Barrett Esophagus–Associated Small Cell Carcinoma

This is the authors' abstract. We don't add key points for this paper.

For many years, the most common malignant tumor of the esophagus was the squamous cell type; it was said to constitute more than 90% of all carcinomas in classic textbooks of pathology. In the last decade, however, there has been a dramatic change in the incidence of adenocarcinoma of the esophagus. During the past 5 years, squamous cell carcinomas accounted for 60% and adenocarcinomas for 38% of all carcinomas at our institution.1The main reason for the rise in incidence of adenocarcinoma has been the recognition of Barrett esophagus. It is now widely accepted that there is a sequence of events, starting with chronic gastroesophageal reflux, that cause inflammation and ulceration of the lower esophagus. The reparative process yields a metaplastic epithelium, so-called columnar-lined esophagus, consistent with intestinal epithelium with goblet cells (Barrett esophagus). The incidence of malignancy in patients with Barrett esophagus is about 3%.2Most Barrett esophagus–associated cancers are adenocarcinomas; there is a small group of Barrett esophagus–associated nonadenocarcinomas, namely squamous cell and small cell carcinomas.Small cell carcinomas associated with Barrett esophagus constitute less than 1% of all reported cases. The case illustrated herein is that of a 54-year-old woman with long-standing gastroesophageal reflux who was complaining of recent onset of dysphagia. Esophagoscopy revealed an obstructing mass at the lower end of the esophagus. The overlying mucosa contained islands of easily recognizable glandular mucosa. The patient underwent a partial esophagogastrectomy. Microscopic examination of the specimen showed a tumor mass extending underneath areas of squamous epithelium adjacent to the intestinal type of epithelium (Figure 1). High magnification of the tumor revealed a cellular mass, composed of small cells, with scanty cytoplasm and irregular, hyperchromatic nuclei. There was numerous mitoses per field (Figure 2). The epithelial nature of the tumor cells was graphically depicted by the immunoreactivity for cytokeratin (Figure 3). Similar to their counterpart in the lung and other sites, the neoplastic cells displayed neuroendocrine differentiation, as shown by their immunoreactivity for synaptophysin (Figure 4) and neuron-specific enolase (Figure 5).