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)

Focal crypt injury by neutrophils (cryptitis/crypt abscesses), or focal active colitis (FAC), is a common isolated finding in endoscopic colorectal biopsies. Focal active colitis is often thought of as a feature of Crohn's disease, but may also be seen in ischemia, infections, partially treated ulcerative colitis, and as an isolated finding in patients undergoing endoscopy to exclude neoplasia. Clinical, endoscopic, and pathological data were retrospectively reviewed from 49 patients with focal active colitis, who had no other diagnostic findings on colorectal biopsy and no history of chronic inflammatory bowel disease. The histological findings were correlated with clinical diagnoses. Follow-up information was available for 42 of 49 focal active colitis patients. None developed inflammatory bowel disease; however, 19 patients had an acute self-limited colitis-like diarrheal illness, 11 had incidental focal active colitis (patients without diarrhea that were endoscoped to exclude colonic neoplasia and found to have asymptomatic FAC), 6 had irritable bowel syndrome, 4 had antibiotic-associated colitis, and 2 had ischemic colitis. Twenty patients were immunosuppressed, and 19 were taking nonsteroidal anti-inflammatory drugs. No histological features predicted final diagnoses. FAC did not predict the development of chronic colitis, even when mild crypt distortion or slight basal plasmacytosis was present. The preponderance of acute self-limited colitis and antibiotic-associated colitis among the FAC patients, along with the high number of immunosuppressed patients, support the conclusion that most FAC cases are infectious. The incidental detection of FAC in patients undergoing endoscopy to exclude colonic neoplasia was not clinically significant. The role of nonsteroidal anti-inflammatory drugs in FAC deserves further study.
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PMID:The clinical significance of focal active colitis. 971 35

Eicosanoids are produced throughout the gastrointestinal tract and are significant mediators of physiologic and pathophysiologic processes. Understanding the precise role(s) of specific eicosanoid metabolites remains a significant challenge, but has led to the development of new pharmacologic strategies for treating NSAID-induced gastroenteropathy and IBD. Given the complex array of arachidonic acid metabolites, the development of more specific and potent inhibitors of these cyclooxygenase isoforms is important for future studies and possible therapeutic applications. Mice have been prepared that lack expression of COX-1 or COX-2. Once these animals have been carefully evaluated, understanding of the role of various pathways of eicosanoid formation in gastrointestinal function, development, and epithelial growth regulation might be improved. Considerable progress has been made in the understanding of arachidonic acid metabolism and in eicosanoid receptor biology. The identification and characterization of an inducible cyclooxygenase isoform has led to important studies evaluating the role of this enzyme in inflammation, neoplasia, and NSAID-induced gastrointestinal injury. The demonstration that COX-2 overexpression in intestinal epithelial cells leads to specific phenotypic changes, such as increased adhesion and inhibition of apoptosis, indicates that this enzyme may alter the tumorigenic potential of epithelial cells and offers hope for the future development of improved chemopreventive agents.
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PMID:Introduction to eicosanoids and the gastroenteric tract. 922 72

A high-fat and low-fiber diet is regarded as a major risk factor for colon cancer by increasing luminal contents of secondary bile acids. Calcium, on the other hand, has been implicated as a possible preventive agent in colon tumor development. In in vitro studies with human colonic epithelium, incubation with the secondary bile acid deoxycholic acid (DCA) induced hyperproliferation of colonic crypt cells which is regarded as a sign of preneoplastic transformation. In the present study the effects of calcium chloride (CaCl2) on DCA-induced hyperproliferation were tested at different stages of DCA-induced cell injury. Colonic biopsies from 36 patients (no tumors, polyps or IBD) were incubated with CaCl2 (1 and 10 mM) and 5 microM DCA which was added to the incubation medium either together with (experiment A), after (experiment B), or before CaCl2 (experiment C). Coincubation of the biopsies with DCA and 10 mM CaCl2 at the same time (experiment A) resulted in a significant reduction of whole crypt labeling index by 12% (p < 0.05), whereas in the other incubation experiments no significant growth-inhibitory effects could be demonstrated for CaCl2. These findings may best be explained by the formation of calcium-bound bile acid salts which lost most of their toxicity for the colonic cells.
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PMID:Effects of calcium and deoxycholic acid on human colonic cell proliferation in vitro. 942 94

