Erosive esophagitis, or breaks in the esophageal mucosa, represents one of the common manifestations of chronic reflux disease. Histologi-cally, erosive esophagitis is defined as superficial necrotic defects that do not penetrate the muscularis mucosae, whereas esophageal ulcerations are described by a deeper invasion through the muscularis mucosae and into the submucosa.2 Several classifications have attempted to grade the severity of esophagitis as observed at the time of upper endoscopy. One such classification system, the Los Angeles classification (Table 4.1) grades the esophageal change from A to D, depending on the severity and extent of erosions determined during endoscopy.
Although the exact population prevalence of erosive esophagitis is not known, it is estimated to vary from 0.7 to 1.2% regardless of symptoms of heartburn.9 This was recently demonstrated in a cross-sectional study performed to explore the complications of GERD in 11,691 patients undergoing endoscopic evaluation. Of these, esophagitis was diagnosed in 1633 patients, with an overall prevalence of 14% (61% men, 39% women).10 However, in those patients with reflux symptoms, approximately 40-60% may have endoscopic evidence of esophageal
MANAGING FAILED ANTI-REFLUX THERAPY
Table 4.1. Los Angeles classification of esophagitis.
Grade A mucosal break confined to folds, no >5mm
Grade B >1 mucosal break >5mm confined to folds but not continuous between tops of folds
Grade C Mucosal breaks that are NOT circumferential, but are continuous between the tops of two or more mucosal folds
Grade D Circumferential mucosal breaks erosions.11 It is unclear if the prevalence of reflux symptoms and erosive esophagitis is increasing. Some studies have in fact noted a decrease in the frequency of erosive esophagitis. Todd and colleagues12 reported results from an endoscopic database in Tayside, Scotland over a 15-year period. A significant decrease in the prevalence of esophagitis was discovered, contrasting sharply with an increase in the incidence of Barrett's esophagus during the same time interval.12
The prevalence of erosive esophagitis may also differ in various ethnic and racial populations indicating that host factors may have an important role in the pathogenesis of this complication of GERD. El-Serag and colleagues13 reported the differences in gastroesophageal reflux between different racial groups in the United States and used logistical regression analysis (controlling for several variables) to find an association between various racial groups and GERD. Among 496 individuals who completed a GERD questionnaire, and 215 who had an endoscopy, the age-adjusted prevalence of heartburn was similar among all racial groups studied (whites, blacks, and hispanics). Of note, however, black patients had a significantly lower risk of esophagitis (adjusted odds ratio 0.22-0.46). Thus, although the prevalence of GERD symptoms may be similar between blacks and whites, blacks seem less likely to have endoscopic evidence of esophagitis.13
In another study, among a mix of 1985 Chinese, Malaysian, and Indian patients, only 6% had evidence of erosive esophagitis (majority with mild esophagitis). Males seemed to have a higher incidence of esophagitis compared with females, as did those of Indian decent and the presence of hiatal hernia also seemed to increase the chances of finding erosive esophagitis.14 In a study from Taiwan, Yeh and colleagues15 evaluated 464 patients with upper gastrointestinal symptoms and 66 (14.5%) of these patients were found to have erosive esophagitis. In addition, a male-to-female pre ponderance of 3.1:1 was witnessed and disease severity was also found to increase with age, particularly in individuals in their 60s and 70s.15
The pathological reflux of gastric and duodenal contents into the esophagus disrupts the normal protective environment. This refluxed material consists not only of acid and pepsin, but also bile and pancreatic juices which contribute to epithelial damage and possibly even to Barrett's metaplasia. The degree and extent of this damage is directly correlated with the type, timing, and duration of the refluxate, but inversely correlated with the speed of esophageal acid clearance and esophageal mucosal resistance.16,17
Much controversy surrounding the pathogen-esis of erosive esophagitis centers around the concept of disease progression. It has been theorized by some investigators that erosive esophagitis represents a continuum to more complex gastroesophageal complications.18 This continuum would include natural progression from nonerosive esophageal disease to erosive esophageal disease to Barrett's and possible esophageal adenocarcinoma.18 Data to the contrary, however, exist as well. A group of 35,725 patients with erosive esophagitis were identified from a database, including some with concurrent ulcerations or strictures and had a follow-up of >4 years. In the group with esophagitis but without stricture or ulcers, no patient had disease progression or developed further esophageal complications.19,20
