Use of accurate diagnostic criteria may increase incidence of stercoral perforation of the colon

PURPOSE: Stercoral perforation of the colon is reported to be a rare disease with poor prognosis. The aim of this study was to determine the frequency of stercoral perforation of the colon, to define diagnostic criteria for stercoral perforation of the colon, and to analyze the patient outcome in a university hospital gastrointestinal surgery unit. METHODS: From November 1993 until November 1998 all surgically treated patients with a colorectal disease were prospectively recorded in a computerized database. Diagnosis of stercoral perforation of the colon was made if 1) the colonic perforation was round or ovoid, exceeded 1 cm in diameter, and lay antimesenteric; 2) fecalomas were present within the colon, protruding through the perforation site or lying within the abdominal cavity; and 3) pressure necrosis or ulcer and chronic inflammatory reaction around the perforation site were present microscopically. Any additional colon pathology led to exclusion from the diagnosis of stercoral perforation of the colon. Using the same criteria, 81 cases in the literature were found to qualify and were further analyzed. RESULTS: In a five-year period 1,295 patients underwent colorectal interventions through laparotomy. A total of 566 (44 percent) cases were emergencies, 220 (17 percent) of these caused by colonic perforation. Seven patients had stercoral perforation of the colon. The incidence of stercoral perforation of the colon was 0.5 percent of all surgical colorectal procedures through laparotomy, 1.2 percent of all emergency colorectal procedures, and 3.2 percent of all colonic perforations. The mean age of the patients was 59 (median, 64; range, 22–85) years. All perforations were situated in the left hemicolon or upper rectum. The round or ovoid perforation had a mean diameter of 3.6 cm. Fecalomas were present in all patients and protruded from the perforation site or were found within the free abdominal cavity in three of them. Generalized stercoral peritonitis was a constant finding. Using a colonic resection without immediate restoration of continuity, an extensive intraoperative lavage, and antibiotics, there was no in-hospital mortality. Analysis of the reports in the literature revealed additionally that 28 percent of patients with stercoral perforation of the colon have multiple stercoral ulcers in the colon and that substantial mortality is encountered if only minor surgical procedures of treatment are used. CONCLUSIONS: The incidence of stercoral perforation of the colon seemed to have been underestimated. The reason for this might be the lack of defined diagnostic criteria for this disease. Low mortality is obtained by early surgical eradication of the affected part of the colon, including all stercoral ulcers, and by aggressive therapy for peritonitis.Presented in part at the meeting of the Swiss Society of Surgery, Lugano, Switzerland, June 9 to 12, 1999.     

Survival of colorectal cancer patients in relation to duration of symptoms and other prognostic factors

The effect of duration of symptoms and other prognostic factors on survival was studied by interview using a population-based sample of 154 colorectal cancer patients. The authors found that symptom durations of up to approximately one year before diagnosis had no effect on survival. In addition, it was found that the total number of symptoms was a statistically significant predictor of survival, although no single symptom had a significant effect. Stage, sex, and site also were found to be significant predictors of survival, whereas age, socioeconomic status, and other factors were not predictive. Research supported by NCI grant 2R18CA-16404. Work performed at the Fred Hutchinson Cancer Research Center.     

