Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021390 (inflammatory bowel disease)
 23,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Preoperative plasma CEA levels were measured in 93 selected patients with histologically defined colorectal adenomata removed at fibroptic colonoscopy in order to determine whether CEA levels are elevated in patients with colonic polyps, or vary with different histologic patterns. None of the patients had inflammatory bowel disease, previous history of carcinoma, or evidence of liver disease. Fifteen percent of the patients had elevated CEA levels (greater than or equal to 2.5 ng/ml; Hansen method), and two-thirds of these were between 2.5 and 4.0 ng/ml. Increased association of elevated CEA levels was noted with old age, villous adenomas (2- to 4-fold), and increased tumor size (greater than 2.3-cm diameter; 2-fold), but not with foci of dysplasia or carcinoma in situ as such. One-half (7/14) of the patients with elevated CEA levels showed the following: two patients had villous tumors with carcinoma in situ, one had a villous adenoma, two had mixed villous and tubular adenomas (with a high proportion of villous pattern), and two were subsequently shown to have carcinoma elsewhere in the colon. It is uncertain that the polyps were the source of the elevated circulating CEA levels; other factors including smoking and patient selection need to be considered. This preliminary study suggests that patients with colorectal adenomata and elevated circulating CEA may be at higher risk for the development of carcinoma. Further follow-up studies of the malignant potential of the polyp-bearing colon are essential.
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PMID:CEA levels in patients with colorectal polyps. 120 57

The risk of colorectal carcinoma is increased among patients with longstanding ulcerative colitis and Crohn's disease. The development of cancer in inflammatory bowel disease is hypothesized to evolve by a multistep process involving genetic instability, clonal expansion and the development of a malignant phenotype. The contribution of nutritional factors such as folate deficiency is of great interest; molecular genetic mechanisms are under study. In contrast to sporadic colorectal carcinoma, carcinomas in ulcerative colitis are associated with a long prior history of chronic inflammation and the subsequent development of epithelial dysplasia. Dysplasia is defined as an unequivocal neoplastic alteration of the colonic mucosa. The object of surveillance is prevention of death from cancer by detection at a premalignant or early curable stage. Patients at greatest risk of cancer who customarily undergo endoscopic surveillance are those with extensive colitis of more than 8 years duration. Dysplastic epithelium may occur in flat mucosa, and may produce a plaque or a nodular/villiform appearance. Dysplasia is not present in all patients with cancer in colitis. It is important to develop more sensitive and specific markers for the presence of precancer or cancer in colitis. Under study are proliferation-associated markers detected by immunohistochemistry, lectin binding, flow cytometry and laser-induced fluorescence coupled with endoscopy.
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PMID:Ulcerative colitis and colon cancer: biology and surveillance. 146 4

The controversy in the treatment of inflammatory bowel disease is how to decide surgical vs. medical management in each case. Of 309 patients with ulcerative colitis in our department, 63 (20%) patients had received surgical treatment. The mean age was 33.5 +/- 13.7 years old and the mean duration from onset to operation was 6.72 +/- 5.51 years. The indications for surgical treatment were 47 (75%) resistant cases against medical treatment, 9 (14%) severe cases and 7 (11%) cancer or dysplasia cases. In surgical cases compared with medical ones, the ratio of total duration (months)/number of admission showed below 10, and the total amount of used steroid was over 300 mg per month. These ratios were considered to be the useful markers for surgical indication. Operative procedures were 15 total proctocolectomy+ileostomy, 29 total colectomy+ileorectal anastomosis, 13 total proctocolectomy+ileoanal anastomosis and 6 others. Restorative proctocolectomy using double stapling method with two stage operation was chosen in 8 patients because of easier and safer operative procedure and a few complications. We conclude that early surgical treatment for the patients resistant against medical management is considered to improve the patients' quality of life.
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PMID:[Controversy--surgical vs. medical management of inflammatory bowel disease]. 147 Jan 22

This article summarizes the data concerning cancer risk in chronic inflammatory bowel disease. Cancer risk of ulcerative colitis and Crohn's disease is highly dependent on the duration of the disease, extent of bowel inflammation, and probably also of the age at onset of the disease. Cancer development follows the dysplasia-carcinoma-sequence. Diagnosis of premalignant changes is the basis for follow-up studies in ulcerative colitis as suggested here.
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PMID:[Risk of cancer in chronic inflammatory bowel diseases]. 162 13

