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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Currently, more than 4,000 newly colorectal cancer are diagnosed each year in Belgium. The individual average-risk for developing colorectal cancer is about 5%. 90% of colorectal cancer occurred after the age of 50, and in 70% of the cases in patients without particular risk factors (average-risk population). Personal and/or familial history of colorectal adenoma, colorectal cancer, inflammatory bowel disease localised to the colon, familial polyposis syndrome or Hereditary Non Polyposis Colorectal Cancer (HNPCC) increase the risk of colorectal cancer. An individual appropriate screening of high-risk patients and average-risk asymptomatic patients older than 50, together with endoscopic resection of adenoma decrease the incidence and the mortality of colorectal cancer. Usual screening methods are fecal occult blood testing which is not proven to be efficient alone for individual screening (but still recommended for general population's screening), sigmoidoscopy (which has to be completed by a colonoscopy, if lesions founded), and colonoscopy. Virtual colonoscopy and genetic testing need further evaluation. Currently, colonoscopy seems to be the goldstandard method providing complete examination of the whole colon and being the most cost-effective method. Screening strategy should be decided on an individual basis considering the patient's benefit with respect to the informed consent.
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PMID:[Individual screening for colorectal cancer: which strategy for which patient?]. 1168 Jan 74

The new WHO-classification of the tumours of the digestive System replaces the "blue books", and are now dealt with completely in a single book. In addition to the histological features of the lesions, the new classification also contains information on epidemiology, aetiology, endoscopy, genetic susceptibility, molecular genetics, prognosis and predictive factors. The erstwhile mostly black-and-white histological photographs have at last again been replaced by numerous colour photographs and supplemented by endoscopic and macroscopic pictures. The changes to the individual tumour classifications are only few. The former classification of the malignant lymphomas of the gastrointestinal tract has now been replaced by the classification of these lesions that has long been in use. New additions are the gastrointestinal tract has long been in use. New additions are the gastrointestinal stroma tumours (GIST) and the gastrointestinal autonomic nerve tumour (GANT). To the epithelial tumours of the oesophagus have now been added the basaloid squamous cell tumours of the vermiform appendix and the colorectum have now been added the serrated adenoma and the small-cell carcinoma. The following new chapter have been included: adenocarcinoma of the oesophagogastric junction, secondary carcinomas of the stomach, secondary tumours of the small bowel and colon, the Peutz-Jeghers syndrome, juvenile polyposis, familial adenomatosis coli, and HNPCC. For the first time the intra-epithelial neoplasias in chronic inflammatory bowel disease have been differentiated, i.e. adenomas distinguished from the dysplasias, while the latter term has now been replaced by the term "intra-epithelial neoplasias". In comparison with the former "blue books", the new WHO-classification, prepared by presentatives of numerous disciplines--for the first time including clinicians--has taken on the character of a text book.
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PMID:[Esophageal, gastric and colorectal tumors]. 1189

This article discusses patients with inflammatory bowel disease (IBD), a group which is at increased risk for colorectal carcinoma based on extent and duration of their disease. Patients with chronic IBD (at least 8-10 years duration) should be screened with colonoscopy every 1 to 2 years with multiple jumbo biopsies every 10 cm through the entire colon. Patients with sporadic adenomas can be followed after complete polypectomy, whereas patients with adenoma-like dysplasia-associated lesion or mass (DALMs) need increased surveillance. Patients with flat dysplasia or non adenoma-like DALMs are at high risk for progression and should undergo colectomy. The patients who have indeterminate lesions can be differentiated based on the endoscopic, histologic, and molecular features of the lesion. Long-term follow-up is necessary to determine the natural history of these lesions.
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PMID:Evaluation of polypoid lesions in inflammatory bowel disease. 1248 42

