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Query: UMLS:C0009319 (colitis)
 19,384 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Enhanced local production of reactive oxygen metabolites has been found in association with colitis, both experimentally and in humans. Cellular and biochemical systems involved have been identified, and 5-aminosalicylic acid-containing drugs but, more effectively, specific scavengers have been found to reduce the intestinal inflammatory process. The multitude of reactions in which oxygen metabolites participate provides a new area of research in intestinal inflammation. These basic studies might bring related clinical studies in an era of new anti-inflammatory drugs for inflammatory bowel disease specifically designed to scavenge toxic oxygen metabolites.
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PMID:Reactive oxygen metabolites and colitis: a disturbed balance between damage and protection. A selective review. 166 60

Cytomegalovirus infections in immunocompromised patients may cause serious illness, particularly in patients with HIV-disease and in transplant recipients. There is an increasing number of reports of cytomegalovirus infections involving the alimentary tract, especially colitis. Diagnosis of cytomegalovirus disease is at present based on specific histological findings. Antibody findings can be difficult to interpret. The slow growth of cytomegalovirus in cultures makes this method less useful in the acute setting of diagnosis. It is important to recognize cytomegalovirus colitis as a differential diagnosis to idiopathic inflammatory bowel disease. In fulminant disease, colectomy should be considered in addition to antiviral treatment.
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PMID:[Cytomegalovirus disease in the gastrointestinal tract]. 166 55

Spontaneous colitis in CTT's presents cytological characteristics similar to chronic ulcerative colitis in humans, e.g. inflammatory cell infiltrate and crypt abscesses. To better characterize CTT colitis as a potential model for human inflammatory bowel disease (IBD), inflammatory mediators identified in colonic tissue of human IBD patients and/or experimental colitis models were assayed. Inflammatory mediator changes in plasma and colon from tamarins with acute (n = 10) and chronic (n = 10) colitis (by mucosal biopsy) were assayed by RIAs. Similar inflammatory mediators were found in the CTT's with acute colitis. In the plasma, PAF and PGE2 levels were lower in acute colitis CTT's, no LTB4 was detected, and histamine levels were not different from chronic colitic animals. In the colon, myeloperoxidase and interleukin-1 beta were significantly higher in acute colitis, PGE2 and LTB4 were higher but not significantly, and PAF was not different from chronic CTT's. These data suggest that a combination of events are occurring in the pathogenesis of tamarin colitis that involves some of the same mediators that are found in the human disease and in other experimental models. The importance of these findings to human IBD remains for further investigation; however, the spontaneous primate model offers an exciting approximation of the disease development and merits further investigation for understanding the pathogenesis of human IBD as well as to aid in development of targeted therapeutics.
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PMID:Inflammatory mediators in cotton-top tamarins (CTT) with acute and chronic colitis. 166 91

Oxygen radicals particularly superoxide and hydroxyl radicals are very reactive species believed to be involved in cell and tissue damage in a variety of diseases including inflammatory bowel disease (IBD). Today there are four major arguments for such a role in IBD: Infiltration of the inflamed intestinal mucosa with myeloperoxidase containing activated neutrophils able to produce superoxide, hydroxyl and hypochlorite, increased chemoluminescence response of peripheral and mucosal phagocytic cells to various stimuli, decreased inflammation following specific scavenger treatment in animal models of colitis and defined radical scavenger and inhibitory properties of drugs, especially aminosalicylates used in the therapy of IBD. In the absence of a specific therapy, radical scavenging and/or inhibition may be an adjunctive modality in IBD.
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PMID:Clinical relevance of oxygen radicals in inflammatory bowel disease--facts and fashion. 166 82