结直肠侧向发育型肿瘤内镜诊断与治疗

目的探讨结直肠侧向发育型肿瘤(LST)内镜诊断方法,经内镜黏膜切除术(EMR)、分片切除术(EPMR)、内镜黏膜下剥离术(ESD)方法治疗LST的疗效、安全性。方法 LST经色素染色放大内镜或NBI-ME观察病变形态、腺管开口分型(pit)及表面微血管分型(MP),分别进行EMR、EPMR、ESD或外科手术治疗,并分析LST的病理特点。结果在399例病人检出有LST,共407个病变。LST大小在10～80mm。LST部位在直肠128个(31.4%),乙状结肠97个(23.8%),降结肠54个(13.3%),横结肠67个(16.5%),升结肠21个(5.2%),盲肠36个(8.8%),回肠末段4例(1.0%)。LST形态呈颗粒均一型145个,结节混合型161个,扁平隆起型63个,假凹陷型38个。LST腺管开口分型以ⅢL和Ⅳ为多。405个LST经肠镜微创电切治疗,228个行EMR切除,165个行EPMR切除,12个行ESD切除,均在内镜下成功电切,另2例LST行外科手术治疗。出血发生率4.0%,术中即刻出血4例,术后3天迟发出血12例,无肠穿孔发生。LST病理结果:管状腺瘤46个(11.3%),管状绒毛状腺瘤146个(35.9%),绒毛状腺瘤181个(44.5%),增生性息肉10个(2.5%),高级别上皮内瘤变19个(4.7%),黏膜内癌3个(0.7%),黏膜下癌2个(0.4%)。术后复查肠镜无复发。结论色素染色放大内镜或NBI-ME方法有利于检出LST,EMR、EPMR、ESD是内镜下治疗LST安全有效的方法。     

结直肠海绵状血管瘤的诊断及外科治疗

目的 总结国内文献中结直肠海绵状血管瘤的临床病例特点和外科治疗方式.方法 回顾性分析北京协和医院1993年至2006年收治的4例和检索1979年至2006年国内文献报道的54例结直肠海绵状血管瘤的病例资料.结果 男女发病比例为100:1.0,43.1%的患者在婴幼儿时期发病,98.3%的患者表现为反复血便,纤维结肠镜、直肠CT和磁共振成像的诊断准确率为100%.91.4%的患者病变呈弥漫浸润性,8.6%的病变表现为局限性.82.8%的患者接受了外科干预治疗,3.5%的患者未接受治疗.结论 纤维结肠镜是诊断结直肠海绵状血管瘤的首选诊断方式.外科手术方式的选择方面应该根据患者的具体情况而定.     

结直肠损伤的特点和处理

目的 探讨结直肠损伤的特点和结肠损伤Ⅰ期修复的适应证以及直肠损伤和医源性结直肠损伤处理的特殊性。方法 总结分析1989年1月～2000年12月收治的结直肠损伤41例临床资料。结果 38例行急诊手术,术中出现并发症11例,占26.8％,2例术中损伤未发现以致形成直肠阴道瘘和腹膜后脓肿,1例结肠镜下息肉切除造成小穿孔在镜下用钛夹修补治愈。本组治愈39例,死亡2例,均死于严重的并发症。结论 了解结直肠损伤的特点,提高结直肠损伤的认识,掌握好结肠Ⅰ期修复手术的适应证、直肠损伤及医源性损伤处理的特殊性是减少结直肠损伤并发症,提高外科治疗效果的关键。     

Flow cytometric DNA analysis of poorly differentiated adenocarcinoma of the colorectum.

DNA ploidy patterns in 11 poorly differentiated adenocarcinomas of the colorectum were examined by flow cytometry using paraffin-embedded specimens. Measurements of DNA content were made of the superficial (Sup) half and deeper (Deep) half of the primary tumors in all cases, and of lymph node metastases in five cases. All the primary tumors showed invasion beyond the muscularis propria of the colorectum. Aneuploidy or polyploidy in either Sup or Deep of the primary tumor was found in six of the 11 (54.5%) tumors. Out of the six aneuploid tumors, five were in Dukes' stage C with distant metastases at the time of operation, and four died within one year of surgery. Conversely, out of five diploid tumors, none had distant metastases at the time of operation and two survived for longer than three years after surgery. The DNA ploidy pattern of Deep differed from that of Sup in four out of six aneuploid tumors, and two showed aneuploidy in Sup and diploidy in Deep. All the lymph node metastases in the five tumors had a diploid pattern, although three had aneuploid patterns in the primary tumors. The findings suggest the DNA ploidy pattern of a primary tumor to be correlated with the degree of metastasis at the time of operation or prognosis, but the population of tumor cells having different DNA contents may be apt to change between Sup and Deep in aneuploid tumor.     

