Inlet Patch: Prevalence, Histologic Type, and Association With Esophagitis, Barrett Esophagus, and Antritis

Inlet patch is a congenital anomaly of the cervical esophagus consisting of gastric mucosa. We report the prevalence and histologic types of the inlet patch as well as its association with Barrett esophagus and Helicobacter pylori–associated gastritis.

In reviewing the pathologic reports of upper gastrointestinal biopsies consecutively obtained from the endoscopies of 1821 patients between 1995 and 2002 at North Shore University Hospital in Manhasset, NY, we identified 20 patients with inlet patch (Table). The inlet patch measured between 5 and 12 mm and occupied between 10% and 20% of the circumference. Clinical indications for upper gastrointestinal endoscopies are shown in the Table. The patients' ages ranged from 16 to 75 years (mean, 55 years); no sex predilection was observed. Four patients had a Barrett esophagus, 3 with a long segment and 1 with a short segment (12, 8, 3, and 2 cm from the gastroesophageal junction). In all but 1 case, at least 1 biopsy was taken from each site of the proximal esophagus, distal esophagus, and gastric antrum, and 2 biopsies were obtained from the inlet patch. In addition to the routine hematoxylin-eosin stain, the Steiner stain for the identification of H pylori was performed in all cases as well as a stain for gastrin-producing cells in the nonoxyntic mucosa of the inlet patch.

An inlet patch occurred in about 1.1% of our study population. The histologic type of the inlet patch included oxyntic-type mucosa in 11 patients, gastrin negative, and therefore cardiac mucosa in 5 and superficial foveolar epithelium in 4. These last 4 specimens were considered too superficial to be classified. Pancreatic acinar tissue was also seen in 2 patients (Table). Eleven of the inlet patches were inflamed, 1 of which was associated with H pylori (Table; Figure 2, A and B). No intestinal metaplasia or dysplasia was found. Pathologic findings in distal esophagus included Barrett esophagus in 4 patients, distal esophagitis in 4 patients characterized by eosinophils in the squamous esophageal mucosa, oxyntic mucosa in 5 patients, and pancreatic acinar tissue in 3 patients (1 coexisting with oxyntic mucosa). The remaining 5 patients with inlet patch had unremarkable squamous esophageal mucosa. Helicobacter pylori was not identified in any of the distal esophageal biopsies. Pathologic findings in the antrum included gastritis in 2 patients—bile-associated chemical gastropathy in one and a hyperplastic polyp with xanthoma and intestinal metaplasia in the other. Helicobacter pylori was seen in 1 patient who also had H pylori in the inlet patch.

The presence of inlet patch (ectopic gastric mucosa in upper esophagus) was first described in 1805 by Schmidt from postmortem examinations.1 Inlet patch is thought to be a congenital anomaly, and it occurs most frequently in the postcricoid portion of the esophagus at or just below the upper esophageal sphincter.2–4 In most cases, inlet patches are asymptomatic and are detected by routine screening or workup for upper gastrointestinal complaints due to Barrett esophagus, esophagitis, or gastritis. However, pain and dysphagia have been described.5,6 Furthermore, inlet patch can occasionally be associated with serious medical complications, such as bleeding,7 perforation,8 esophageal web,9 and stricture.10,11 It has also been associated with adenocarcinoma.12–15 Intestinal metaplasia has often been reported in association with adenocarcinoma developing in the inlet patch, but dysplasia has been reported only occasionally.15 

The incidence of inlet patch was reported as 4.5% based on a study from Rector and Connerly16 on 1000 autopsies in children, with a range of from 0.3% to 10%.17,18 An inlet patch was noted in about 1% of our patient population in whom an inlet patch was searched for endoscopically and a biopsy performed. The relatively high prevalence of inlet patch in some studies compared to others may be explained by the special interest of certain endoscopists who intentionally look for it.19 Maconi et al19 report a prevalence of inlet patch of 0.29% (operator unaware) versus 2.27% (operator aware) of evaluated patients. In fact, 50% of the inlet patches in the present study were identified by a single gastroenterologist.

In our study, the histologic type of the inlet patch included oxyntic mucosa and cardiac mucosa, with oxyntic mucosa being the most common type. This is in agreement with other studies.16,20 One case of pancreatic acinar tissue has been reported in an inlet patch21; we identified 2 in this study. Pancreatic acinar tissue is most frequently in the gastroesophageal junction and in Barrett esophagus, indicating either a metaplastic or congenital origin.22 Our previous study favors a congenital origin.23 By studying the histology of gastroesophageal junction from 69 children and young adults, we found 16% of the study population with pancreatic acinar tissue not associated with Barrett esophagus; the prevalence of esophagitis and/or gastritis did not vary significantly between patients with or without pancreatic acinar tissue. These results suggest a congenital rather than a metaplastic origin for pancreatic acinar tissue at the gastroesophageal junction.

Several groups have reported a possible association between inlet patch and Barrett esophagus. Malhi-Chowla et al24 proposed that inlet patch is a possible marker for the severity of Barrett esophagus, whereas Avidan et al25 suggested that both conditions share a similar embryonic etiology. Immunohistochemical studies have demonstrated that inlet patches possess a distinctive embryonic gastric mucosa profile, while Barrett esophagus is considered an acquired condition that originates from immature gastrointestinal stem cells.26 Based on a retrospective review of endoscopies performed at our institution by one endoscopist who carefully searched for inlet patches, we noted an increased prevalence of Barrett esophagus in patients with inlet patches.27 An increased prevalence of inlet patches was also noted in the patients with Barrett esophagus. We postulated that the acid secretion from the inlet patches had contributed to the pathogenesis of Barrett esophagus and that patients with inlet patches were inherently predisposed to developing columnar metaplasia in the distal esophagus. In this current study of pathologic specimens, we have observed 20% coexistence between these 2 conditions (4/20 patients with inlet patch have Barrett esophagus). This coexistence could reflect the selective patient population with upper gastrointestinal symptoms who underwent upper gastrointestinal endoscopies in our hospital and the special attention of the endoscopist in trying to identify inlet patch. Alternatively, the 2 conditions could be related. All 4 patients with Barrett esophagus had gastroesophageal reflux disease.

Helicobacter pylori is a spiral or curved gram-negative non–spore-forming bacillus. It transmits through oral-oral or fecal-oral routes, lives within or beneath the mucous layer adjacent to the epithelium, and is found transiently in the duodenum, saliva, and feces. Studies have shown that the ectopic gastric mucosa of inlet patch can produce acid.28–30 Therefore, it would be the ideal location for H pylori colonization. Among 11 patients with inflamed inlet patch, 1 was positive for H pylori, and this patient also had H pylori in the antrum. Inflammation of the gastric mucosa of the inlet patch in the remaining patients may be explained by the coexistence of gastroesophageal reflux disease or a reaction to acid secreted by the oxyntic mucosa. Coinfection of H pylori in the inlet patch and gastric antrum has also been reported by others.19,31 Since the infection of H pylori is through an oral route, inlet patch may be an important site in H pylori infection in the upper gastrointestinal tract because of its more proximal location. We believe that the elimination of H pylori in both the inlet patch and antrum is very important in the treatment of patients with coinfection.

In summary, inlet patch occurred in about 1% of our study population. Oxyntic mucosa is the most common histologic type for inlet patch. Helicobacter pylori infection of the inlet patch correlates with that of the antrum.

The authors thank Ira Goldman, MD, Andrea Sacknoff, MD, Michael Goldstein, MD, Lisa Lih-Brody, MD, David Berger, MD, Gary Weissman, MD, Paul Berg, MD, and Jeffrey Berger, MD, for providing biopsy material.