The recent data indicate a clear difference in the distribution of CG in the proximal stomach among different ethnic populations, and might explain different disease pathogenesis mechanisms among various ethnic patient groups. Cardiac

glands (CG) in a healthy human consist of primarily mucus cells, scattered parietal cells, a few undifferentiated cells in the neck, and many endocrine cells in the base, but no chief cells.1–3 When the number of parietal cells increases, often in the basal half of gastric mucosa, parietal cells admix with mucus cells to form oxyntocardiac glands. CG show two growth patterns: (i) tubular, similar to gastric pyloric glands; and (ii) compound acinar or racemose, mimicking the duodenal Brunner glands. CG secrete mucus that forms a protective blanket on the gastric surface. At the subcellular level, these mucus cells Lumacaftor concentration are equipped with short microvilli at the apical surface and

secretory granules in the apical cytoplasm, which can be highlighted with periodic acid–Schiff (PAS) reaction for carbohydrates and negative on the alcian Smoothened antagonist blue stain at pH 2.5 or lower, which is similar to the staining pattern of mucus cells elsewhere in the stomach.1,2 Anatomically, CG and oxyntocardiac glands are mainly concentrated around the esophagogastric junction (EGJ) in a narrow zone and also clustered in small numbers at the upper esophagus, and rarely in other parts of the esophagus.2–4 In the distal esophagus, CG might be present underneath the squamous mucosa 上海皓元 and above the muscularis mucosae; these are also known as superficial esophageal CG.4–7 Traditional

teaching holds that the CG, along with oxyntocardiac glands, are congenital and form the cardiac mucosa (CM) in the most proximal part of the stomach, a transition zone of 10–30 mm in length, which abuts proximally with the esophageal squamous mucosa and distally with gastric fundic oxyntic glands.2,4 Recent research results, mainly from the Chandrasoma groups, challenge this doctrine.8–10 They reported that in the EGJ region of unselected adult autopsies, CG were present in only 29% of cases and oxyntocardiac glands in 44%; even in selected autopsies with the entire EGJ examined microscopically, CG were detected in only 44%. Recent autopsy studies further found that the length of the CM was in fact not 10–30 mm, but varied between 1 mm and 4 mm in pediatric patients,8,11 and approximately 5 mm in most adults.8,12 Therefore, CG, regardless of whether or not present in the proximal stomach or in the distal esophagus, are believed to be an acquired metaplastic lesion.10 As such, the CM is no longer considered to be part of the proximal stomach, but the distal esophagus.