Using a combination of cytochrome P450 1B1 and β-catenin for early diagnosis and prevention of colorectal cancer

Background: Although fecal occult blood test and invasive endoscopic examination are common used to detect colorectal adenomas and cancers, non-invasive and specific biomarkers are still under investigation. The objective is to evaluate the biomarker CYP1B1 alone or in combination with aryl hydrocarbon receptor (AhR), nuclear β-catenin, p53 or bcl-2 for early diagnosis and prevention of colorectal cancer. Methods: These biomarkers were analyzed semi-quantified across 231 colonic tissues including 97 adenocarcinomas, 85 adenomas and 49 non-neoplastic colons using immunohistochemistry. In order to differentiate non-neoplastic colons from colorectal neoplasms (adenoma and carcinoma), the values for CYP1B1, AhR, nuclear β-catenin, p53 and bcl-2 expressions were subjected to discrimination analysis, then the cross-validation, sensitivity and specificity of these models were calculated. Results: Expressions of CYP1B1, p53, nuclear β-catenin and bcl-2 were significantly associated with colorectal carcinogenesis (p < 0.01 for the trend test). The overexpression rates for CYP1B1, p53, nuclear β-catenin and bcl-2 were significantly higher in the adenoma and carcinoma groups than in the non-neoplastic colon group (p < 0.05). The discrimination models showed that a combination of two biomarkers was better than a single biomarker, and provided specificity ranging from 39% to 100% and sensitivity ranging from 43% to 82% for colorectal carcinoma. Conclusions: The increase in expression of CYP1B1 occurred not only in colorectal carcinoma and but also in adenoma. Moreover, a screening panel of CYP1B1 in combination with nuclear β-catenin was the most suitable marker pair to screen for colorectal carcinoma based on this study.     

Neuroendocrine cells in colorectal adenomas

A consecutive series of 218 endoscopically resected colorectal adenomas was investigated for the occurrence of neuroendocrine cells. In 59 per cent of these adenomas argyrophil cells were detected. In 8 per cent of the adenomas these cells were numerous and so intricately blended in with the other cell types that they were regarded as an intrinsic part of the tumour. In these adenomas subsequently immunocytochemistry revealed the presence of the neuro-hormonal peptides glucagon, pancreatic polypeptide and somatostatin as well as serotonin, in a pattern similar to that seen in normal colorectal mucosa. The presence of neuroendocrine cells did not correlate with any clinical or pathological parameter. The occurrence of neuroendocrine cells in colorectal adenomas is in agreement with the unitarian theory of the development of the various epithelial cell types in large bowel mucosa.     

Altered JS-2 expression in colorectal cancers and its clinical pathological relevance

JS-2 is a novel gene located at 5p15.2 and originally detected in primary oesophageal cancer. There is no study on the role of JS-2 in colorectal cancer. The aim of this study is to determine the gene copy number and expression of JS-2 in a large cohort of patients with colorectal tumours and correlate these to the clinicopathological features of the cancer patients. We evaluated the DNA copy number and mRNA expression of JS-2 in 176 colorectal tissues (116 adenocarcinomas, 30 adenomas and 30 non-neoplastic tissues) using real-time polymerase chain reaction. JS-2 expression was also evaluated in two colorectal cancer cell lines and a benign colorectal cell line. JS-2 amplification was noted in 35% of the colorectal adenocarcinomas. Significant differences in relative expression levels for JS-2 mRNA between different colorectal tissues were noted (p = 0.05). Distal colorectal adenocarcinoma had significantly higher copy number than proximal adenocarcinoma (p = 0.005). The relative expression level of JS-2 was different between colonic and rectal adenocarcinoma (p = 0.007). Mucinous adenocarcinoma showed higher JS-2 expression than non-mucinous adenocarcinoma (p = 0.02). Early T-stage cancers appear to have higher JS-2 copy number and lower expression of JS-2 mRNA than later stage cancers (p = 0.001 and 0.03 respectively). Colorectal cancer cell lines showed lower expression of JS-2 than the benign colorectal cell line. JS-2 copy number change and expression were shown for the first time to be altered in the carcinogenesis of colorectal cancer. In addition, genetic alteration of JS-2 was found to be related to location, pathological subtypes and staging of colorectal cancer.