The endoscopic biopsy specimens obtained from 91 patients were analyzed. Ten were cases of long-segment Barrett's esophagus (LSBE) and 81 had SSBE. Expression of MUC2, MUC5AC, Con A and CD10 was evaluated using immunohistochemical staining. RESULTS: All samples from LSBE (n = 9) were histologically diagnosed as specialized columnar epithelium. The 81 SSBE samples were divided into gastric fundic-type (n = 26), junctional-type (n = 16) and specialized columnar epithelium (n = 39). In the specialized columnar epithelium of SSBE, there was a predominance of goblet cell-type metaplasia proposed by Watanabe et al. which is characterized by MUC2-positive pyloric epithelium (66.7%). The total percentage of non-goblet cell-type and goblet cell-type was 76.9%. In contrast, 80% of LSBE revealed the large intestinal-type or the large and small intestinal-type. The long oval and villous pit by magnifying endoscope suggests the presence of the specialized columnar epithelium, but the phenotypic classification of Watanabe's criteria was not associated with the endoscopic pit pattern. CONCLUSION: Intestinal metaplasia in Barrett's esophagus changes immunohistochemically with progress of the disease.     

Barrett's esophagus

Barrett's esophagus is an acquired condition resulting from severe esophageal mucosal injury. It still remains unclear why some patients with gastroesophageal reflux disease develop Barrett's esophagus whereas others do not. The diagnosis of Barrett's esophagus is established if the squamocolumnar junction is displaced proximal to the gastroesophageal junction and if intestinal metaplasia is detected by biopsy. Despite this seemingly simple definition, 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 of the esophagus. The incidence of esophageal adenocarcinoma continues to increase and the 5-year survival rate for this cancer remains dismal. However, cancer risk for a given patient with Barrett's esophagus is lower than previously estimated. Current strategies for improved survival in patients with esophageal adenocarcinoma 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, antireflux surgery, chemoprevention, and ablation therapy, but there is still no clear consensus on the optimal treatment for these patients.     

Barrett's esophagus

Barrett's oesophagus is a premalignant metaplastic change of the oesophageal mucosa. Due to its relationship with oesophageal reflux disease and the development of adenoma-carcinoma of the oesophagus the problem arouses increasing interest. In the wide pathogenesis of the disease most probably the composite effect of the refluxed HCl content and duodenal juices play a part. In the diagnosis in addition to fundamental methods--endoscopy and histology--increasingly chromoendoscopy and fluorescent endoscopy are involved. Dispensarization of patients is essential and depends on the degree of pathohistological epithelial changes. Treatment of Barrett's oesophagus can be divided into conservative, where the drug of choice are proton pump inhibitors, and surgical treatment. Promising is endoscopic ablation of the epithelium in combination with subsequent antisecretory therapy.     

Barrett's esophagus

Barrett's esophagus is an acquired metaplastic abnormality in which the normal stratified squamous epithelium lining of the esophagus is replaced by an intestinal-like columnar epithelium. While in itself a benign and asymptomatic disorder, the clinical importance of this relatively common condition relates to its role as a precursor lesion to esophageal adenocarcinoma, the incidence of which has dramatically increased in Western populations in recent years. Although known to arise as a consequence of chronic gastroesophageal reflux, the cellular and molecular mechanisms underlying development Barrett's esophagus and its progression to cancer remain unclear.     

Achalasia and hiatal hernia

Several reports have emphasized the rarity of hiatal hernia in achalasia, despite the lack of inherent incompatibility of the two conditions and despite the relatively high frequency of hiatal hernia in the general population. We reviewed the radiographs of 71 of 94 consecutive patients with manometrically proven achalasia referred to Yale-New Haven Hospital. Unequivocal hiatal hernia was seen in 10 (14.1%) patients and was seen in nine of 35 (25.7%) patients 51 years old or more. Review of the radiographic reports from these 10 patients indicated that only two were properly recognized as showing both achalasia and hiatal hernia. All five patients who underwent pneumatic dilatation had excellent results. We conclude that hiatal hernia in achalasia is frequently unrecognized and underreported but is not rare, with a frequency probably similar to that of the general population.     

Partial regression of Barrett's esophagus by long-term therapy with high-dose omeprazole

Background: Barrett's esophagus is mainly regarded as an acquired condition related to increased gastroesophageal reflux. Thus it is conceivable that abolition of acid reflux would lead to its regression. The aim of this study was to assess whether long-term treatment with high-dose omeprazole (60 mg/day) produces a consistent control of gastric acid production and normalizes the esophageal acid exposure, thus reducing the length of Barrett's epithelium. Methods: Fourteen patients (8 men and 6 women, mean age 52 years) with histologic diagnosis of columnar epithelium longer than 3 cm in the distal part of the esophagus were enrolled and began receiving 60 mg of omeprazole in a single daily morning dose. Before therapy and after 6 and 12 months of therapy, all patients had endoscopy with four-quadrant biopsies at 2 cm intervals. A 24-hour esophagogastric pH recording was performed at entry and after 10 days, 6 months, and 12 months of treatment in all patients. Results: The initial length of Barrett's epithelium (4.5 ± 1.9 cm) was significantly reduced after 6 months (3.1 ± 1.1; p < 0.01) and 12 months (2.1 ± 1.6; p < 0.005) of treatment. Values were significantly lower at 12 than at 6 months (p < 0.03). The 24-hour mean gastric pH after 10 days (5.89 ± 0.58), 6 months (5.71 ± 0.55), and 12 months (5.54 ± 0.76) of therapy was always higher (p < 0.001) than the basal level (1.9 ± 0.49). No significant difference in gastric pH was seen over the treatment period. The 24-hour mean percent of time in which pH in the esophagus was below 4.0 decreased significantly (p < 0.001) from a basal rate of 29.4% to 3.5%, 3.0%, and 4.9% in the various time intervals of therapy. There was a normalization of esophageal acid exposure in all patients but two. Conclusions: It can be concluded that the antisecretory effect of 60 mg/day of omeprazole is consistent and is kept constant throughout the entire 1-year treatment period. The consequent normalization of esophageal acid exposure in almost all patients in our series led to a partial, but significant, regression in the length of Barrett's epithelium. (Gastrointest Endosc 1996;44:700-5)