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DOI: 10.1055/s-2003-40228
Routine Chromoendoscopy for Gastrointestinal Diseases: Indications Revised
Publikationsverlauf
Publikationsdatum:
24. Juni 2003 (online)
![](https://www.thieme-connect.de/media/endoscopy/200307/lookinside/thumbnails/10.1055-s-2003-40228-1.jpg)
Introduction
Can we be sure that we have identified every lesion after an endoscopic examination? We may believe we have seen all of the sites that need to be examined - but what percentage of the cancers diagnosed are early ones? In our department, some 50-60 % of lesions identified are early gastric cancers, but this still means that 40-50 % of lesions found represent advanced gastric cancer. Of course, the principal reason for late diagnosis is late presentation; however, a proportion of cases are likely to be due to lesions being overlooked during endoscopy.
Endoscopic treatment methods such as endoscopic mucosal resection (EMR), photodynamic therapy (PDT), and argon plasma coagulation (APC) are now meeting with acceptance throughout the world as radical methods of treating early esophageal and gastrointestinal cancers. These methods have the advantages of reduced invasiveness, improved cost-effectiveness, and shorter hospital stays. However, if it is not possible to identify early cancers conclusively as an indication for endoscopic therapy, then such treatments cannot be offered. Early cancers - generally involving flat, but not always small, lesions - need to be detected more frequently. Chromoendoscopy first came into clinical use some 40 years ago as a method of identifying lesions and studying them in detail, and several types of chromoendoscopy stain have since been developed (Table [1]). These stains can be extremely helpful for identifying early cancers, and they are discussed in detail below.
Table 1 Routine chromoendoscopy stains in gastrointestinal endoscopy Stain type Main organs Mechanism What stains Positive stain Clinical aims Contrast stains Indigo carmine Stomach, colon, small intestine Pools in mucosal grooves and depressed areas Cells do not stain; only pooling effects Blue Screening of early cancer; differentiation between malignant and benign lesions; pit-pattern analysis; diagnosis of spread and depth; observation of inflammatory diseases; evaluation of ulcer healing Vital stains Lugol’s solution Methylene blue Toluidine blue Esophagus Esophagus, small intestine, colon Esophagus Binds iodine in nonkeratinized cells Active absorption into cells Diffusion into cells Normal squamous cells with glycogen Small- and large-intestinal cells, intestinal metaplasiaBinds to cellular nuclei Dark brown Blue Blue Screening of early esophageal cancer; reflux esophagitis; columnar epithelium in the esophagus; follow-up after mucosal ablation in Barrett’s esophagusSpecialized epithelium in Barrett’s esophagus; intestinal metaplasia in the stomach; ectopic gastric mucosa in the duodenumSquamous-cell carcinoma; reflux esophagitis; gastric or intestinal metaplasia in Barrett’s esophagus Reactive stains Congo red Phenol red Stomach Stomach pH < 3 results in color changes Alkaline pH results in color changes Acid-secreting gastric cells H. pylori-infected gastric mucosa Turns red to blue-black Turns yellow to red Mapping of acid-secreting gastric mucosa; diagnosis of ectopic gastric mucosa Diagnosis of H. pylori infection
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M. Kida, M.D.
Dept. of Gastroenterology · Kitasato University East Hospital
2-1-1 Asamizodai, Sagamihara · Kanagawa 228-8520 · Japan
Fax: +81-42-749-8690
eMail: m-kida@kitasato-u.ac.jp