Hepatocyte paraffin 1 immunoexpression in esophageal brush samples

Abstract

With interest, we read the article by Zhang et al.1 entitled “Hepatocyte paraffin 1 immunoexpression in esophageal brush samples, a sensitive marker for Barrett esophagus with intestinal metaplasia.” First, the authors have to be congratulated for the presentation of a novel cytopathologic tool, thus increasing the armamentarium in the diagnosis of morphologic changes associated with gastroesophageal reflux disease. In addition, the technology presented may be suitable for the detection of molecular abnormalities that precede histopathologic changes involving the development of Barrett esophagus (BE). The article by Zhang et al. pointed out semantic discrepancies related to the definition of BE. The question to be raised is, “Is it to be termed BE without intestinal metaplasia, in the absence of goblet cells?” According to a consensus meeting, a diagnosis of BE requires the presence of goblet cells (“no goblets, no Barrett's”).2 The statement that “the working definition of BE is displacement of the squamocolumnar junction proximal to the gastroesophageal junction with the presence of intestinal metaplasia” was accepted by 16 of 18 participants in an American Gastroenterological Association workshop on the diagnosis of BE.3 In contrast, based on the report by Spechler and Goyal,4 pathohistologic criteria for BE include replacement of distal esophageal squamous epithelium by columnar-type epithelium in the presence or absence of goblet cells (with and without intestinal metaplasia; intestinal vs. cardiac type metaplasia). Thus, the morphologic sequence of BE would be considered to commence with the presence of columnar epithelium in the distal esophagus. This semantic concept is favored by our clinical experience. Due to the patchy distribution of intestinal metaplasia in a BE lesion, the absence of goblet cells in segments of gastric-type mucosa in the distal esophagus never can be ruled out.2, 3 Consequently, the number of patients diagnosed with BE and those enrolled into surveillance programs is supposed to vary, depending on the definition applied (BE with or without intestinal metaplasia). Future studies will have to determine whether the type of pathohistologic definition of BE may affect economic issues and the statistical risk of developing adenocarcinoma of the esophagus.2-4 In addition, attention has to be drawn to the fact that the diagnosis of BE cannot be established without the inclusion of endoscopic information (gastric vs. esophageal pathology).2, 3 Taken together, the issue clearly demands clarification of the linguistic confusion related to BE. Finally, difficulties with describing a disease meaningfully also may reflect the complexity of factors involved in the pathogenesis of a disease, a condition reminiscent of inflammatory bowel disease.5 The authors are asked kindly to comment on the issues discussed and to propose a recommendation of how to solve the Babylonian confusion around BE.