Detailed colonoscopy for detecting early superficial carcinoma: recent developments.

Early superficial colorectal carcinoma (CRC) has been commonly detected by routine colonoscopic examination in Japan. A series of 769 early CRCs and 4821 adenomas were diagnosed by colonoscopy at Hiroshima University Medical Hospital between 1991 and 1998. Of early CRCs, macroscopically superficial early CRCs accounted for 209 lesions (28%). Among 5590 lesions of adenomas and carcinomas, depressed-type lesions showed a significantly higher malignant potential for cancerous and submucosal invasion than elevated lesions (polypoid, IIa-type lesions, and G-LST). As one of the quantitative examinations for early CRC, pit pattern observed by magnifying video-colonoscopy was useful. We performed magnifying observations for 265 lesions of colorectal neoplasias using Kudo's pit pattern classification for 2 years. Depressed-type lesions characterized the Ills and V pit patterns, and elevated lesions characterized the III(L) pit pattern. The incidence of cancer was significantly higher in lesions with IIIs and V pit patterns. Furthermore, the V(N) pit pattern was considered a significant indicator of submucosal invasion. These results indicated that superficial early CRC could be considered to constitute about one-third of all early CRCs. Of them, the depressed-type lesions showed a significantly higher malignant potential than elevated lesions. Pit pattern observation by magnifying videocolonoscopy is useful for predicting the histology/invasion depth of early CRC.

Characteristics of teen-age patients with juvenile duodenal ulcer. Relation between inherited hyperpepsinogenemia I and duodenal ulcer.

We analyzed environmental factors, family history of peptic ulcer, gastric acid secretion, and serum levels of pepsinogen I (PG I) and gastrin in 56 juvenile patients with duodenal ulcer and 39 normal teenage subjects. Basal acid output and maximal acid output were significantly higher in our duodenal ulcer patients than in controls without ulcer (both, p < 0.01), and patients with duodenal ulcer showed significantly higher serum levels of PG I and gastrin than the controls (both, p < 0.001). There were no significant differences in any environmental factor between the patients and controls. Fifteen of the 17 patients who had one or both parents with hyperpepsinogenemia I had high serum PG I levels. Over half of the duodenal ulcer patients had high serum gastrin levels, irrespective of family history of hypergastrinemia. Our findings suggest that hyperpepsinogenemia I and hypergastrinemia are important characteristics and that genetic background, particularly the inheritance of a gastric mucosal trait expressed as hyperpepsinogenemia I, is frequently involved in the pathogenesis of juvenile duodenal ulcer.