Hiatal Hernia and the Risk of Barrett's Esophagus

Juliana Andrici; Martin Tio; Michael R Cox; Guy D Eslick


J Gastroenterol Hepatol. 2013;28(3):415-431. 

In This Article

Abstract and Introduction


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.


Barrett's Esophagus (BE) is a condition in which the normal squamous esophageal lining is replaced by specialized or intestinal columnar epithelium.[1,2] According to current guidelines in North America,[3] BE is diagnosed when columnar mucosa is identified above the gastroesophageal junction on endoscopy and is confirmed to contain specialized intestinal epithelia (characterized by the presence of goblet cells) on histological examination. Since 1994, BE has been classified as either short segment BE (SSBE) or long segment BE (LSBE) according to the length of the metaplastic change observed on endoscopic examination.[4] If the intestinal metaplasia extends less than 3 cm above the gastroesophageal junction, it is termed SSBE, and if it extends 3 cm or more, it is termed LSBE. The prevalence of BE in the general US population is uncertain, due to the fact that many individuals are asymptomatic, and because diagnosis requires endoscopy. A study from Sweden found a prevalence of 1.6% in a random sample of 3000 individuals from the general population.[5] Among patients with gastroesophageal reflux disease (GERD), the prevalence of BE has been reported to be between 3% and 15%.[6,7] The clinical significance of BE is its association with an increased risk in developing esophageal adenocarcinoma.[8,9] Although esophageal adenocarcinoma is a relatively uncommon disease, its incidence has been increasing in the US and other Western countries in recent decades.[10–15]

Risk factors for BE include white race, male sex, older age, obesity[16] and persistent gastroesophageal reflux.[17] Hiatal hernia has also been associated with BE. Hiatal hernia refers to the prolapse of elements of the abdominal cavity, most commonly parts of the stomach, through the esophageal hiatus of the diaphragm and into the thoracic cavity. The most common type is Type I, or sliding hernia, in which the lower esophageal sphincter and a portion of the gastric cardia herniate upwards due to a widening of the muscular hiatal aperture and circumferential laxity of the phrenoesophageal membrane.[18–20] The presence of hiatal hernia results in anatomical impairment of the esophagogastric junction, which leads to reflux of gastric material into the esophagus. This includes gastric products such as hydrochloric acid and pepsin, as well as pancreatic enzymes and bile.[17,19] It is hypothesized that chronic exposure to these substances is a contributing factor to the development of BE.

Although individual studies have shown a higher prevalence of hiatal hernia in BE patients compared with non-BE GERD patients,[21–23] to date no meta-analysis of the relationship between BE and hiatal hernia has been performed. The purpose of this study was to conduct a meta-analysis combining the results of studies reporting the prevalence of hiatal hernia in BE subjects, and thus provide a quantitative estimate of the increased risk of BE associated with hiatal hernia. We hypothesized that hiatal hernia is associated with an increased risk BE, and that we would see a stronger association with LSBE than with SSBE.