(Radiographics. 1999;19:1686-1688.)
© RSNA, 1999
Gastrointestinal Case of the Day1
Branko M. Plavsic, MD, PhD,
Bradley S. Shore, MD,
Harry B. Rosenthal, MD and
Michelle M. Payette, MD
1 From the Department of Radiology, Tulane University, 1430 Tulane Ave, New Orleans, LA 70112. Received December 14, 1998 and accepted January 20, 1999. Address reprint requests to B.M.P.
Index Terms: Esophagus, CT, 713.1211, 714.1211 • Esophagus, diseases, 713.744, 714.744 • Esophagus, neoplasms, 713.35, 714.35
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HISTORY
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A 60-year-old white man presented with a complaint of heartburn and symptoms of chronic gastroesophageal reflux. The patient had difficulty swallowing, particularly solid food. He had undergone an upper gastrointestinal series 5 years earlier but had not undergone endoscopy or follow-up examination. An upper gastrointestinal series and contrast material–enhanced computed tomography (CT) of the chest and abdomen were performed.
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FINDINGS
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Initial upper gastrointestinal examination had revealed a 70-mm-long midesophageal stricture and moderate granularity of the mucosa of thedistal two-thirds of the esophagus (Fig 1). Upper gastrointestinal examination performed 5 years later demonstrated narrowing of the distal two-thirds of the esophagus by polypoid masses that extended into the proximal stomach (Fig 2). Contrast-enhanced CT demonstrated thickening of the esophageal wall (Fig 3).
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Figures 1, 2. (1) Initial double-contrast esophagogram demonstrates a midesophageal stricture (arrows) and granularity of the mucosa of the middle and distal esophagus. (2a) Barium esophagogram shows polypoid masses narrowing the distal two-thirds of the esophagus. (2b) Barium esophagogram demonstrates masses in the distal esophagus (arrowheads) and proximal stomach (arrows).
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Figures 1, 2. (1) Initial double-contrast esophagogram demonstrates a midesophageal stricture (arrows) and granularity of the mucosa of the middle and distal esophagus. (2a) Barium esophagogram shows polypoid masses narrowing the distal two-thirds of the esophagus. (2b) Barium esophagogram demonstrates masses in the distal esophagus (arrowheads) and proximal stomach (arrows).
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Figures 1, 2. (1) Initial double-contrast esophagogram demonstrates a midesophageal stricture (arrows) and granularity of the mucosa of the middle and distal esophagus. (2a) Barium esophagogram shows polypoid masses narrowing the distal two-thirds of the esophagus. (2b) Barium esophagogram demonstrates masses in the distal esophagus (arrowheads) and proximal stomach (arrows).
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DIAGNOSIS: Barrett adenocarcinoma.
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DISCUSSION
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Only 2 decades ago, adenocarcinoma of the esophagus represented less than 5% of all esophageal cancers. Today, adenocarcinoma accounts for approximately 30% of all newly diagnosed esophageal cancers. Esophageal adenocarcinoma is the most rapidly proliferating malignancy in the United States, with approximately 2,500 new cases being diagnosed each year. The disease has a more than 7:1 male predilection and predominantly affects whites (1). Most esophageal adenocarcinomas originate in the distal esophagus. The lesions are stenosing or polypoid neoplasms that tend to affect long segments of the esophagus; however, they may appear as plaquelike tumors and may be ulcerated. Esophageal adenocarcinoma may arise from Barrett esophagus, gastric adenocarcinoma involving the esophagus, submucosal and deep esophageal glands, or elements of ectopic gastric mucosa in the esophagus. The latter two causes are rare. Although squamous cell carcinoma and adenocarcinoma have similar gross morphologic appearances, they tend to differ with respect to pathways of metastasis. For lower esophageal neoplasms such as adenocarcinoma, mediastinal lymph nodes, the celiac axis region, and nodes in the gastrohepatic ligament are considered regional. In squamous cell carcinoma, palliative chemotherapy and radiation therapy are indicated, whereas palliative surgery is recommended for adenocarcinoma (2).
The importance of diagnosing Barrett esophagus lies in the potential for early detection and treatment of esophageal adenocarcinoma. Barrett esophagus is seen in 10% of patients with advanced chronic reflux esophagitis (1,3). In Barrett esophagus, squamous epithelium is replaced with columnar epithelium in the distal esophagus (4). The columnar epithelium is continuous with the epithelium of gastric mucosa but does not secrete hydrochloric acid. There are no parietal cells; however, goblet cells are often present. The mucosal lining in Barrett esophagus is characterized by chronic inflammation. Metaplastic epithelium does not cause clinical symptoms.