This review summarizes current diagnostic problems and advances with regard to patterns of inflammation and dysplasia in ulcerative colitis and Crohn's disease. Ulcerative colitis and Crohn's disease have a variety of characteristic but non-specific pathologic features. In approximately 5% of inflammatory bowel disease cases, a definite diagnosis of ulcerative colitis or Crohn's disease cannot be established, in which case the term "indeterminate" colitis is used. Most cases of indeterminate colitis are related to fulminant colitis, a condition in which the classic features of ulcerative colitis or Crohn's disease may be obscured by severe ulceration with early superficial fissuring ulceration, transmural lymphoid aggregates, and relative rectal sparing. Approximately 20% of patients with indeterminate colitis develop severe pouch complications, which is intermediate in frequency between ulcerative colitis (8-10%) and Crohn's disease (30-40%). In order to establish a diagnosis of ulcerative colitis or Crohn's disease, it is important to evaluate pathologic material in conjunction with clinical, laboratory, radiologic, and endoscopic features and to recognize the variety of changes that may be seen in fulminant ulcerative colitis. There are a number of exceptions to the classic principles of inflammatory bowel disease pathology that may lead to diagnostic confusion. For instance, apparent skip lesions on biopsy analysis may occur in patients with ulcerative colitis in the following settings; long term oral or topical therapy, focal ascending colon, cecum and/or appendiceal involvement in patients with left sided ulcerative colitis, upper gastrointestinal involvement in patients with ulcerative colitis, and at initial presentation of ulcerative colitis in pediatric patients. In all of these circumstances, the finding of patchy disease and/or rectal sparing should not be misinterpreted as either evidence against a diagnosis of ulcerative colitis, or as representing skip areas characteristic of Crohn's disease. Patients with ulcerative colitis and Crohn's disease are at increased risk for the development of dysplasia and carcinoma. Recent studies suggest that given a similar duration and extent of disease, patients with Crohn's disease have a similar risk of dysplasia and cancer as patients with ulcerative colitis. Dysplasia in ulcerative colitis may be classified as flat or elevated (dysplasia associated lesion or mass [DALM]). Patients with flat high grade dysplasia are generally treated with colectomy. However, there is recent evidence to suggest that patients with flat low grade dysplasia, particularly if detected at the time of initial endoscopic exam, or if its multifocal or synchronous, should also be treated with colectomy. Elevated lesions in ulcerative colitis (DALM) are subdivided into "adenoma-like" and "non-adenoma-like" lesions based on their endoscopic appearance. Recent data suggests that adenoma-like lesions, regardless of the grade of dysplasia, or the location of the lesion (i.e., inside or outside areas of established colitis) may be treated adequately by polypectomy if there are no other areas of flat dysplasia in the patient. Although there are some histologic and molecular features that can help differentiate sporadic adenomas from adenoma-like polypoid dysplastic lesions related to ulcerative colitis, none of these adjunctive techniques can help distinguish these lesions definitively in any single patient. Patients with a non-adenoma-like DALM, (irregular, broad based, or strictured lesion) should be treated with colectomy because of the high probability of adenocarcinoma. The surveillance and treatment options for patients with flat and elevated dysplasia in ulcerative colitis are reviewed in detail.
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PMID:Diagnostic problems and advances in inflammatory bowel disease. 1269

Patients with ulcerative colitis are at an increased risk of developing dysplasia and carcinoma. The histologic recognition of dysplasia arising in this setting, particularly when patients have active colitis, can be challenging. However, even if it is clear that the patient has dysplasia, further challenges include the distinction of low-grade dysplasia from high-grade dysplasia and the distinction of an inflammatory bowel disease-related dysplastic lesion from a sporadic adenoma. This review article will summarize some of these issues from the gastrointestinal pathologist's perspective.
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PMID:The histologic diagnosis of dysplasia, dysplasia-associated lesion or mass, and adenoma: a pathologist's perspective. 1270 68

The fact that there is an increase in cases of ulcerative colitis-associated dysplasia and colitic cancer raises some problems for clinical practice and pathological diagnosis. How to detect ulcerative colitis-associated dysplasia and early cancer endoscopically? How to discriminate inflammatory regenerative epithelium from UC-associated dysplasia and aberrant crypt foci histologically? How to distinguish dysplasia-associated lesion or mass from sporadic adenoma pathologically? UCAC has established risk factors including, among others, long duration of disease, large extent and low activity of disease, and the lack of adequate surveillance and therapy. Colonoscopic and histological evidence of low grade and high grade dysplasia means the possible evidence of coexisting carcinoma. Carcinoma typically may occur in the entire colon, is often multiple and has undifferentiated histology. Important factor is the effectiveness of dysplasia surveillance as a population based strategy to decrease colorectal cancer mortality in inflammatory bowel disease patients. Colitis-related cancer may have distinct pathogenesis to sporadic colorectal cancer.
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PMID:[The pathogenesis of ulcerative colitis-associated colorectal cancer]. 1510 94

