Ulcerative Colitis: Li F

He G, Ouyang Q, Chen D, Li F, Zhou J. · Department of Gastroenterology, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, China. · Dig Dis Sci. · Pubmed #17429731 No free full text.

Abstract: Mucosal microvascular thrombi in rectal biopsies were observed in some ulcerative colitis (UC). Heparin may be effective in steroid resistant UC in some studies, however, the new results of meta-analysis demonstrated a non-significant effect of heparin in controlled clinical trials, differing markedly from observational studies. The objective of this study was to identify colonic microvascular thrombi in larger cases with UC, and analyse its possible risk factors: age, gender, histologic score, extent of lesions and operation or biopsy specimens, and assess the significance of microvascular thrombosis in patients with UC. The microvascular thrombi were identified by immunohistochemical staining with anti-CD61 monoclonal antibody and Martius scarlet blue (MSB) staining in 40 colonic tissue samples of UC (31 biopsy specimens and nine operated cases) and 12 cases of normal colon tissue from operated colonic carcinoma. Logistic regression analysis was used to assess the relationship of age, gender, degree of histology, origin of the specimens, extent of lesions and microvascular thrombi examined. Microvascular thrombi were positive in 14 of 40 UC cases, and none in the controls. The presence of microvascular thrombi was related to operation specimens with odds ratio 11.667, P=0.0179, it might be also related to histologic score (OR=1.350) and extent of lesions (OR=1.619). These results suggest that microvascular thrombosis may be one of the important pathogenesis in some UC, and that the effect of anticoagulant treatment still needs to be assessed.

Cai J, Li F, Zhou W, Luo HS. · Department of Gastroenterology, Renmin Hospital, Wuhan University, Jie Fang Road 238, Wuchang 430060, Wuhan, P R China. · Dig Dis Sci. · Pubmed #17404880 No free full text.

Abstract: Diseases of the ileocecal junction are mostly ulcerative. The aim of this study was to investigate the value of colonoscopy on the diagnosis of the causes of ileocecal ulcer. Clinical manifestations, diagnosis, and endoscopic and histopathologic features of 52 hospitalized cases of ileocecal ulcer were retrospectively analyzed. In this study, the causes of ileocecal ulcer were intestinal tuberculosis (32.7%), Crohn's disease (19.2%), carcinoma of the cecum (17.3%), ulcerative colitis (UC; 13.5%), solitary ulcer of the colon (9.6%), lymphoma (5.8%), and leiomyoma (1.9%).The concordance rate of diagnosis at endoscopy to final diagnosis was 78.8%; the rate of endoscopic misdiagnosis was 21.2%. The concordance rate of clinical diagnosis before colonoscopy to the final diagnosis was 17.3%. Colonoscopy plays an important role in the diagnosis of the diseases that lead to ileocecal ulcer. However, colonoscopy may cause some erroneous diagnosis. To attain the correct diagnosis, endoscopic features, pathologic results, and the other clinical data should be analyzed together.

Yan B, Wang H, Rabbani ZN, Zhao Y, Li W, Yuan Y, Li F, Dewhirst MW, Li CY. · Department of Radiation Oncology, Duke University Medical Center, Durham, North Carolina, USA. · Cancer Res. · Pubmed #17178846 links to  free full text

Abstract: Tumor necrosis factor-alpha (TNF-alpha) is an important inflammation cytokine without known direct effect on DNA. In this study, we found that TNF-alpha can cause DNA damages through reactive oxygen species. The mutagenic effect of TNF-alpha is comparable with that of ionizing radiation. TNF-alpha treatment in cultured cells resulted in increased gene mutations, gene amplification, micronuclei formation, and chromosomal instability. Antioxidants significantly reduced TNF-alpha-induced genetic damage. TNF-alpha also induced oxidative stress and nucleotide damages in mouse tissues in vivo. Moreover, TNF-alpha treatment alone led to increased malignant transformation of mouse embryo fibroblasts, which could be partially suppressed by antioxidants. As TNF-alpha is involved in chronic inflammatory diseases, such as chronic hepatitis, ulcerative colitis, and chronic skin ulcers, and these diseases predispose the patients to cancer development, our results suggest a novel pathway through which TNF-alpha promotes cancer development through induction of gene mutations, in addition to the previously reported mechanisms, in which nuclear factor-kappaB activation was implicated.