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Objective To discuss the indication,technique,effect,and safety of colonoscopic resection of colorectal submucosal tumor(SMT).Methods A total of 33 patients with SMT,which was diagnosed colonoscopically and pathologically,were treated by endoscopy.The sizes of the tumors were 0.2-2.2 cm in diameter,and 0.2-1.2 cm in the diameter of the roots.After injecting adequate adrenalin saline deeply into the root of SMT,the mass of those,who had negative nonlifting sign,was attracted,snared,and then cut using high frequency electrotome.In 7 cases of smaller SMT,the tumor was gripped.Results No perforation,large amount of hemorrhage,or burns of the colorectal wall was found.Complete resection was achieved(no tumor tissue was detected on the edge or bottom of the SMTs after endoscopic resection,or pathological examination found no tumor tissue after open surgery) in 29 cases,including 18 carcinoids,6 leiomyomas,2 hamartomas,2 lipomas,and 1 neurofibroma.Except 3 patients with leiomyoma were lost,26 of the patients were followed up for a median of 44.5 months(3 months to 12 years and 7 months).No recurrence was found during the follow-up.The 4 carcinoids were resected partially(there were tumor tissues remained on the edge or bottom of the SMTs after endoscopic resection,or the pathological examination after open surgery showed tumors).Two of the 4 were transferred to open surgery(one was followed up for 2 years and 3 months,the other was lost).The other two patients refused operation and received a followed-up of 5 months and 2 years and 4 month respectively.None of the 4 patients had recurrence during follow-up.Conclusions Colonoscopic treatment can be applied to the patients with SMT sized ≤1.2 cm at the root and negative nonlifting sign.The method is safe,effective,and minimal invasion.Pathological examination is recommended after the colonoscopic resection,open surgery is necessary for the partially resected SMTs.
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Objective:To investigate the correlation between the disease activity of ulcerative colitis (UC) and the immunohistochemical distribution of calprotectin in colon mucosa,as well as the levels of calprotectin in fecal. Methods:Monoclonal antibody against calprotectin was used to investigate the distribution of these proteins in colon mucosa from 42 patients with ulcerative colitis and 20 healthy controls. ELISA assay was used to measure the concentrations of calprotectin in fecal. The disease activity of UC was determined by Truelove-Witts histological criteria. Results: Calprotectin was demonstrated in the majority of granulocytes and macrophages in colon mucosa of patients with active UC, while negative in patients with unactive UC and healthy controls. A strong calprotectin immunoreactivity was presented in ulcerative and erosion lesions in the colon. The concentration of calprotectin was significantly higher in patients with active UC than that with unactive UC and healthy controls (P
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Objective:To assess the mechanism of exacerbation of colonic damage in rat colitis model induced by trinitrobenzene sulfonic acid(TNBS)treated wi th celecoxib(a selective COX-2 inhibitor).Methods:The rats w ere randomized in to four groups.Group 1 and Group 2 were study groups.Group 3 and Group 4 were control groups.Colitis was induced by intracolonic administration of TNBS(25 g /L)in a vehicle of 50% ethanol(0.25 mL)of study groups.The rats of study gro ups were treated orally,beginning 3 h before induction of colitis and continuin g twice per day thereafter for up to 7 d,with celecoxib(1.25 mg/kg,Group 1)a nd distilled water(1 mL/0.3 kg,Group 2)respectively.In control experiments,the rats of Group 4 were treated orally with celecoxib(1.25 mg/kg)twice per da y for up to 7 d.Group 3 rats were healthy control rats.All the rats that survi ved until the end of the experiment(d 7)were killed and the severity of coloni c inflammation was assessed.The COX-2 protein expression in colon tissues was e xamined by immunohistochemistry.Results:The colonic damage of Group 1 was exac erbated as compared with Group 2.The inflammatory index of colon tissues of Gro up 1(8.5?2.5)was significantly reduced,as compared with Group 2(13.5?1.9,P
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Objective: To compare effects of sulindac, PPAR? activator and PPAR? antagonist on the proliferation and apoptosis of the colonic cancer cells, and to investigate whether sulindac exerts its colonic neoplasm inhibiting activity through pathway of PPAR?. Methods: Cell strain HT-29 of colonic cancer was divided into six groups: the control group, sulindac group, 15d-PGJ2 (PPAR? activator) group, GW9662 (PPAR? antagonist) group, sulindac+GW9662 group and 15d-PGJ2+ GW9662 group. After 24 and 48 hours’culturing, proliferation status of each group was determined by immunocytochemical staining of PCNA, and cell apoptosis status was determined by double staining method of AnnexinV-FITC/PI, examined on flow cytometer. Results: (1) Proliferation status of the colonic cancer cells of each group: 24 and 48 hours after medication, PCNA positive ratios were 33.2%?4.5% and 25.0%?4.7% of the control group, 11.8%?3.7% and 8.6%?1.9% of sulindac group, 11.2%?2.5% and 11.4%?2.1% of 15d-PGJ2 group, 35.3%?4.3% and 26.8%?3.9% of GW9662 group, 16.5%?5.3% and 12.2 %?2.4% of sulindac + GW9662 group, 21.0%?4.8% and 21.5%?4.2% of 15d-PGJ2+GW9662 group. (2) Apoptosis ratio of colonic cancer cells of each group: 24 hours after medication, apoptosis rate of colonic cancer cells was 13.0%?1.0% of the control group, 41.0%? 2.6% of sulindac group, 11.5%?0.6% of 15d-PGJ2 group, 12.4%?0.9% of GW9662 group, 33.6%?2.3% of sulindac+GW9662 group, and 13.0%?1.0% of 15d-PGJ2 + GW9662 group. 48 hours after medication, apoptosis rate was 14.0%?3.4% of the control group, 95.3%?1.5% of sulindac group, 31.5%?2.3% of 15d-PGJ2 group, 13.0%?1.9% of GW9662 group, 86.8%?0.4% of sulindac+GW9662 group, and 12.9%?1.0% of 15d-PGJ2+GW9662 group. Conclusion: Both sulindac and PPAR? activator can inhibit proliferation and promote apoptosis of colonic cancer cells, and their effects can be antagonized by PPAR? antagonist, which indicates that as a kind of PPAR? ligand, sulindac can inhibit proliferation of colonic cancer cells via activating PPAR?.
