Hidetaka Mochizuki

PURPOSE: This study was designed to clarify indication and benefit of pelvic sidewall dissection for rectal cancer. METHODS: The retrospective, multicenter study collected the data of rectal cancer patients who underwent surgery between 1991 and 1998 and were prospectively followed. RESULTS: Of 1,977 patients with rectal cancers, 930 underwent pelvic sidewall dissection without adjuvant radiotherapy. Positive lateral lymph nodes were found in 129. Multivariate analysis disclosed a significantly increased incidence of positive lateral lymph nodes in female gender, lower rectal cancers, non-well-differentiated adenocarcinoma, tumor size of > or =4 cm and T3-T4. The five-year survival rate for 1,977 patients was 79.7 percent. The survival of patients with positive lateral lymph nodes was significantly worse than that of Stage III patients with negative lateral lymph nodes (45.8 vs. 71.2 percent, P<0.0001). Multivariate analysis showed significantly worse prognosis in male gender, pelvic sidewall dissection, lower rectal cancers, T3-T4, perirectal lymph node metastasis, and positive lateral lymph nodes. During the median follow-up time of 57 months, recurrence developed in 19.7 percent: 17 percent in negative and 58.1 percent in positive lateral lymph nodes (P<0.0001). Local recurrence was found in 8 percent: 6.8 percent in negative and 25.6 percent in positive lateral lymph nodes (P<0.0001). Multivariate analysis disclosed that lower rectal cancers, non-well-differentiated adenocarcinoma, T3-T4, perirectal lymph node metastasis, and positive lateral lymph nodes were significantly associated with an increased local recurrence. CONCLUSIONS: Positive lateral lymph node was the strongest predictor in both survival and local recurrence. Pelvic sidewall dissection may be indicated for patients with T3-T4 lower rectal cancers because of the greater probability of positive lateral lymph nodes.

This study was performed to investigate the mechanism whereby immediate enteral feeding after burn injury reduces postburn hypermetabolism and hypercatabolism. Fifty-seven burned guinea pigs (30% TBSA) were divided into three groups: A (N = 19), given 175 kcal/kg/day beginning 2 hours after burn; B (N = 20), given 175 kcal/kg/day with an initial 72-hour adaptation period; and C (N = 18), given 200 kcal/kg/day with the same adaptation period as B. Resting metabolic expenditure (RME) on PBD 13 was lowest in group A (109% of preburn level), compared with group B (144%, p less than 0.001) and group C (137%, p less than 0.01). On PBD 1, group A had the greatest jejunal mucosal weight and thickness (p less than 0.001), and mucosal weight had negative correlations with plasma cortisol (r = 0.829, p less than 0.001) and glucagon (r = 0.888, p less than 0.001). Two weeks after burn, urinary vanillyl mandelic acid (VMA) excretion, plasma cortisol, and glucagon were lowest in group A (p less than 0.05 to p less than 0.01). These hormones also significantly correlated with RME (p less than 0.01 to p less than 0.001). These findings suggest that immediate postburn enteral feeding can prevent hypermetabolism via preservation of gut mucosal integrity and prevention of excessive secretion of catabolic hormones.

Although recent studies have demonstrated that cyclooxygenase (COX)-2 is overexpressed in various cancers including gastric cancer, the mechanisms underlying the contribution of COX-2 to tumorigenesis and tumor promotion still remain unclear. To determine the role of COX-2, we investigated the COX-2 expression, the prostaglandin (PG) levels, and the microvessel density in 42 patients with primary gastric adenocarcinoma. COX-2 protein was over-expressed in 31 (74%) of 42 gastric cancers based on an immunoblot analysis. The intensity of COX-2 expression was found to significantly correlate with lymph node involvement. The COX-2 overexpressed cases showed significantly elevated levels of prostaglandin E2 (PGE2) in cancer tissues in comparison with the normal gastric mucosa by an immunoassay (201 +/- 90 versus 161 +/- 57 ng/mg protein; P < 0.05). However, the COX-2 overexpression was not related to the levels of thromboxane B2 and 6-keto-prostaglandin F1alpha. The density of microvessel immunostained with CD34 was significantly higher in patients demonstrating COX-2 overexpression than in those without such expression (63 +/-21 versus 45 +/- 17/200 x; P < 0.01). Our data thus suggested COX-2 overexpression to be associated with increased PGE2 biosynthesis and angiogenesis in gastric cancer, which indicates that COX-2 may play a role in the development of gastric cancer.