A 54-year-old Hispanic male presented to the clinic with chronic dyspepsia and uncontrolled reflux symptoms not responding to acid-suppression therapy with a proton pump inhibitor (PPI). His past history was remarkable for sleeve gastrectomy one year previously. PPI therapy was stopped two weeks prior to endoscopy to promote the yield of a Helicobacter pylori (H. pylori) test. Esophagogastroduodenoscopy revealed gastric-like mucosa 2 cm in diameter in the proximal esophagus, suggestive of an inlet patch (Fig. 1). The biopsy of the esophageal lesion confirmed the gastric mucosa, showing mild chronic inflammation and a positive immunohistochemical stain for H. pylori (Fig. 2). Biopsies from the gastric mucosa were only significant for chronic gastritis, with a negative H. pylori stain.
Figure 1 Narrow-band imaging of the gastric-like mucosa in the upper esophagus
Figure 2 Immunohistochemical stain reveals that the inlet patch gastric mucosa is positive for Helicobacter pylori microorganisms (immunoperoxidase 20x)
Gutierrez et al suggested that 73% of cases of H. pylori gastritis were associated with H. pylori infection of an inlet patch and that such an infection is highly related with the density of H. pylori colonies in the stomach [1]. To our knowledge and to date, this report is the first case of isolated H. pylori infection in a cervical inlet patch without concurrent H. pylori gastritis [2,3].
The case is also unique because of the prior history of sleeve gastrectomy. The mechanism of isolated H. pylori infection in patients who have undergone sleeve gastrostomy remains unclear; our proposed theory is that the altered stomach anatomy reduces its isolation and promotes H. pylori colonization in other parts of the gastrointestinal tract.
Further studies are warranted to confirm the mechanism of isolated H. pylori colonization in a cervical inlet patch and its association with sleeve gastrectomy.