Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022104 (irritable bowel syndrome)
 8,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It was investigated whether Hemoccult-II test (H-II) could reduce the number of colonic examinations in patients with the irritable bowel syndrome, with normal rigid proctoscopic findings. A negative H-II was obtained in 299 patients from general practice and a positive test in nine. Colonoscopy was done in 157 and double contrast barium enema in 142 after random allocation. The nine patients with positive H-II all had colonoscopy. Among the 299 with negative H-II, colonic adenomas were detected in ten and an early cancer in an adenoma in the sigmoid colon; overlooked rectal adenomas were found in three, rectal cancer in one, rectal carcinoid in another and a coecal cancer, which could be palpated, in a third patient. Two patients with colonic cancer and one with adenoma were detected among those with positive H-II. All patients were followed by clinical examination after one year. In conclusion, colonic examination should carry a low priority in patients with symptoms of irritable bowel, negative Hemoccult-II and normal rigid proctoscopic findings performed by an experienced examiner. The investigation confirmed the recommendation of total colonoscopy in patients with a positive H-II and added support for increasing number of endoscopy services in contrast to those of diagnostic radiology, which should be reduced.
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PMID:[Rectoscopy and Hemoccult II in irritable colon. A prospective study]. 194 12

Previous studies have suggested that patients with Barrett's oesophagus may be at increased risk of colorectal neoplasia, though the association is disputed. In a multicentre prospective study we compared the prevalence of colorectal adenomas in patients with Barrett's oesophagus and controls. Barrett's oesophagus patients (n = 104) had histological confirmation of columnar epithelium extending more than 3 cm above the gastro-oesophageal junction. The 537 controls were patients with symptoms suggesting irritable bowel syndrome. No participant had a personal history of colonic neoplasm. Each patient underwent colonoscopy. Histologically proven adenomas were found in 26 Barrett's patients (25%) and 75 controls (14%). Three colorectal cancers were discovered in each group. The prevalence of adenomas was greater in the Barrett's oesophagus group than in the control group (p < 0.01) but the relation became non-significant after adjustment for age and sex and control for other known risk factors by a logistic regression model (odds ratio 1.4 [0.7-2.7]). The relative risk of adenoma was significantly higher in patients older than 59 than in younger patients (2.2 [1.3-3.5]) and in men than in women (3.4 [2.0-5.7]). Other factors contributing significantly to the risk of adenoma were a family history of colorectal cancer (2.3 [1.1-4.8]), rectal bleeding (2.1 [1.1-3.9]), previous colonic investigation (0.3 [0.1-0.7]), and complete as opposed to partial colonoscopy (6.4 [0.8-48.3]). We conclude that Barrett's oesophagus is not an independent risk factor for colorectal neoplasia and, therefore, is not, in itself an indication for colorectal screening.
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PMID:Multicentre prospective controlled study of Barrett's oesophagus and colorectal adenomas. Groupe d'Etude de l'Oesophage de Barrett. 853 84

Forty-nine acromegalics and 57 controls matched for age and sex underwent colonoscopy. The control group consisted of patients investigated because of atypical abdominal complaints compatible with irritable bowel syndrome or constipation. The exclusion criteria for both groups included: age over 75 years, previous colonic polyps or cancer, previous colonic surgery, rectal blood loss, anemia, previous abdominal radiation, sigmoidoscopy, colonoscopy or barium enema performed for any indication within 3 years prior to the present study. Colonoscopy was successful in reaching the cecum in 72 and 77% of the controls and acromegalics, respectively (p = NS). Eleven (22%) of 49 acromegalics had biopsy-proven colonic adenomas versus only five (9%) of the control group (p < or = 0.05). Multiple adenomas were found in three of the 11 acromegalics and in none of the controls. In five of these 11 patients and in only one of the controls, at least one adenoma was located in the right colon. In addition, acromegalics tended to have larger adenomas. The group of acromegalics with and without adenomas did not differ significantly in age or duration of active disease. In conclusion, the present study shows that acromegalic patients have an increased risk of developing colonic adenomas.
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PMID:Increased prevalence of colonic adenomas in patients with acromegaly. 792 Dec 6