Collen and associates20 have suggested that older individuals are at an increased risk for the development of erosive esophagitis. These investigators studied 228 consecutive patients with reflux symptoms who underwent upper endoscopy and reported that patients older than 60 years had increased risk for complications of chronic reflux such as erosive esophagitis, and that this risk increased with every decade of life above age 30.21 A study by Johnson and
COMPLICATIONS OF GERD: ESOPHAGITIS, STRICTURE, BARRETT'S, AND CANCER
Fennerty11 echoed this sentiment. Of 11,945 patients studied, only 12% of those <21 years were found to have erosive esophagitis, compared with 37% of those >70 years. It was also found that although heartburn was a good indicator for the presence of severe esophagitis in the elderly, they presented more often with respiratory symptoms or even dysphagia.11
Why do only some GERD patients develop erosive esophagitis whereas others do not? Although the exact reasons for this are unclear, a number of factors have been recently identified that may contribute to the development of erosive esophagitis. Most recently, investigators have focused on lower esophageal sphincter pressure, presence of a hiatal hernia, impaired esophageal clearance of refluxed material (decreased peristalsis), and presence of bile reflux,to name a few.22 To date,there has not been a consistently observed difference in rates of esophagitis between males and females, although it seems that the risk may be slightly higher in males. Esophageal ulcerations have also been found to be more common in Caucasians than other races.23 Investigators have questioned whether Western influences, particularly changes in diet and social habits, may have led to the increased incidence of reflux complications in the Asian subcontinent.
Although the majority of patients with erosive esophagitis experience typical symptoms of esophageal reflux (i.e., heartburn, regurgitation), symptoms do not seem to necessarily predict the presence of erosive esophagitis in GERD patients. A study by Sonnenberg and col-leagues24 revealed that duration, frequency, and severity of heartburn symptoms did not correlate with esophagitis. It was shown that, in fact, there was a large degree of overlap in the severity and frequency of symptoms between patients with erosive esophagitis and nonero-sive reflux.24
Another study evaluated a total of 644 GERD outpatients who underwent an endoscopy, followed by esophageal manometry, and 24-hour pH monitoring. Analysis of resulting data suggested that there was no clear-cut association between the degree of acid reflux and the presence and severity of erosive esophagitis. In addition, the amount of upright or supine acid contact time, frequency of all or only long reflux episodes, and an overall summary score of pH-metry, did not correlate with the severity of erosive esophagitis.25
Treatment of erosive esophagitis continues to center around the use of acid suppression therapy. Healing appears to be most apparent and successful with the use of proton pump inhibitors (PPIs), with patients treated up to 12 weeks. Chiba et al.26 demonstrated healing rates approaching 85% [95% confidence interval (CI): 79.1-88.1%] with use of these medicines compared with approximately 52% (95% CI: 46.9-56.9%) with histamine antagonists. Healing rates, however, have largely been found to be dependent on the baseline grade of erosive esophagitis. In addition, Holtmann and col-leagues27 have also suggested that patients infected with Helicobacter pylori may actually have better response rates to PPIs in the treatment of erosive esophagitis. Maintenance of healing of erosive esophagitis is also helped by use of PPIs. A study by Lundell and colleagues,28 among others, followed a group of patients with documented erosive esophagitis after being treated with daily omeprazole therapy. After completion of 8 weeks of PPI therapy, these patients were followed up to 6 months to monitor for relapse of erosive esophagitis. In the absence of acid suppression therapy, it was shown that it was possible for all grades of erosive esophagitis (Los Angeles grade A) to relapse.
Anti-reflux surgery can also be an option for the long-term treatment of erosive esophagitis in some patients. A study by Lundell and col-leagues29 randomized 155 patients to medical therapy (omeprazole) or surgical anti-reflux therapy. Over a 3-year follow-up period, 139 of the medically treated patients, and 129 of the surgically treated were evaluated and compared by symptomatology, 24-hour pH monitoring, and endoscopy. Of the surgically treated group, 97 remained in clinical remission, compared with 77 in the medically treated group (P = 0.0016); however, when dose adjustments were made in the medically treated group (i.e., increasing omeprazole dose), the failure rates between the two types of treatment were not significantly different.
MANAGING FAILED ANTI-REFLUX THERAPY
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Gastroesophageal reflux disease is the medical term for what we know as acid reflux. Acid reflux occurs when the stomach releases its liquid back into the esophagus, causing inflammation and damage to the esophageal lining. The regurgitated acid most often consists of a few compoundsbr acid, bile, and pepsin.