Adenocarcinomas of the colon arise from adenomatous polyps. We hypothesized that sucrase-isomaltase (SI), a glycoprotein hydrolase, found in normal small intestine, fetal colon, and colon carcinomas is a marker associated with progression of adenomatous polyps with dysplasia to adenocarcinomas. To examine this hypothesis, we performed immunostaining using a polyclonal antihuman SI antibody in 32 adenomatous polyps with varying degrees of dysplasia. In addition, sucrase enzyme activity was determined in three sets of simultaneously harvested polyps, cancer, and adjacent normal mucosa from the same patient. All severely dysplastic polyps (6/6) exhibited SI staining. Most polyps (85%) with 3+ staining (i.e., greater than 10% of polyp positive for SI) had severe dysplasia, whereas those with mild dysplasia had either 1% to 5% staining or no staining in 95% of the cases. These data indicate that the extent of SI immunostaining in polyps correlates with the degree of dysplasia (p = 0.0001). Sucrase-isomaltase activity in the polyps was 18.1 +/- 1.8 mU/mg (mean +/- SD); in adjacent carcinoma SI activity was 29.1 +/- 1.8 mU/mg. Adjacent mucosa showed no activity in all cases. In summary, our results suggest that SI expression correlates with the progression of dysplastic adenomatous polyps to carcinoma. Sucrase-isomaltase expression may be useful as a clinical marker to improve our prognostic capabilities in patients with dysplastic lesions of the colon, that is, inflammatory bowel disease.
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PMID:Sucrase-isomaltase: a marker associated with the progression of adenomatous polyps to adenocarcinomas. 169

Campylobacter jejuni is a major cause of human enteritis which mimics the inflammatory bowel disease (IBD). In this study, microstructural changes on the surfaces of the murine gastrointestinal tract persistently colonized by Campylobacter jejuni, strain GJ-S131, were investigated by using scanning electron microscopy (SEM) and transmission electron microscopy (TEM). The results revealed that the appearance of the gastrointestinal mucosa in both BALB/C and KM mice resembled that in human with inflammatory bowel disease. Under SEM, the mucosa of the jejunum and ileum, with broken or distorted villi had a "worm eaten" look; crypts were irregular in shape and size, and the mucosa showed atrophy, especially in the colon. Epithelial junctions demonstrated furrows, clefts or deep crevasses, with exudates containing a large number of leukocytes. Cytologic appearances were characterized by microvilli dysplasia and/or atrophy, patchy erosions or necrosis and pelade-like appearance due to absence of microvilli, which were similar to the findings under TEM.
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PMID:Electron microscopic appearance of the chronic Campylobacter jejuni enteritis of mice. 178 9

Histocompatibility antigens (HLA) play an important part in immunoregulation and in cell differentiation. This study analyses the expression of HLA class I and class II antigens (DR, DP, DQ) in intestinal biopsy specimen from patients with Crohn's disease, ulcerative colitis, GvHD, radiation colitis and intestinal adenomas using the indirect immunoperoxidase technique. 92 of 94 inflamed specimen from patients with inflammatory bowel disease showed a neoexpression of HLA II (DR greater than DP greater than DQ) on their epithelial cells. The intensity of HLA-DR neoexpression was significantly dependent on an endoscopic as well as a histological index of inflammation. All 75 non-inflamed specimen except 4 from patients with Crohn's disease did not show any evidence of HLA II display on the epithelium. 4 of 18 intestinal adenomas expressed HLA II on their epithelial cells without any correlation to the type of adenoma or the degree of cell dysplasia. Furthermore all specimen from a patient with intestinal GvHD showed an aberrant epithelial HLA II expression, but not that from radiation colitis. The expression of HLA class I antigens was similar in all biopsies studied. Our results suggest, that the epithelial neoexpression of HLA class II antigens may be an important event in the pathogenesis of various bowel diseases.
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PMID:[Immunohistologic studies of differential HLA expression in patients with various intestinal diseases]. 205 37