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Objective: To evaluate the long-term effectiveness of sulindac on the pathology of colorectal adenomas of familial adenomatous polyposis (FAP) patients. Methods: FAP patients were treated with sulindac 400 mg per day. The change of colorectal polyps was assessed every 3 months in the first year. After the significant regression of colorectal polyps was achieved, sulindac was used to maintain the effects. The patients received colonoscopy examination regularly. Biopsies of remnant polyps and other lesions were obtained. The type and dysplasia grade of biopsies were evaluated and compared with baseline. Results: Before the study, 90.8% of adenoma biopsies were tubular, while 9.2% was tubulovillous adenoma. The dysplasia of grades Ⅰ, Ⅱ and Ⅲ were 42.1%, 45.6% and 12.3%, respectively. After sulindac treatment, 99.8% of adenoma biopsies were tubular, while 0.2% tubulovillous adenoma. There was significant difference compared with baseline (P
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Objective: To investigate the chemopreventive effects of pioglitazone (exogenous PPAR? ligand) on rat colon aberrant crypt foci, a rat carcinogenesis model induced by dimethylhydrazine (DMH),and to compare pioglitazone with sulindac (a NSAID). Methods: Thirty two, 8 week old, female Sprague Dawley rats were randomly divided into four groups ( n =8 each). Group 1 rats were injected with DMH alone (120 mg?kg -1 , single subcutaneous injection). Group 2 rats were injected with saline alone. Group 3 rats were pre treated with sulindac (320 mg?kg -1 ) for 7 days before DMH initiation. Group 4 rats were treated with pioglitazone (100 mg?kg -1 ). The animals were killed at the end of the experiment (week 5) and the colons were stained with methylene blue. The aberrant crypt foci (ACF) of the colonic mucosa were assessed. Results: In Group 1 rats (DMH only), the average numbers of ACF/colon and AC/colon were (182?93) and (263?198), respectively. In Group 2 (saline group) rats, no ACF were found. In Group 3 (sulindac group) rats, the average numbers of ACF/colon and AC/colon were (91?49) and (140?69), respectively. Both of them were decreased significantly compared with the values in Group 1 ( P
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Objective To investigate the features of pit patterns by magnifying endoscopy on neo-plastic colorectal polyps. Methods The materials consisted of 129 polyps in 108 patients. Dye-assisted magnifying endoscopies were used to ascertain the pit patterns of polyps. Results Of 129 polyps, 106 were diagnosed pathologically as neoplastic lesions(adenomas and carcinomas) , in which 10 demonstratedⅡpit pattern with only mild to moderate atypia and no severe atypia; 73 ⅢL pit pattern; 1Ⅲs pit pattern; 7 Ⅳ pit pattern and 15 Ⅴ pit patterns which includes malignant change in 10 cases, and severe atypia in 5 cases. Ten lesions all demonstrated Ⅴ pit pattern were found to be carcinoma (7 mucosal and 2 submucosal and 1 advanced carcinomas). Of 7 mucosal carcinomas,6 showed ⅤA pit pattern,1 , Ⅴ N pit pattern; 2 submuco-sal carcinomas all showed VN pit pattern; 1 advanced carcinoma showed ⅤN pit pattern. Ten lateral sprea-ding tumors were also investigated, their pit patterns under magnifying endoscopy were Ⅲ LⅥor V pit pat-tern among them one case with malignant change. Conclusion The images of pit pattern obtained by magnif-ying endoscopy were essentially concordance to those provided by stereomicroscopy. The differentiation of tu-morous lesion or non-tumorous lesion can be fairly performed under the observation of pit patterns; it gives an important practical significance in diagnosing tumorous lesions.