Dysplasia is a morphological term that ethymologically means 'malformation'. For the definition of inflammatory bowel disease-related dysplasia, the nature and origin of the malformation are stressed and the lesion is defined as an epithelial malformation that is unequivocally neoplastic but noninvasive. The use of a precise definition is necessary because of the clinical consequences related to the finding of dysplasia in IBD. The microscopic diagnosis of dysplasia, however, remains difficult. Clinically, it is important to make a proper differential diagnosis between polypoid IBD-related dysplasia and sporadic adenoma occurring in IBD, and between therapy-related 'pseudodysplasia' and genuine dysplasia. When dysplasia is diagnosed, a second opinion may be indicated because of the clinical consequences. Additional techniques to search for genetic defects associated with carcinogenesis can help to support the diagnosis. They can identify changes in DNA content and molecular changes resulting from defects of genes controlling cell proliferation and death or tissue structure. These changes can, however, be absent, appear early or late in the transition from normality toward dysplasia and cancer, or appear during repair. Positive findings indicate an increased cancer risk, but the magnitude of the risk remains to be defined. A positive diagnosis of genuine dysplasia necessitates clinical action - either follow-up of the patient or treatment. In practice, treatment means surgery because dysplasia can be a precursor and/or a marker of malignancy, except for sporadic adenomas, which can be removed locally.
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PMID:Dysplasia in inflammatory bowel diseases: definition and clinical impact. 1054 55

The aim of this study was to assess the spectrum of radiographic findings in primary hyperparathyroidism (PHPT). The study group consisted of 16 women and 7 men whose Ca levels were at least two or three times higher than normal. The average age was 55.3 in women and 49.4 in men. We detected carcinoma in 1, hyperplasia in 1, multiple adenomas in 4, single adenoma in 17 patients. The most common finding in the skeletal system was the decreased bone mineral density (BMD) and the complete loss of the lamina durae dentium. BMD was found lower in women than in men. This result attributed the increased number of postmenopausal patients in our study group. The second most common finding in our study group was subperiosteal bone resorption. Brown tumors (BTs) were located at maxilla in one, widespread in one, mandibula in two, long tubular bones in four patients. Renal stone disease was found in five, spastic colon in two, gastric ulcer in one, mitral valve calcification in one patients. We demonstrated no pathologic changes consistent with PHPT in remaining seven patients.
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PMID:The spectrum of radiographic findings in primary hyperparathyroidism. 1198 74

There has been a major improvement in our understanding in the area of the genetics of CRC in the last decade. Reason for this is partly that CRC has a strong hereditary trait and premalignant lesions are frequent and easily accessible. In the 1990-ies the mutations responsible for the adenoma-carcinoma sequence were discovered on after the other. In the second part of the review the authors discuss the genetic background of sporadic and IBD associated colorectal cancers as well as the role of genetics in the diagnosis, prognosis and prediction of therapy. Chromosomal instability (85%) and microsatellite instability with or without change in DNA methylation (15%) are the main mechanisms involved in the pathogenesis of sporadic colorectal cancers. It became evident that no ultimate mutations exist. Most of neoplasms are genetically heterogeneous, independent pathways and simultaneous tumorigenesis may exist within the same organ, also in the colon. Gene expression profile, clinical phenotype and prognosis may also vary according to the location. Similar genetic mutations may be found in IBD associated colorectal cancers, however, the typical sequence and importance of mutations is different. In future, fecal DNA testing may be an important screening tool for colorectal cancer; however, its routine use is still limited by its low sensitivity. Similarly, genetic investigation may play an increasing role in the prediction of prognosis, therapy and complication of chemotherapy. A more distant goal may be the individualization of the therapy.
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PMID:[Current concepts in the genetics of hereditary and sporadic colorectal cancer and the role of genetics in clinical practice: sporadic and IBD-associated colorectal tumors, significance of genetic tests in diagnosis, prognosis and assessment of chemotherapy outcome]. 1657 74

Colorectal cancer (CRC) is still a disease with a high incidence and mortality. Prevention of (pre-) cancerous lesions of CRC by endoscopic screening is promising, but costs are high and identification of high-risk populations is difficult. Since screening both average-risk and high-risk populations for CRC has its logistic and financial limitations, new primary prevention strategies are sought. Substantial evidence has shown that non-steroidal anti-inflammatory drugs (NSAIDs) and selective COX-2 inhibitors can reduce the incidence and mortality of CRC. However, long-term use of NSAIDs is associated with substantial gastrointestinal toxicity and may cause an exacerbation in IBD patients. Selective COX-2 inhibitors, with a better toxicity profile and no flare-up in IBD disease activity, are therefore attractive candidates for prevention. Chemoprevention with low-dose aspirin can be considered for individuals carrying a high risk for CRC. Folate supplementation is beneficial to the folate-depleted patients, since significant risk reductions for CRC are reported. Moreover, it might be applicable to the general population because it is safe, inexpensive and protects against vascular diseases. In line with drugs beneficial for multiple disease entities, statins have recently been proposed to reduce CRC risk. Ursodeoxycholic acid has been shown to decrease the incidence of colonic dysplasia in patients with ulcerative colitis and PSC and possibly reduces recurrence rates of polyps in general. Unfortunately, prospective randomized trials, in both high-risk and general population, are not available and the evidence is still controversial. Furthermore, cumulative epidemiological and observational data suggest the potential role of hormones as a chemoprotective agent. An increase in CRC in females with an early menopause, as well as a decrease of CRC in women with hormone replacement therapy justify further research into this issue. In IBD patients, both the severity and duration of the inflammation are the most evident risk factors for the development of dysplasia and subsequently cancer. Remission of inflammation, clinically, endoscopically and histologically, in IBD is the major goal. Long-term use of 5-aminosalicylates (5-ASA) has been shown to decrease the incidence of CRC and may hold the best promise as a chemoprotective agent in IBD. In parallel with primary prevention strategies in vascular medicine, the aim might be to postpone adenoma formation, for instance for 10 years, thereby achieving a significant risk reduction for CRC. In current practice, folate supplementation along with low-dose aspirin use in high-risk patients may be most attractive candidates, while future studies will have to clarify the role of these and other chemoprotective agents.
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PMID:Chemoprevention for colon cancer: new opportunities, fact or fiction? 1678 36