Inflammatory bowel disease (IBD) has a multifactorial etiology and includes ulcerative colitis (UC) and Crohn's disease (CD). Powerful epidemiologic and genetic studies have provided ample evidence that a subset of both CD and UC are attributable to a likely primary genetic etiology. This is evidenced by the recent identification of the IBD1 gene ( NOD2 ) mutations which show an association with susceptibility to CD. The IBD complex shows a significant increased frequency in Jews when compared to non-Jews. While there is an increased incidence of colorectal cancer (CRC) in patients with IBD, it nevertheless is important to realize that IBD likely accounts for no more than 1-3% of all cases of CRC in Ashkenazi Jews. Importantly, however, awareness of the increased CRC risk in IBD may aid immeasurably in preventive interventions. The molecular pathway leading to CRC in IBD appears to differ from the well-known adenoma-to-CRC sequence, given the fact that these cancers appear to arise from either flat, dysplastic tissue or dysplasia-associated lesions or masses (DALMs). An important model, but by no means an absolute one, for colon carcinogenesis in IBD follows progression from an absence of dysplasia, to indefinite dysplasia, to low-grade dysplasia, on to high-grade dysplasia, and ultimately to invasive CRC. This carcinogenic process relates to the disease duration with respect to the extent of colonic involvement and may also involve primary sclerosing cholangitis. Given this knowledge of an increased risk for CRC in UC and CD, surveillance colonoscopy should initially be performed 8-10 years after onset of symptoms as opposed to diagnosis, and it should be performed 1-2 years after 8 years of disease in patients with pancolitis or after 15 years in those with left-sided colitis. A search for dysplasia of colonic mucosa with biopsies performed in all four quadrants every 10 cm throughout the colon is exceedingly important. Additional biopsies should be taken of any flat lesions, masses, or strictures. Prophylactic colectomy may then be indicated when severe dysplasia is confirmed by knowledgeable pathologists.
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PMID:Inflammatory bowel disease in Ashkenazi Jews: implications for familial colorectal cancer. 1551 46

Patients with inflammatory bowel disease (IBD), both ulcerative colitis (UC) and Crohn's disease (CD), are at an increased risk for developing colorectal carcinoma (CRC). The accurate diagnosis of dysplasia in biopsies taken during periodic surveillance of long-standing IBD patients is most important in prevention of UC and CD related cancer. Distinction of low from high grade IBD-related dysplasia and differential diagnosis between IBD-related dysplasia and dysplasia in sporadic adenoma as well as distinction from pseudodysplastic lesions in inflammatory pseudopolyps or reparative lesions is often very subtle and difficult and demands expertise of second experienced gastrointestinal pathologist. Although surveillance colonoscopy with multiple biopsies does not reduce the cancer mortality, it offers a reasonable chance of detecting precancer and performed prophylactic colectomy. Novel methods of detecting dysplasia are continuously being evaluated, including chromoscopy and molecular biology markers. In the future, one may expect, from these new markers to detect the dysplasia in IBD patients before development of histological evidence of neoplastic changes.
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PMID:The histological diagnosis of dysplastic and neoplastic lesions in inflammatory bowel disease: a pathological perspective. 1577 1

Adnab-9 binding in colonic tissue and effluent has been associated with an increased risk for colorectal neoplasia. We investigated if fecal binding by Adnab-9 may be used as a marker for colorectal neoplasia. A fecal-Adnab-9 ELISA was performed on samples of 249 patients and colonoscopic pathology results correlated. Fecal Adnab-9 binding was seen in 63% of patients with colorectal neoplasia (59% with colorectal cancer and 83% with adenoma), 33% with inflammatory bowel disease, 0% with hyperplastic polyps and 10% of controls. We conclude that fecal Adnab-9 binding is a promising risk marker for colorectal neoplasia.
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PMID:Fecal Adnab-9 binding as a risk marker for colorectal neoplasia. 1589 19

This review highlights areas of clinical research in gastroenterology and hepatology that were published during the last year and were summarized during the most recent American Gastroenterological Association Plenary Session. The topics include a comparison of the risk of recurrent bleeding in patients taking clopidogrel versus aspirin plus a proton pump inhibitor, the introduction of rifaximin for the treatment of traveler's diarrhea, and the results of an oral vaccine for cholera tested in a high endemic area where there is also a high prevalence of human immunodeficiency virus infection. In inflammatory bowel disease, the impact of a biomarker of inflammation, C-reactive protein, to the response to a new biologic therapy is identified as potentially important because it might facilitate the selection of patients for these treatments. Results of device, endoscopic, and surgical treatment of obesity are reviewed, including the evidence of significant impact of surgery-induced weight loss on comorbid diseases. In the field of cancer, colonoscopic screening results in more polyps detected, down-staging of cancers identified, and improved cancer survival. A new familial syndrome associated with a serrated adenoma/carcinoma phenotype and variability in microsatellite instability is described. A controlled study demonstrates that a urine-derived substance, ulinastatin, reduces the risk of post-endoscopic retrograde cholangiopancreatography pancreatitis. Hepatic stellate cells are involved in the fibrogenesis associated with nonalcoholic fatty liver disease. These areas of clinical research demonstrate the breadth of significant advances that will impact on the clinical practice of gastroenterology and hepatology.
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PMID:GIH clinical research update: 2004-2005. 1636 Oct 39


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