Intestinal metaplasia may develop in the cardia in patients either with short-segment BE or carditis especially caused by H. pylori. Distinction between these two entities is important since the etiology and risk of developing adenocarcinoma are different . BE is believed to be caused by GERD and associated with an increased risk of esophageal adenocarcinoma [1, 2, 4]. Microscopically, BE can be defined as replacement of the esophageal squamous epithelium by metaplastic specialized (intestinalized) columnar epithelium. Other epithelial types are junctional type and fundal type of epithelia. The diagnosis of BE requires biopsy confirmation of intestinal metaplasia with Alcian blue pH2.5 positive goblet cells in addition to typical endoscopic findings. The exact level of SCJ, proximal aspect of the gastric folds, and linearly oriented mucosal vessels in the distal esophagus and EGJ should be identified . SCJ normally corresponds to the proximal margin of the linear gastric folds which means EGJ. The small vessels oriented parallel to the long axis of the esophagus disappear at the normally located SCJ. However, detection of abnormal extension of these vessels below the SCJ and above the proximal margin of gastric folds is an evidence of the presence of columnar epithelium in the distal esophagus .
Distinguishing BE from other entities which may render similar histopathologic features is paramount. Because of no absolute histological criteria for diagnosing Barrett mucosa has been established yet, recent studies [8–11, 15–19] mainly depend on patterns of some cytokeratin subsets, especially two distinct patterns of CK7/20 staining. Cytokeratins are highly conserved polypeptides and represent a group of cytoskeletal structural proteins present in all epithelia. There are at least 20 distinct forms of cytokeratins in epithelial cells and variable patterns of expression depending on the type, location, and differentiation of the epithelium . CK7, essentially, is not expressed in normal epithelium of the gastrointestinal tract, whereas CK20 is expressed in intestinal epithelium, gastric foveolar epithelium, and endocrine cells in the upper portions of the pyloric glands. Barrett CK7/20 pattern was first defined by Ormsby et al.  as staining of the superficial epithelium for CK20 and staining of both superficial and deep metaplastic epithelium for CK7. The designated gastric CK7/20 pattern was grouped into two patterns regarding the type of the intestinal metaplasia (incomplete/complete) by the same authors. According to their suggestion, patchy CK7 expression with variable involvement of deep glands was seen in incomplete gastric intestinal metaplasia, whereas strong CK20 expression in superficial and deep glands with the absence of CK7 expression was seen in complete gastric intestinal metaplasia. In this pioneering study, Barrett CK7/20 pattern was highly sensitive and specific when compared to cases with gastric intestinal metaplasia. However, H. pylori status of the cases was not mentioned. Studies by Glickman et al  and Jovanovic et al.  confirmed Ormsby's findings in 91% and 94% of their cases with long-segment BE, respectively. On the other hand, studies by some other researchers have not been able to support Ormsby's findings; the proposed Barrett CK7/20 pattern was found in 54% of patients with long-segment BE by Mohammed et al.  and only 39% of patients with long-segment BE by El-Zimaity et al. .
Ormsby et al.  later assessed the utility of CK7/20 patterns in short-segment BE in another study and found that "diagnostic" Barrett CK7/20 pattern was present in 82% of patients with short-segment BE. Although Mohammed et al.  found almost the same percentage (81%) for the short-segment BE cases with Ormsby et al. , they found the same pattern in 30.7% of patients with intestinal metaplasia in cardia and more interestingly in 55% of biopsies which had either normal or inflamed gastric mucosa without intestinal metaplasia.
In the present study, 10% of patients with short-segment BE showed the anticipated CK7/20 pattern and 40% of patients with gastric intestinal metaplasia showed the anticipated gastric CK7/20 pattern with appropriate complete or incomplete intestinal metaplasia. The sensitivity of Barrett CK7/20 pattern was very low (10%) in the BE group despite its high specificity (100%). The sensitivity of gastric CK7/20 pattern was also low (40%) in gastric intestinal metaplasia group, although the specificity was high (100%) in this group as well. Gastric CK7/20 pattern was significantly higher in gastric intestinal metaplasia group than in BE group (P = 0.02), whereas Barrett CK7/20 pattern did not significantly differ between the two groups (P = 0.487). Based on these results, to use two distinct patterns of CK7/20 staining could not be accepted as a reliable method in differentiating short-segment BE from gastric intestinal metaplasia since both patterns have very low sensitivity and very high false-negativity values.
In the Couvelard's study  31% of patients and in the Ormsby's study 15% of patients with short-segment BE associated with Barrett CK7/20 pattern had H. pylori infection. Although the percentage of the positive H. pylori cases in patients with short-segment BE associated with a Barrett CK7/20 pattern was not mentioned in the Mohammed's study , 6% of patients had H. pylori infection with short-segment BE. Since intestinal metaplasia may be seen both in H. pylori infection and BE, combination of these entities should not be of the interpreted for evaluating the utility of the cytokeratin subsets. We excluded the H. pylori positive cases even if it was diagnosed as BE. Therefore, the differences between our study and previously reported results may have been due to this strict distinction of H. pylori positive BE cases in the present study. Differences in biopsy protocols between previous studies and the present study (number, size or site of the specimen, anterograd or retroflexed approach) might have been another reason for differences in the results. To identify the exact location of the cardia anterograd approach should be used. However, regarding the normal cardiac epithelium, its existence remains still unclear, since the results of different studies are contradictory [21–23]. While the two studies suggest that normal cardiac epithelium represents a form of metaplastic epithelium secondary to gastro-esophageal reflux [21, 22], another study reported by Kilgore et al suggests that cardiac mucosa exists as a native structure . Further studies may provide information on the cardiac mucosa, especially its' relation with reflux changes and BE.