There are no specific radiologic signs in Barrett esophagus. Most signs of Barrett esophagus are found in advanced reflux esophagitis, reflecting a common pathophysiologic basis. These include thickening and irregularity of the esophageal folds, diffuse granularity and a fine reticular pattern of the esophageal mucosa, erosion, and peptic ulcer of the esophagus. The distal esophagus has decreased tone at manometry. Scintigraphy demonstrates the inherent dysmotility of the esophagus in patients with Barrett esophagus (5). Radiologic signs of high risk for Barrett esophagus include ulcer, high or midesophageal stricture, and a reticular mucosal pattern. Less than one-third of affected patients have an esophageal ulcer. Patients with distal esophageal stricture or thickened, irregular mucosal folds are at moderate risk for Barrett esophagus (6). Sensitive radiologic signs in Barrett esophagus are not specific, and specific signs are not sensitive. Approximately 20%–30% of patients with Barrett esophagus may demonstrate normal radiologic findings. Because our patient had a midesophageal stricture, he was considered to be at high risk for Barrett esophagus.
The probability of developing esophageal adenocarcinoma is 40 times higher in patients with Barrett esophagus than in the general population. The reported prevalence of esophageal adenocarcinoma among patients with Barrett esophagus ranges from 0% to 46% (mean, 10%) (1,3,7). However, it seems that this figure is exaggerated (7).
The progression from squamous cells to Barrett epithelium, which may then evolve into nests of dysplastic epithelium, is best described as neoplastic progression. Low-grade dysplasia may develop into high-grade dysplasia and intramucosal adenocarcinoma (7). High-grade dysplasia progresses into carcinoma in 15%–20% of patients (3). Indicators of neoplasia include biomarkers (ornithine decarboxylase, carcinoembryonic antigen, mucus abnormalities), chromosomal abnormalities (tumor suppressor genes, oncogenes), flow cytometry (aneuploidy, cellular proliferation), and growth regulatory factors. Endoscopic ultrasonography can provide information about the depth of invasion of the esophageal wall and the status of adjacent lymph nodes (2).
If the diagnosis of Barrett esophagus is suspected radiologically, it should be confirmed endoscopically. Endoscopic surveillance with four-quadrant biopsy is recommended every other year. Patients with low-grade dysplasia are treated aggressively with omeprazole. Intensity of treatment and surveillance is based on resolution or persistence of dysplasia. If the presence of foci of high-grade dysplasia is confirmed, resection is recommended. Regression of Barrett esophagus is uncommon. Antireflux surgery does not prevent development of adenocarcinoma (7,8).
Our patient refused surgical treatment and died 1 month following radiologic diagnosis of adenocarcinoma. The gross pathologic specimen demonstrated infiltrative esophageal wall thickening in the distal two-thirds of the esophagus (Fig 4a). Pathologic analysis revealed abnormal glandular structures and hyperchromatic cells (Fig 4b), findings that are consistent with adenocarcinoma of the esophagus.
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Figure 4a. (a) Gross specimen of the esophagus and lungs shows a thickened esophageal wall (arrows), a finding indicative of esophageal adenocarcinoma. (b) Low-power photomicrograph (original magnification, x15; hematoxylin-eosin stain) demonstrates tumor cells forming abnormal glandular structures.
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Figure 4b. (a) Gross specimen of the esophagus and lungs shows a thickened esophageal wall (arrows), a finding indicative of esophageal adenocarcinoma. (b) Low-power photomicrograph (original magnification, x15; hematoxylin-eosin stain) demonstrates tumor cells forming abnormal glandular structures.
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References
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Gore RM. Esophageal cancer: clinical and pathologic features. Radiol Clin North Am 1997; 35:243-263.[Medline]
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Thompson WT. Esophageal carcinoma. Abdom Imaging 1997; 22:138-142.[Medline]
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Levine MS, Herman JB, Furth EE. Barrett's esophagus and esophageal adenocarcinoma: the scope of the problem. Abdom Imaging 1996; 20:291-298.
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Barrett NR. Chronic peptic ulcer of the esophagus and "esophagitis.". Br J Surg 1950; 38:174-182.
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Plavsic BM, Robinson AE, Jeffery BR. Gastrointestinal radiology: a concise text New York, NY: McGraw-Hill, 1992; 206-223.
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Gilchrist AM, Levine MS, Carr FR, et al. Barrett's esophagus: diagnosis by double-contrast esophagography. AJR 1988; 150:97-102.[Abstract/Free Full Text]
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Spechler SJ, Goyal RK. Barrett's esophagus. N Engl J Med 1986; 315:362-371.[Medline]
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Phillips RW, Wong RKH. Barrett's esophagus: natural history, incidence, etiology and complications. Gastroenterol Clin North Am 1991; 20:791-816.[Medline]
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HISTORY
FINDINGS