The cyclooxygenase (COX) is a key enzyme in the conversion of arachidonic acid to prostaglandins. COX-1 is constitutively expressed and is a critical housekeeping gene, whereas COX-2 is rapidly upregulated by growth factors and cytokines and thus responsible for inflammation. COX-2 is frequently overexpressed in colonic adenoma and carcinoma. Specific inhibitors of COX-2 have been shown to induce apoptosis in tumor cells and to inhibit tumor growth in animal models and in humans. Long-standing IBD patients have increased risk of developing colorectal cancer compared to general population. IBD-associated colorectal carcinogenesis is probably promoted by chronic inflammation and closely related to COX-2. In a recent study, powerful chemopreventive ability of selective COX-2 inhibitor was observed in colitis-related colon carcinogenesis in mouse model. But it was reported that even selective COX inhibitors aggravated the DSS-induced colonic inflammation. It is assumed that endogenous PGs are involved in the mucosal defense against DSS-induced colonic ulcerations which are produced by COX-1 at early phase and by COX-2 at late phase. Long-term use of COX-2 inhibitors for the chemoprevention of colitic cancer is needed to define their mechanism of action, that reduce side effects and have specific tumor target.
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PMID:[COX-2 inhibitors in inflammatory bowel disease: friends or foes?]. 1815 71

Patients with long-standing and extensive ulcerative colitis (UC) and colonic Chron's disease (CD) have an increased risk of CRC compared with the general population. Although no large controlled trials have proven that surveillance reduces mortality, cancer prevention in inflammatory bowel disease depends on the detection of dysplasia during scheduled surveillance colonoscopy and is widely recommended by gastroenterological associations. Dysplasia in IBD may occur in flat mucosa or in raised lesions (DALM) which have sometimes endoscopic features similar to adenoma (adenoma-like DALM). Recently, new endoscopic techniques to facilitate the distinction between dysplastic and actively inflamed or normal mucosa have been proposed. Chromoendoscopy significantly increases the sensitivity of detecting subtle dysplastic lesions and has emerged as the new standard of cancer surveillance in patients with IBD. Confocal laser endomicroscopy (CLE) is a novel technique that enables the endoscopist to obtain real time in vivo microscopic images of the gastrointestinal mucosa and can be used for targeting biopsies to relevant areas. CLE in conjunction with chromoendoscopy proved able to increase the diagnostic yield of dysplasia in ulcerative colitis and reduce the number of biopsies needed. The role of digital filtering technologies (virtual chromoendoscopy) and autofluorescence in IBD surveillance will be also discussed.
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PMID:Evolving endoscopic technologies for the detection of dysplasia in inflammatory bowel diseases. 2165 52

Little is known about the significance of inflammation in neoplastic colon polyps: tubular, tubulovillous, and villous polyps/adenomas (TVPs) and hyperplastic/serrated polyps (HSPs). We undertake this study to ascertain the significance of acute and chronic inflammation in neoplastic polyps. Eighty-one consecutive, randomized TVPs and fifty-four randomized HSPs accessioned in the UCHC surgical pathology laboratory were selected for final analysis. The TVPs display increased acute and chronic inflammation compared to normal and adjacent non-dysplastic colonic mucosa. Adenoma size correlates with degree of acute and chronic inflammation. TVPs show increased overall acute and chronic inflammation compared to HSPs of the same size. This difference was statistically highly significant (p<.001). The number of adenomas exhibiting high grade dysplasia was insufficient to evaluate the relationship between polyp inflammation, polyp size, and degree of dysplasia. The HSPs showed significantly lower incidence and severity of acute and chronic inflammation compared to the TVPs. No correlation was seen in the HSP group between polyp size and acute or chronic inflammation. The prevalence of IBD was higher in patients with HSP showing acute inflammation than in the general population, but this statistic may be skewed by the low overall incidence of acute inflammation in the HSP group.
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PMID:Inflammation associated with neoplastic colonic polyps. 2296 14


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