Neuroendocrine gastroenteropancreatic tumor diagnosis is a very difficult and expensive procedure. This study compared Chromogranin A (CgA) to Neuron-specific enolase (NSE) in 55 patients affected by neuroendocrine tumors. Advanced local or metastatic neoplasia was found in 43 patients. Radical operation was performed in 12 patients. Seventeen cases of lung microcystoma, 23 cases of other intestinal tumors and 19 patients affected by irritable bowel syndrome were used as controls. CgA sampling demonstrated sensitivity of 73% and specificity of 66%, a positive predictive value of 77% and a negative predictive value of 61% while NSE sampling showed sensitivity of 100%, specificity of 36%, a positive predictive value of 15% and a negative predictive value of 100%. CgA values demonstrated a statistically significant difference between patients with neuroendocrine tumors and tumor-free resected patients (p = 0.0015), microcystoma patients (p = 0.0087), other types of neoplasia (p = 0.01) and irritable bowel syndrome patients (p = 0.0004). No significant difference was found among the same groups when NSE values were analyzed. The high diagnostic accuracy of CgA sampling renders it very useful in early neoplastic detection, even in cases of nonfunctioning neoplasms or absence of liver metastases. In addition, CgA sampling may be an effective screening test in patients with irritable bowel syndrome or with liver or lung metastases when there is no evidence of the primitive tumor.
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PMID:[Usefulness of chromogranin A determination in the diagnosis of neuroendocrine neoplasia]. 1051 16

Endogenously formed nitrogen and oxygen free radicals are believed to be involved in human cancer etiology. Plasma nitrate/nitrite originates from endogenous nitric oxide production in fasting humans, decrease in superoxide scavenger activity (SSA), and free sulfhydryl groups (SH) reflects the amount of superoxide anion generated, and nitrotyrosine is believed to be formed by the interaction of tyrosine and peroxynitrite in vivo. The aim of the current study was to measure plasma nitrate/ nitrite, SSA, and SH in 69 patients (mean age +/- standard deviation, 66 +/- 11 years) with colorectal carcinoma. Nitrotyrosine was measured from both the plasma and tumor tissues in 32 patients. All patients had adenocarcinoma of the colon or rectum. Twenty-five patients were classified as stage B according to Dukes classification as modified by Astler-Coller, 13 were classified as stage C, and 31 patients were classified as stage D. To determine whether the changes are specific for colorectal cancer, 20 patients with active inflammatory bowel disease (IBD; mean age, 52 +/- 18 years) and 30 healthy volunteers, who served as control subjects (mean age, 48 +/- 11 years), were studied. Plasma nitrate/nitrite was measured by the modified Griess method, SSA was measured by an electron/spin resonance spin trapping method, free SH was measured by Ellman's method, and the presence of nitrotyrosine in the plasma and tumor tissue was detected by high performance liquid chromatography (HPLC) using C- 18-derivatized silica (5 microm) column (C18S, Crestpaque, New York, NY, USA) and at a wavelength of 274 nm. Patients with colorectal carcinoma and with active IBD had a significantly higher plasma nitrate/ nitrite level (51.2 +/- 26.2 microm and 56.0 +/- 14.6 microm versus. 29.6 +/- 6.3 microm; p < 0.01), and a lower SSA level (39 +/- 11.5 U/g protein and 52.0 +/- 18.9 U/g protein versus. 88 +/- 25.1 U/g protein; p < 0.05) and SH level (7.7 +/- 3.89 microm protein and 6.4
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PMID:Evidence of in vivo peroxynitrite formation in patients with colorectal carcinoma, higher plasma nitrate/nitrite levels, and lower protection against oxygen free radicals. 1063 9

The Authors report a case of sigmoid obstruction due to endometriosis and review the literature about. Unusual localisation and difficult preoperative differential diagnosis with IBD and bowel carcinoma are stressed. A 45-years old woman with previous history of oophorectomy was admitted at the hospital with symptomatic bowel obstruction. A barium enema showed a sigmoid stenosis thought to a carcinoma of bowel. A laparoscopic approach confirmed the diagnosis and a laparotomy was performed with a subsequent anterior resection (end-to-end anastomosis with stapler) plus myomectomy. The Authors do believed, during surgery, to be treating a carcinoma which disappeared with opening the specimen. The mucosa were intact and muscular layers so think to form a strong ring to be able to invaginate the upper colon for 3-4 cm. A stromal tumor was supposed and the definite diagnosis of endometriosis was very surprisingly. Intestinal resection to be necessary, with associated salpingo-oophorectomy and hysterectomy in older patients and treatment with oral contraceptive in younger female. Laparoscopy may be helpful in the diagnosis showing pelvic endometriosis with bowel wall involvement. Laparoscopic treatment in our opinion must be confirmed to particular situation and to well experience of surgeons.
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PMID:[Sigmoid occlusion due to endometriosis. A case report]. 1181 43

GI protein loss can result from a heterogeneous group of diseases, including lymphangiectasia, IBD, neoplasia, ulceration, intussusception, and histoplasmosis. PLE should be suspected in any hypoalbuminemic patient with no evidence of exudative protein loss, proteinuria, or HI. A minimum laboratory database for the suspected PLE patient should include a complete blood cell count, a biochemical and electrolyte profile, urinalysis (+/- urine protein:cretinine ratio), and pre- and postprandial bile acid determinations. Fecal alpha 1-PI concentrations may be used to confirm the presence of GI protein loss in cases with concurrent renal or hepatic disease. Because PLE is a syndrome and not a specific disease, the most effective therapy must be directed at the underlying cause. Multiple high-quality endoscopic biopsies are sufficient to diagnose most patients with PLE, although full-thickness biopsies are required in some cases. Patients with PLE are often clinically "fragile," and careful symptomatic therapy must be integrated with dietary and medical management strategies in most cases.
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PMID:Protein-losing enteropathies. 1455 61