The aetiology of inflammatory bowel disease (IBD) remains unknown, and many methods of treatment have been advocated. Patients with IBD are often nutritionally deficient and in negative nitrogen balance. The cause is multifactorial and includes decreased intake and absorption due to previous resection or mucosal involvement or increased exudation. General recommendations of vitamin and mineral supplements are usually made for these patients. Diet may have a more fundamental role in the aetiology and treatment of Crohn's disease, although this is not certain. Several controlled studies have confirmed that an elemental diet is as effective as steroids in inducing a remission in patients with acute Crohn's disease. Bacteria have also been implicated in the aetiology of Crohn's disease. Dietary measures may alter the intestinal flora and could result in a decrease of toxin production, which has been shown to correlate with clinical improvement. Although elemental diets are not effective in the treatment of ulcerative colitis, dietary measures may still be important. Preliminary studies suggest that eicosapentaenoic acid, which inhibits the production of mediators of inflammation by competing with enzymes in the arachidonic acid pathway, may be effective. Recent findings of increased faecal bile acids in patients with long-standing ulcerative colitis who developed dysplasia or carcinoma suggest that dietary measures may counteract these developments. It does appear that nutritional therapy in patients with IBD has both a primary and adjunctive role.
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PMID:Does nutritional therapy in inflammatory bowel disease have a primary or an adjunctive role? 211 81

Previous studies have found a widely variable prevalence of dysplasia and cancer in colonic strictures in patients with ulcerative colitis. Consequently, therapeutic recommendations are conflicting. To better assess the prevalence, we reviewed the clinical and pathological findings in all 27 patients with ulcerative colitis complicated by stricture who were entered into our Inflammatory Bowel Disease Registry. A true stricture was defined as a persistent localized narrowing of the colon found on air-contrast barium enema or on colonoscopy. Upon careful review, 12 of 27 patients were found to have transient colonic spasm, not a stricture, and were excluded. The remaining 15 patients with true strictures represented 3.2% of all ulcerative colitis patients in the registry. Strictures were identified at 13.3 +/- 9.9 years following the diagnosis of ulcerative colitis. Eleven patients had multiple strictures that were principally located in the left colon. Of the 15 patients, 11 had dysplasia and two had cancer found on colonoscopic biopsy. Ultimately, six patients had carcinoma found at colonoscopy or colectomy (three modified Dukes' stage A, one stage B, and two stage D). All cancers were at the site of a stricture. These findings indicate that a true colonic stricture in ulcerative colitis is frequently associated with dysplasia and cancer, which can be diagnosed with colonoscopic biopsy. A stricture should be considered a strong risk factor for cancer, requiring intensive colonoscopic surveillance. If dysplasia is discovered, or if the stricture cannot be adequately biopsied, consideration should be given to total colectomy.
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PMID:Dysplasia and cancer complicating strictures in ulcerative colitis. 230 80

Chronic inflammatory bowel disease (CIBD) and colorectal adenoma are considered as precancerous conditions and lesions of large bowel carcinoma, respectively. They, therefore, may be used to study the behavior of such different factors as tumor-associated antigens and nuclear DNA content abnormalities in colorectal carcinogenesis. Tissue concentrations of carcinoembryonic antigen (CEA) were significantly higher in those precancerous lesions (CIBD: 61 +/- 11.2 ng/mg, adenoma: 70 +/- 6 ng/mg; mean +/- standard error of the mean) than in normal colonic mucosa (36 +/- 4.7 ng/mg). Colorectal carcinoma had still higher tissue levels (437 +/- 108.2 ng/mg). No correlation between tissue CEA and tumor differentiation could be found, but there was a significant difference between aneuploid (747 +/- 354 ng/mg) and diploid (139 +/- 43 ng/mg) tumors. Using flow cytometry DNA aneuploidy was present in 31.6%, 10.5%, and 51.6% of CIBD, colorectal adenoma, and carcinoma, respectively. These data suggest that the occurrence of aneuploidy is not strongly dependent on a malignant transformation, but it may also be present in premalignant colorectal lesions without cellular dysplasia.
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PMID:Tissue carcinoembryonic antigen and DNA aneuploidy in precancerous and cancerous colorectal lesions. 231 59


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