A model of experimentally induced inflammatory bowel disease (IBD) featuring colitis, originally devised by Onderdonk and co-workers in guinea pigs, was modified to establish the optimal conditions for ulcer development. Upon varying the time of subcutaneous immunization with Bacteroides vulgatus and concomitant oral administration of acid-degraded iota-carrageenan and viable B. vulgatus, it was found that the optimal times of administering these agents were one to two weeks and five to six days, respectively. Light microscopy of the colon and cecum of the guinea pigs given the optimized treatment for ulcer induction revealed pronounced edema, inflammation, and lesions of the mucosa. Transmission electron microscopy of the mucosa from these animals showed the presence of large numbers of leukocytes in the subepithelial region, the majority being polymorphonuclear neutrophils which possessed large electron-dense granules or rods. Oral administration of 300 mg/kg/day sulfasalazine (salicylazosulfapyridine) for 14 days to guinea pigs given the optimized treatment for ulcer induction failed to reduce the numbers of ulcers or the histopathology gradings and fine structural changes of the mucosal inflammatory changes, but did reduce the symptoms of diarrhea.
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PMID:Inflammatory bowel disease induced by combined bacterial immunization and oral carrageenan in guinea pigs. Model development, histopathology, and effects of sulfasalazine. 167 17

Although the aetiology of inflammatory bowel disease remains elusive, many agents are available for the control of symptoms and inflammation. Knowledge of drug pharmacology, indications and side effects is essential to ensure the best possible clinical care while minimising toxicity and inappropriate use. Sulfasalazine consists of sulfapyridine linked to mesalazine (5-aminosalicylic acid) via an azobond. Its use is indicated in the treatment of mild to moderately active ulcerative colitis and in the prevention of relapse in patients with quiescent disease. Patients with mild to moderate colonic or ileocolonic Crohn's disease also benefit from this drug, as do a proportion of patients with isolated small bowel disease. Sulfasalazine has not been uniformly effective in preventing relapse in Crohn's disease, although many clinicians continue its use in patients who respond initially. A high incidence of side effects which limit therapy include intolerance, hypersensitivity reactions and impairment of male infertility. The newer aminosalicylates offer targeted delivery of mesalazine to the bowel, with fewer side effects. Topical mesalazine has proved extremely effective in patients with distal ulcerative colitis; oral forms are effective in the treatment of mild to moderately active ulcerative colitis and in relapse. Both types appear to be effective in the treatment of Crohn's disease, and possibly in preventing relapse. There is no current clinical advantage of one mesalazine preparation over another, nor is there an indication for their use in sulfasalazine-treated patients who have satisfactory response without adverse effects. Corticosteroids are indicated for more severe disease activity where the aminosalicylates have limited efficacy-specifically to induce remission in patients with severe or refractory ulcerative colitis or Crohn's disease. They should not be used to maintain disease remission or in the prevention of postoperative recurrence. Topical corticosteroids allow their local use in distal colitis with minimal systemic side effects. Long term use is limited by side effects, many of which are dose related, although alternate-day therapy may lessen the incidence. Immunosuppressive agents are beneficial for the treatment of refractory inflammatory bowel disease unresponsive to other medications, and may also facilitate the withdrawal of steroids in refractory patients. Mercaptopurine has an added benefit in the treatment of Crohn's disease fistulae; the role of cyclosporin in bowel disease has not been established and its use cannot currently be recommended. The potential toxicity of immunosuppressive agents warrants careful consideration of their use by both physician and patient. Metronidazole is indicated for the treatment of mild to moderate Crohn's disease, including perineal disease. Common side effects include peripheral neuropathy and nausea.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Risk-benefit assessment of drugs used in the treatment of inflammatory bowel disease. 167 90

Morphological evidence of activation in vivo of circulating neutrophils in patients with inflammatory bowel disease (IBD) was sought by quantitative light microscope examination of toluidine blue-stained preparations made from peripheral venous bloods that had been fixed immediately ex vivo. The proportion of spherical (unactivated) circulating neutrophils was reduced in active Crohn's disease (73%; 46-96 (median; range), n = 11) compared with inactive Crohn's (90%; 45-99; n = 18, P less than 0.01) and normal subjects (94%; 44-98; n = 13, P less than 0.05). There tended to be fewer spherical neutrophils in active ulcerative colitis (77%; 13-96; n = 17) than in quiescent colitis (88%; 57-99, n = 13, P less than 0.1) or normal subjects (P less than 0.05). Activated neutrophils occur in the circulating pool of patients with active IBD and can be detected by light microscopy of peripheral venous blood leucocyte preparations.
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PMID:Peripheral blood neutrophils in inflammatory bowel disease: morphological evidence of in vivo activation in active disease. 168 41