Due to the development of more effective medications, those infected with HIV are living longer. Consequently, more tumors and infections have been added to the AIDS-defining criteria in the last decade. Our aim was to review the occurrence and clinical course of colorectal (CR) malignancies in HIV infected/AIDS patients from a single institution. A retrospective review of HIV/AIDS patients with colorectal malignant tumors was undertaken. We included adult patients, with ELISA and Western blot test positive for HIV, and primary malignant tumors located in the colon or rectum. Malignant neoplasms of the anus were excluded for the purposes of this study. Twelve patients (9 males and 3 females), mean age 41 years, were identified with the following neoplasm: 6 adenocarcinomas (ACA), 5 non-Hodgkin lymphomas (NHL), and 1 small-cell carcinoma. Intravenous drug abuse was the main risk factor for HIV. No patient had identified risk factors for colorectal neoplasm. Five out of six patients with ACA had metastatic disease at the time of diagnosis. One patient with stage II ACA developed early liver metastases after colonic resection. Seven out of 12 patients underwent surgery. Six (85.7%) of these sustained postoperative complications, primarily wound infection. The overall survival in our series was dismal, averaging 20 months. For NHL average survival was 29 months, and 12 months for CR-ACA. This is the largest series of cases of colorectal cancer in the HIV/AIDS patient population published in the English language and the largest number of colorectal ACA reported in this unique population. Early in our experience, tumors frequently found in immunoincompetent patients were detected (NHL). More recently, we have only treated patients with colorectal ACA; none of them had no risk factors for colorectal cancer (family history, IBD, FAP, HNPCC). These patients developed tumors at earlier ages and were diagnosed at an advanced stage. Therefore, these tumors may be associated with the grade of immunosuppression induced during the course of the HIV infection and with a tumorigenic effect of the HIV on the colonic epithelium. Consequently, a high index of suspicion when evaluating chronic abdominal complaints in such patients is warranted. The use of the new antiretroviral therapy regimens should be further evaluated to know its impact in the survival.
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PMID:Colorectal malignancies in HIV-positive patients. 1462 61

Guanylin, uroguanylin, and the bacterial heat-stable enterotoxin (ST) peptides comprise a new family of cyclic guanosine 3'-5' monophosphate (cGMP)-regulating agonists. The discovery of guanylin and uroguanylin peptides stems from studies of cellular mechanisms underlying a form of secretory diarrhea caused by enteric bacteria. Guanylin, uroguanylin, and microbial ST peptides activate a common apical membrane receptor-guanylate cyclase (R-GC) that elicits large increases in the intestinal secretion of chloride and bicarbonate via the intracellular second messenger, cGMP. Guanylin and uroguanylin were isolated from rat jejunum and opossum urine, respectively. These peptides are endogenous peptide hormones that physiologically regulate R-GC signaling proteins in target cells. Physiological roles for these peptides include the regulation of epithelial cell balance in the intestinal epithelium and modulation of sodium balance through actions in the kidney. The guanylin-uroguanylin-ST peptides are candidate therapeutic agents targeting receptors in the intestine, kidney, and other epithelia. For example, uroguanylin has anti-tumor actions in an animal model for human colon cancer. The ST peptides can be used as diagnostic agents to detect secondary colon cancers by single photon-emitting computed tomography (SPECT) imaging, thus localizing metastatic forms of colon cancer. Other examples of potential therapeutic applications for the guanylin family of cGMP-regulating agonists are: (1) the irritable bowel syndrome (IBS) with constipation, (2) salt-dependent forms of high blood pressure, (3) liver regeneration and repair, and (4) respiratory diseases such as asthma. Competitive pharmacological antagonists of bacterial ST peptides offer a means for treating the diarrhea caused by ST-secreting strains of enteric bacteria.
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PMID:Uroguanylin and guanylin peptides: pharmacology and experimental therapeutics. 1551 84

There remain technical challenges to the accurate prediction and diagnosis of neoplasia in IBD; therefore, prevention strategies are based on limited evidence and instead, consensus opinions and guidelines. Existing guidelines and published expert opinions are in agreement that given the increased risk of cancer in IBD and well-described associated risks, prevention strategies are warranted. The preponderance of existing prevention is focused on secondary prevention by performance of screening and surveillance colonoscopies with random biopsies to identify neoplasia and trigger surgical resection for prevention of invasive cancer and death. Substantial technical and practical challenges remain, however, and there is a great need for improved understanding of the compounded risks of neoplasia, the natural history of dysplasia, and more accurate detection and diagnostic techniques. A future approach to prevention is likely to stratify patients based on individualized risks that include, among things, the histologic degree of inflammation present. In meantime, existing guidelines should be emphasized and ongoing education of clinicians and patients must occur.
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PMID:Surveillance for cancer and dysplasia in inflammatory bowel disease. 1695 42


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