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Esophageal Disorders

Long-standing esophagitis

Achalasia

Plummer-Vinson syndrome

Genetic Predisposition

Long-standing celiac disease

Ectodermal dysplasia

Epidermolysis bullosa

Racial disposition

States are attributable to alcohol and tobacco usage. Some alcoholic drinks contain significant amounts of such carcinogens as polycyclic hydrocarbons, fuel oils, and nitrosamines, along

with other mutagenic compounds. Nutritional deficiencies associated with alcoholism may contribute to the process of carcinogenesis.

Alcohol and tobacco cannot be invoked as risk factors in many high-incidence regions of the world. The presence of carcinogens, such as fungus-contaminated and nitrosamine-containing

foodstuffs in China, may play a significant role in the extraordinary high incidence of carcinoma in this region. Dietary deficiencies in vitamins and essential metals have been documented

in China and South Africa. Human papillomavirus DNA is found frequently in esophageal squamous cell carcinomas from high-incidence regions, but is infrequent in cancer-bearing

patients in North America. [13]

Based on the above considerations, dietary and environmental factors have been proposed to increase risk, with nutritional deficiencies acting as promoters or potentiators of the

tumorigenic effects of environmental carcinogens. For example, methylating nitroso compounds in the diet and in tobacco smoke may be the reason for the broad spectrum of p53 point

mutations present in over half of esophageal cancers. Other genetic alterations, such as mutations in p16INK4, and amplification of CYCLIN D1, C-MYC, and epithelial growth factor

receptor (EGFR), are prevalent in these cancers as well. This is in keeping with the concept that stepwise acquisition and accumulation of genetic alterations ultimately give rise to cancer.

[14] Notably rare in esophageal squamous cell carcinomas are K-RAS and adenomatous polyposis coli (APC) mutations.

Finally, the chronic esophagitis so commonly observed in persons living in areas of high incidence may itself be the result of sustained exposure to the carcinogens listed earlier. This

chronic esophagitis results in an increased epithelial cell turnover, which, over a length of time in a continuously carcinogenic environment, progresses to dysplasia and eventually to

carcinoma. The rate of progression along the chronic esophagitis-dysplasia-cancer sequence may well be modified or modulated by genetic or racial factors.

Morphology.

Like squamous cell carcinomas arising in other locations, those of the esophagus begin as apparent in situ lesions (intraepithelial neoplasm or carcinoma in situ). When they become

overt, about 20% of these tumors are located in the upper third, 50% in the middle third, and 30% in the lower third of the esophagus. Early lesions appear as small, gray-white, plaque-like

thickenings or elevations of the mucosa. In months to years, these lesions become tumorous masses and may eventually encircle the lumen. Three morphologic patterns are described: (1)



protruded (60%), a polypoid exophytic lesion that protrudes into the lumen; (2) flat (15%), a diffuse, infiltrative form that tends to spread within the wall of the esophagus, causing

thickening, rigidity, and narrowing of the lumen; and (3) excavated (ulcerated, 25%; Fig. 17-8 ), a necrotic cancerous ulceration that excavates deeply into surrounding structures and may

erode into the respiratory tree (with resultant fistula and pneumonia) or aorta (with catastrophic exsanguination) or may permeate the mediastinum and pericardium. The fortunate patient is

found at the stage of superficial esophageal carcinoma, in which the malignant lesion is confined to the epithelial layer (in situ) or is superficially invading the lamina propria or submucosa

( Fig. 17-9 ).

Most squamous cell carcinomas are moderately to well differentiated. Several histologic variants may be seen, such as verrucous squamous cell carcinoma, spindle cell carcinoma, and

basaloid squamous cell carcinoma. Irrespective of their degree of differentiation, most symptomatic tumors are quite large by the time they are diagnosed and have already invaded the wall

or beyond. The rich lymphatic network in the submucosa

Figure 17-8Large ulcerated squamous cell carcinoma of the esophagus.

Figure 17-9Squamous cell carcinoma of the esophagus: low-power microscopic view showing invasion into the submucosa.

Figure 17-10Transition from Barrett esophagus to adenocarcinoma.

Figure 17-11Adenocarcinoma of the esophagus. A, Gross view of an ulcerated, exophytic mass at the gastroesophageal junction, arising from the granular mucosa of Barrett esophagus.

The gray-white esophageal mucosa is on the top, and the folds of gastric mucosa are below. (A, courtesy of Dr. James Gulizia, Brigham and Women's Hospital, Boston, MA.) B,

Microscopic view of malignant intestinal-type glands in adenocarcinoma arising from Barrett esophagus.

 

Figure 17-12Anatomy and histology of the stomach. A, Gross anatomy. B, Microscopic view of antral mucosa. C, Microscopic view of fundic mucosa.

Figure 17-13Acute gastritis. A, Gross view showing punctate erosions in an otherwise unremarkable mucosa; adherent blood is dark due to exposure to gastric acid. B, Low-power

microscopic view of focal mucosal disruption with hemorrhage; the adjacent mucosa is normal.

TABLE 17-2-- Diseases Associated with Helicobacter pylori Infection


Date: 2016-04-22; view: 720


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