Wilhelm G. Doos

The increasing frequency of adenocarcinoma of the esophagus

Adenocarcinoma of the esophagus has been considered an uncommon tumor, accounting for fewer than 8% of all cases of esophageal cancer. To determine the current frequency of adenocarcinoma of the esophagus, we reviewed data from the tumor registries of the Commonwealth of Massachusetts, the University Hospital (UH), and the Boston VA Medical Center (BVAMC). From 1982 to 1984, 868 esophageal cancers were reported in Massachusetts, of which 231 (27%) were adenocarcinomas. In comparison with squamous cell carcinomas of the esophagus, esophageal adenocarcinomas occurred more frequently in males (P < 0.01) and were uncommon among blacks (P < 0.01). From 1980 to 1986, 262 cases of esophageal cancer were seen at the UH and the BVAMC, of which 81 (31%) were adenocarcinomas. An analysis of the latter group to identify true esophageal adenocarcinomas (tumors confined to the esophagus without gastric involvement) yielded 47 cases. Thus, true esophageal adenocarcinoma accounted for 18% of esophageal malignancies at our hospitals, a frequency threefold to fivefold higher than that found in four prior studies that used comparable anatomic diagnostic criteria. We conclude that adenocarcinoma of the esophagus is now being recognized at a substantially higher frequency than reported in the past.

Diagnostic inconsistencies in Barrett's esophagus

Abstract Background/Aims: Few studies have compared the precision of various diagnostic tests used to determine the presence of Barretts esophagus. The aim of this study was to compare the results of histological, endoscopic, and manometric tests for patients with Barretts esophagus in two closely spaced examinations. Methods: In a Veterans Administration Cooperative Study, 192 patients with complicated gastroesophageal reflux disease had esophageal manometry and endoscopy performed at baseline and after 6 weeks. At each examination, the endoscopist localized the most proximal level of Barretts epithelium and the lower esophageal sphincter and obtained esophageal biopsy specimens. Results: One hundred sixteen patients met the criteria for Barretts esophagus on at least one of the two endoscopic examinations. Among patients with specialized columnar epithelium, 20% had specialized columnar epithelium found on only one of the two examinations. Although the mean lower esophageal sphincter level did not change, approximately 10% of patients had a change ≥4 cm on endoscopy and manometry between examinations. This led to an apparent change in the diagnosis in 18% of patients with Barretts esophagus. Conclusions: From one endoscopic examination to another, inconsistencies in the ability to detect specialized columnar epithelium are common. This may lead to substantial problems in establishing an accurate diagnosis of Barretts esophagus.

Detection by scanning electron microscopy of a distinctive esophageal surface cell at the junction of squamous and Barrett's epithelium

Metaplastic columnar epithelium replaces the normal squamous epithelium in Barretts esophagus. We characterized the surface epithelial cells of the junction between squamous and Barretts epithelium using scanning electron microscopy and light microscopy. In four biopsy specimens from the squamous-Barretts junction in three patients, we found a distinctive cell type having features intermediate between those of squamous and columnar epithelium. Its distinguishing characteristic is the presence on its surface of two disparate structures not normally present on the same cell in the gastrointestinal tract: microvilli (a scanning electron microscopy feature of glandular epithelium) and intercellular ridges (a scanning electron microscopy feature of squamous mucosa). The surface characteristics of this newly recognized cell were strikingly similar to those of cells found in the transformation zone of the uterine cervix, an area in which squamous epithelium physiologically replaces columnar epithelium. We also examined 28 biopsies of the gastroesophageal junction area from 14 patients with and without a history of heartburn but with no evidence of Barretts esophagus. None of these biosies showed the distinctive cell. We hypothesize that this distinctive cell represents an intermediate step in either the development or the healing of Barretts epithelium, during which surface characteristics of two different cell types, columnar and squamous, coexist on the same cell.

The Prevalence of Barrett's Esophagus in Patients with Chronic Peptic Esophageal Strictures

Both Barretts esophagus and peptic stricture of the esophagus are consequences of chronic reflux esophagitis. Barretts esophagus appears to be a premalignant condition, and continued histologic surveillance for dysplasia and carcinoma has been recommended for affected patients. While patients with peptic esophageal strictures and persistent reflux are at risk for the development of Barretts epithelium, such patients often do not receive continued histologic surveillance if Barretts epithelium is not identified on the initial endoscopic evaluation. Using endoscopic and peroral aspiration biopsy techniques, we studied the prevalence of Barretts esophagus in 25 patients with chronic peptic esophageal strictures in whom Barretts epithelium had not been identified did not have Barretts esophagus was found to have an undifferentiated esophageal carcinoma. We conclude that patients with chronic peptic esophageal strictures frequently have Barretts esophagus. A program of continued histologic surveillance seems advisable for such patients.

