Risk factors for recurrence of artificial gastric ulcers after endoscopic submucosal dissection.

It has been reported previously that artificial gastric ulcers caused by endoscopic submucosal dissection (ESD) would heal within 8 weeks, irrespective of their size and location. The aim of this retrospective study was to describe long-term outcomes of gastric ESD ulcers. Check-up of ulcers was performed by periodic endoscopy. The rate of ESD ulcer recurrence and clinicopathological factors that may relate to recurrence were assessed. During the median observation period of 33 months, a benign ulcer recurrence occurred in 10 lesions in 10 patients (2.1%). Univariate analysis showed that Helicobacter pylori infection and presence of pathological ulcer findings within the ESD specimen were significantly related to the risk of ESD ulcer recurrence. Although the frequency is low, there is a possibility of ESD ulcer recurrence in patients with H. pylori infection and in patients who undergo ESD for a lesion with ulceration.

Gastric perforation during endoscopic resection for gastric carcinoma and the risk of peritoneal dissemination.

BACKGROUND: The potential risk of peritoneal seeding following perforation caused by endoscopic mucosal resection (EMR) or endoscopic submucosal dissection (ESD) is unknown. METHODS: Between January 1991 and December 2003, 90 patients suffered gastric perforation during EMR or ESD at the National Cancer Centre Hospital, Tokyo. The clinical and pathological evidence for peritoneal dissemination in these patients was assessed retrospectively. RESULTS: Eighty-four patients were followed up at this hospital for a median of 53.6 (range 7.0-136.6) months; the remaining six patients were followed up at other institutions. In 83 patients the perforation was repaired by endoscopic clip application and seven patients underwent emergency surgery. Gastrectomy was carried out in 33 patients who had non-curative endoscopic surgery. Among these, peritoneal fluid was sampled during operation in nine patients and was cytologically negative for malignancy. The other 24 patients who had a gastrectomy did not have ascites so cytology was not performed. No peritoneal dissemination was noted during follow-up. CONCLUSION: This study suggests that perforation associated with EMR and ESD does not lead to peritoneal dissemination even in the long term.

Endoscopic indications for endoscopic mucosal resection of laterally spreading tumours in the colorectum.

BACKGROUND: Laterally spreading tumours (LSTs) in the colorectum are usually removed by endoscopic mucosal resection (EMR) even when large in size. LSTs with deeper submucosal (sm) invasion, however, should not be treated by EMR because of the higher risk of lymph node metastasis. AIMS: To determine which endoscopic criteria, including high magnification pit pattern analysis, are associated with sm invasion in LSTs and clarify indications for EMR. METHODS: Eight endoscopic criteria from 511 colorectal LSTs (granular type (LST-G type); non-granular type (LST-NG type)) were evaluated retrospectively for association with sm invasion, and compared with histopathological findings. RESULTS: LST-NG type had a significantly higher frequency of sm invasion than LST-G type (14% v 7%; p<0.01). Presence of a large nodule in LST-G type was associated with higher sm invasion while pit pattern (invasive pattern), sclerous wall change, and larger tumour size were significantly associated with higher sm invasion in LST-NG type. In 19 LST-G type with sm invasion, sm penetration determined histopathologically occurred under the largest nodules (84%; 16/19) and depressed areas (16%; 3/19). Deepest sm penetration in 32 LST-NG type was either under depressed areas (72%; 23/32) or lymph follicular or multifocal sm invasion (28%; 1/32 and 8/32, respectively). CONCLUSIONS: When considering the most suitable therapeutic strategy for LST-G type, we recommend endoscopic piecemeal resection with the area including the large nodule resected first. In contrast, LST-NG type should be removed en bloc because of the higher potential for malignancy and greater difficulty in diagnosing sm depth and extent of invasion compared with LST-G type.

K-ras gene mutation related to histological atypias in human colorectal adenomas.

To investigate the relationship of oncogene analysis to morphology, we analyzed K-ras gene mutations by dot-blot hybridization with and without consideration of histological atypias in individual colorectal adenomas. Each of 54 colon polyps were divided into two parts after fixation. One part was used as a mass to assess point mutations; the remaining portion of each polyp was paraffin-embedded, stained with hematoxylin and eosin, and examined for point mutations related to histological atypias. In the first part of our study, K-ras gene mutations at codon 12 were detected in 13 cases (24%). In the second part of our study, 12 cases had distinctly different histological atypias. From each of these 12 cases, two areas, one with higher or one with lower grade atypia in the same polyp were excised to analyze for K-ras gene mutation. Two of these 12 cases (17%) had the mutation in different areas of the same tumor. These two cases contained the mutation only in the areas with higher grade atypia, and only one case added information regarding ras mutation upon microdissection when compared to the entire biopsy. These results suggest that oligonucleotide hybridization can identify the majority of cases containing ras mutations despite regional morphologic variation. Individual cases, however, may contain clonal subpopulations within adenomas with different ras sequences from other regions within the same adenoma.

Appearance of Ulex europaeus agglutinin-1 and Griffonia simplicifolia agglutinin-1 binding sites on cancer cells in sigmo-rectal polyps.

Ninety-three polypectomized cases from the sigmo-rectal region were examined by lectin histochemistry. On the apical surface, the UEA-1 binding sites were positive in 24/29 carcinomas and in 25/62 adenomas; while the GSA-1 binding sites were positive in 16/29 carcinomas and in 0/62 adenomas. In 2 non-neoplastic polyps, only one case was UEA-1 positive; none was GSA-1 positive. In neighbouring regions, adenomas adjacent to carcinomas were UEA-1 positive in 9/27 cases and GSA-1 positive in 3/37 cases. Thus, the GSA-1 binding sites were expressed more specifically on carcinomas. In the Golgi area, none of the polyps was UEA-1 positive while most of the cells showing GSA-1 positivity were apt to do so within the cells without showing GSA-1 positivity on the apical surface. There were no correlations between the positive rate of the lectin binding sites on the apical surface and the stage of cancer development or the histology of the adenoma on which a cancer developed. The meaning of this restricted appearance of the GSA-1 binding sites on the cancer cell surface was discussed in relation to observations previously reported in the literature.