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In this chapter the clinical differences in the diagnosis and endoscopic treatment of gastrointestinal tract carcinoma between Europe and Japan are reviewed.

Gastrointestinal carcinoma has been detected and diagnosed by barium meal X-ray study and endoscopic study with or without biopsy study. In particular, early and minute carcinoma can be detected only by endoscopic study. Due to the development and refinement of endoscopy, the diagnosis of early gastrointestinal (GI) carcinoma is now easily accomplished by endoscopic observation and biopsy study. Endoscopic detection of gastrointestinal lesions depends on the recognition of visible mucosal changes. However, the final diagnosis is performed by histopathological study of biopsy materials. Biopsy study is still very important to obtain the correct diagnosis of the lesion as carcinoma, dysplasia, adenoma, and hyperplasia, although it is sometimes possible to diagnose the lesion from the endoscopic investigation of mucosal surface details. In this chapter, endoscopic diagnosis of early carcinoma in the upper GI tract will be described.

Endoscopic treatments for early gastric cancers are divided into two groups: mucosal resection methods and coagulation methods (e.g., laser therapies). Mucosal resection methods are usually preferred because through these we can obtain pathological specimens to evaluate. This chapter will present an overview of the current techniques and their future directions.

Recent progress in endoscopic techniques and instruments and interest in the diagnosis of early-stage colorectal cancers has enabled the detection of early colorectal cancers []. Early colorectal cancer is defined as “a cancer where the depth of invasion is limited to the mucosal or submucosal layer of the colon and rectum, regardless of the presence of lymph node metastasis” []. Although surgical therapy has enabled a high cure rate for early colorectal cancers, increasing evidence suggests that endoscopic treatment can be an effective alternative for localized colorectal cancers without lymph node metastasis or hematogenous spread. As a matter of fact, complete endoscopic resection of mucosal cancer is accepted as a curative procedure because of the absence of a risk of lymph node metastasis. However, the endoscopic resection of submucosal cancers remains controversial, because submucosal cancers have some risk of lymph node or distant metastasis []. In cases with metastasis, endoscopic treatment is not curative. Therefore, the indications for the endoscopic resection of early colorectal cancers must be carefully considered.

Cancer can sometimes be diagnosed on endoscopy, but small carcinomas in adenomas are difficult to detect. When cancer is suspected, resection of the lesion is required either endoscopically or surgically, depending on the estimated depth of invasion in cases of cancer. Endoscopic treatment must be supported by clear-cut evidence that the lesion is superficial and can be completely resected by endoscopic techniques. Endoscopic procedures can be used only when tumor invasion is confined to the mucosa or is estimated to be within 1000µm from the muscularis mucosae. Magnification and dye techniques are often used to estimate the depth of invasion. Endoscopic ultrasonography (EUS) is also used. With the former technique, lesions invading the submucosa that are exposed and have lost their glandular structure are not indicated for endoscopic therapy. With EUS, lesions in which the third layer is interrupted or the fourth layer is displaced also cannot be treated endoscopically. For convenience, physiological saline solution can be locally injected immediately below the lesion just before endoscopic treatment.

Neoplastic lesions develop in the squamous lining of the esophagus (squamous cell cancer) or in a segment of columnar metaplasia in Barrett’s esophagus with a specialized epithelium (intestinal metaplasia). Esophageal adenocarcinoma is increasing in Western countries. At the esophagogastric junction there is often confusion between neoplasia in a short Barrett’s esophagus and neoplasia at the cardia.

Endoscopic mucosal resection (EMR) was introduced to the clinical field of treatment for early esophageal cancer in Japan in 1989.This had been developed owing to widespread use of slender panendoscopy and iodine staining throughout Japan [].

It is thought that it takes 15–30 years from the appearance of a gastric cancer cell to patient death [, ], and in the course of the process, cancers observable to clinicians have already reached their late stages. In some cases, the growth of gastric cancer increases drastically and in others, there is almost no change in the growth of cancer cells for years. Thus, the growth of gastric cancer can take various forms, because various factors such as the degree of differentiation, the presence of an ulcer in the lesion, and differences in immunity among individuals exert influence. In the past, the progress of gastric cancer was estimated by retrospective studies, prospective observations, or assumptions based on the growth curve. However, none of the previous research efforts based on these methods have succeeded in elucidating fully the natural course of gastric cancer [].

The natural course of colorectal cancers is not well understood because of the difficulties of investigation. It is not allowed ethically to observe the index lesions in situ in order to investigate their natural course.

The incidence of colorectal neoplasia is increased in patients with long-standing and extensive ulcerative colitis (UC), and death from colorectal neoplasia is the most important factor for long-term mortality in patients with UC. To improve the prognosis of patients with UC-associated neoplasia, it is very important to diagnose it at an early or precancerous state in patients with long-standing UC. However, UC-associated neoplasia is often difficult to detect endoscopically and difficult to discriminate from inflammatory regenerative epithelium pathologically. There are three important problems in diagnosing UC-associated neoplasia: the first is how to detect UC-associated dysplasia and early cancer endoscopically; the second is how to discriminate UC-associated dysplasia from inflammatory regenerative epithelium pathologically; and the third is how to identify individuals at increased risk of neoplasia, especially dysplasia, in patients with long-standing and extensive UC. We reviewed the clinicopathological and genetic characteristics of UC-associated neoplasia focusing on these three problems.