Scanning electron microscopy of Barrett's epithelium and its correlation with light microscopy and mucin stains

The surface epithelial cells of Barretts esophagus were characterized using quantitative scanning electron microscopy and light microscopy with mucin histochemical stains. Fifty-one biopsy specimens of Barretts esophagus from 15 patients and 31 control specimens of the stomach and intestines from 9 patients were examined. Three distinct surface cell types, in addition to the goblet cell, were recognized in Barretts epithelium: the gastric-like cell in 31% of specimens, which was similar to the normal gastric surface cell by quantitative scanning electron microscopy; the intestinal-like cell in 41%, which was most similar to the normal small intestinal surface cell; and the variant cell in 80%, which had a range of surface features. By light microscopy, all specimens with variant and intestinal-like cells were classified as specialized columnar epithelium. The surface mucous cells in Barretts epithelium displayed a variety of mucin staining patterns with acid nonsulfated (small intestinal-like) mucin present in 90% of specimens and acid sulfated (colonic-like) mucin in 43% of specimens. Quantitative scanning electron microscopy and mucin histochemical stains reveal a striking cellular heterogeneity not apparent by routine light microscopy.

Gastric carcinoid (gastrinoma). Associated with achlorhydria (pernicious anemia)

This report presents a case of multicentric gastric carcinoid (gastrin containing) tumors of the fundus associated with achlorhydria and pernicious anemia. It is suggested that stimulation of the antral G cells and possibly fundic argyrophilic cells by achlorhydria associated with atrophic gastritis may lead to hyperplasia, and eventually to neoplasia in the latter, in the form of gastric carcinoid with gastrin production.

CEA levels in patients with colorectal polyps

Preoperative plasma CEA levels were measured in 93 selected patients with histologically defined colorectal adenomata removed at fibroptic colonoscopy in order to determine whether CEA levels are elevated in patients with colonic polyps, or vary with different histologic patterns. None of the patients had inflammatory bowel disease, previous history of carcinoma, or evidence of liver disease. Fifteen percent of the patients had elevated CEA levels (≥2.5 ng/ml; Hansen method), and two‐thirds of these were between 2.5 and 4.0 ng/ml. Increased association of elevated CEA levels was noted with old age, villous adenomas (2‐to 4‐fold), and increased tumor size ((2.3‐cm diameter; 2‐fold), but not with foci of dysplasia or carcinoma in situ as such. One‐half (7/14) of the patients with elevated CEA levels showed the following: two patients had villous tumors with carcinoma in situ, one had a villous adenoma, two had mixed villous and tubular adenomas (with a high proportion of villous pattern), and two were subsequently shown to have carcinoma elsewhere in the colon. It is uncertain that the polyps were the source of the elevated circulating CEA levels; other factors including smoking and patient selection need to be considered. This preliminary study suggests that patients with colorectal adenomata and elevated circulating CEA may be at higher risk for the development of carcinoma. Further follow‐up studies of the malignant potential of the polyp‐bearing colon are essential.

Cholestasis and toxic epidermal necrolysis associated with phenytoin sodium ingestion: the role of bile duct injury.

Excerpt Despite more than 4 decades of extensive clinical experience with phenytoin sodium, reports of important hepatic dysfunction induced by this anticonvulsant drug are uncommon (1). The clinic...

Chemotherapy for primary retroperitoneal yolk sac tumor: Report of a case

A case of primary extragonadal yolk sac tumor occurring in the retroperitoneum of a young adult male was studied. The chemotherapy of this tumor has not previously been described for cases of extragonadal origin. A combination of cyclophosphamide, vinblastine, bleomycin, cis‐diamminedichloroplatinum, actinomycin‐D, and chlorambucil was used. A partial response and dramatic prolongation of survival was achieved, compared with previously reported cases.

Transformation of lymphoma to amyloidoma following radiation therapy

A 62-year-old man presented with a localized upper-extremity small cell lymphoma with plasmacytoid features and an associated IgM lambda serum immunoglobulin level of 1,730 g/dl. The tumor was treated with 5,960 rad over 47 days. On completion of radiation therapy, the tumor had regressed only minimally, and the monoclonal immunoglobulin level had decreased by 63 per cent; repeat biopsy revealed that the lymphoma had been replaced by a virtually acellular mass of amyloid. It is postulated that radiation therapy accelerated the tissue conversion of lambda light chain into the beta-pleated sheet structure characteristic of amyloid fibrils.