Factors associated with incomplete colonoscopy at a Japanese academic hospital.

AIM: To evaluate significant risk factors for incomplete colonoscopy at a Japanese academic hospital. METHODS: A total of 11812 consecutive Japanese people were identified who underwent a colonoscopy at an academic hospital. A multiple logistic regression model was used to evaluate retrospectively the significant risk factors for incomplete colonoscopy. RESULTS: The cecal intubation rate was 95.0%. By univariate analysis, age, female sex, poor bowel cleansing, and a history of abdominal or pelvic surgery were significant risk factors for incomplete colonoscopy (P < 0.001). Moreover, age- and sex-adjusted analysis showed that significant risk factors for incomplete colonoscopy were female sex (OR = 1.38, 95%CI: 1.17-1.64, P = 0.0002), age ≥ 60 years old (OR = 1.44, 95%CI: 1.22-1.71, P < 0.0001), a history of prior abdominal or pelvic surgery (OR = 1.55, 95%CI: 1.28-1.86, P < 0.0001), poor bowel cleansing (OR = 4.64, 95%CI: 3.69-5.84, P < 0.0001), and inflammatory bowel disease (IBD) (OR = 1.48, 95%CI: 1.13-1.95, P = 0.0048). In Japanese men, by age-adjusted analysis, IBD (OR = 1.69, 95%CI: 1.18-2.43, P = 0.005) was an independent risk factor for incomplete colonoscopy. CONCLUSION: Several characteristics in the Japanese population were identified that could predict technical difficulty with colonoscopy.

MUC5AC/ß-catenin expression and KRAS gene alteration in laterally spreading colorectal tumors.

AIM: To clarify differences in mucin phenotype, proliferative activity and oncogenetic alteration among subtypes of colorectal laterally spreading tumor (LST). METHODS: LSTs, defined as superficial elevated lesions greater than 10 mm in diameter with a low vertical axis, were macroscopically classified into two subtypes: (1) a granular type (Gr-LST) composed of superficially spreading aggregates of nodules forming a flat-based lesion with a granulonodular and uneven surface; and (2) a non-granular type (NGr-LST) with a flat smooth surface and an absence of granulonodular formation. A total of 69 LSTs, comprising 36 Gr-LSTs and 33 NGr-LSTs, were immunohistochemically stained with MUC2, MUC5AC, MUC6, CD10 (markers of gastrointestinal cell lineage), p53, ß-catenin and Ki-67 antibodies, and examined for alteration in exon 1 of v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) and exon 15 of v-raf murine sarcoma viral oncogene homologue B1 (BRAF) by polymerase chain reaction followed by direct sequencing. RESULTS: Histologically, 15 Gr-LST samples were adenomas with low-grade dysplasia (LGD), 12 were high-grade dysplasia (HGD) and 9 were adenocarcinomas invading the submucosa (INV), while 12 NGr-LSTs demonstrated LGD, 14 HGD and 7 INV. In the proximal colon, MUC5AC expression was significantly higher in the Gr-type than the NGr-type. MUC6 was expressed only in NGr-LST. MUC2 or CD10 did not differ. P53 expression demonstrated a significant stepwise increment in progression through LGD-HGD-INV with both types of LST. Nuclear ß-catenin expression was significantly higher in the NGr-type. Ki-67 expression was significantly higher in the Gr-type in the lower one third zone of the tumor. In proximal, but not distal colon tumors, the incidence of KRAS provided mutation was significantly higher in the Gr-type harboring a specific mutational pattern (G12V). BRAF mutations (V600E) were detected only in two Gr-LSTs. CONCLUSION: The two subtypes of LST, especially in the proximal colon, have differing phenotypes of gastrointestinal cell lineage, proliferation and activation of Wnt/ß-catenin or RAS/RAF/extracellular signal-regulated kinase signaling.

Establishment of a reflux esophago-laryngitis model in rats.

BACKGROUND: To investigate the pathophysiology of reflux laryngitis, an experimental model is required. AIM: The aim of this study is to establish an animal model of reflux esophago-laryngitis, modifying our previously reported model of chronic acid reflux esophagitis. METHODS: The modified chronic acid reflux esophagitis (m-RE) group (n = 10), in which the duodenum was wrapped with 2.5 mm of Nelaton catheter, was not treated with any drugs. Also postoperatively, two treatment groups (n = 10 in each) received different dosages of rabeprazole (RPZ): 1.0 mg/kg/day (RPZ 1.0 group) or 10.0 mg/kg/day (RPZ 10.0 group). As a control group (n = 5), other rats underwent sham operation. The esophagus and larynx were resected on day 14 after the operation, and ulcer score of the esophagus was assessed. The epithelial thickness and leukocyte infiltration of the supraglottic and subglottic laryngeal mucosae were investigated. The number of interleukin (IL)-1ß-positive cells was also counted and defined as the IL-1ß labeling index. RESULTS: In the m-RE group, the epithelial thickness, leukocyte infiltration, and IL-1ß labeling index of the supraglottic and subglottic laryngeal mucosae were increased compared with controls (P < 0.01). In the RPZ groups, not only the ulcer score of esophagus but also the epithelial thickness, leukocyte infiltration, and IL-1ß labeling index of both the supraglottic and subglottic laryngeal mucosae were decreased dose-dependently relative to the m-RE group (P < 0.05). CONCLUSIONS: Our modified chronic acid reflux esophagitis model proved useful in establishing a rat reflux esophago-laryngitis model, with both pathological laryngeal findings and reflux esophagitis shown to be improved by administration of a proton pump inhibitor.