Olsalazine (sodium azodisalicylate; azodisal sodium) is an anti-inflammatory agent designed to deliver its active moiety, mesalazine (5-aminosalicylic acid; mesalamine), to the colon while avoiding the adverse effects associated with the use of a sulfapyridine carrier. As a prodrug, olsalazine is an effective oral treatment for both active ulcerative colitis and for maintenance of disease remission and may possibly be of benefit in patients with Crohn's colitis. Findings from both short and long term noncomparative and comparative studies demonstrate that olsalazine 1 to 3g daily in divided doses improves clinical signs and symptoms of colitis in approximately 60 to 80% of patients with acute ulcerative colitis of mild to moderate severity. This improvement rate was similar to that obtained with sulfasalazine. Lower doses of olsalazine, usually 1g daily in divided doses, also maintained remission in patients with chronic ulcerative colitis. While olsalazine effectively delivers mesalazine to the colon, the prodrug itself increases net luminal water secretion and accelerates gastrointestinal transit of a meal. The resulting diarrhoea (occurring in approximately 17% of patients and resulting in withdrawal from therapy in 6% of patients) is distinguishable from that associated with inflammatory bowel disease by the high water content and the absence of blood. Olsalazine-induced diarrhoea usually occurred soon after initiation of olsalazine therapy or dosage increase, was more frequent with higher doses and was usually transient. Dosage reduction, increases in frequency of dosing and concomitant administration with food reduced the severity in many patients with persistent olsalazine-induced diarrhoea. With the exception of diarrhoea, olsalazine was generally well tolerated. Fewer than 14% of patients allergic to or intolerant of sulfasalazine had similar reactions to olsalazine. Olsalazine appears to be a suitable therapy for the treatment of first attacks as well as acute exacerbation of mild to moderate acute ulcerative colitis, and for the maintenance of remission in patients with chronic ulcerative colitis.
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PMID:Olsalazine. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in inflammatory bowel disease. 171 64

To determine whether intravenous immunoglobulin produces demonstrable clinical improvement in patients with refractory idiopathic inflammatory bowel disease, a pilot, open-label, nonrandomized, safety and therapeutic efficacy study was carried out at a tertiary care referral medical center. Twelve consecutive patients with refractory idiopathic colitis (nine ulcerative colitis, three Crohn's colitis) who were reluctant to receive immunosuppressive therapy or have surgical intervention were referred by physicians not participating as investigators in this study. Eleven patients were symptomatic for at least 6 months, with endoscopically moderate or severe mucosal inflammation despite medical therapy, including systemic corticosteroids in all cases, and one patient was dependent on oral prednisone to remain in clinical remission. Ten patients had extensive colitis, six of whom had pancolitis and four of whom had colitis extending to the hepatic flexure or transverse colon. Nine patients required hospitalization for treatment of colitis. Intravenous immunoglobulin was administered in one or two induction phases (2 g/kg over 2 or 5 days), followed by a maintenance phase (200-500 mg/kg every 2 wk for 12 or 24 wk). Tapering of systemic corticosteroid therapy was attempted, whereas other medications for idiopathic colitis were continued. Treatment response was assessed clinically and by colonoscopy with multiple biopsies whenever possible. Immunoglobulin therapy was well-tolerated and did not produce any biochemical abnormalities. In six patients who completed the treatment protocol, mean reductions +/- SE were achieved in subjective symptoms as quantified by a colitis activity score, 13.3 +/- 1.2 to 4.7 +/- 0.9 (p less than 0.001), and daily mg dose of prednisone, 41.7 +/- 8.0 to 1.9 +/- 1.2 (p less than 0.001). For all 12 patients, statistically significant reductions were achieved in the colitis activity score and daily prednisone dose. Of five patients who completed the treatment protocol and improved clinically, four underwent post-treatment colonoscopic and biopsy evaluations and had unequivocal reductions in the intensity of colonic mucosal inflammation. Three patients who had objective improvement with intravenous immunoglobulin experienced relapses of colitis after discontinuation of this therapy. Six patients did not complete the treatment protocol, two of whom required surgical intervention and four of whom withdrew to undergo colectomy electively. Intravenous immunoglobulin may be beneficial in subsets of patients with idiopathic colitis. The results of our pilot study justify the undertaking of a prospective, randomized controlled trial to determine the efficacy of intravenous immunoglobulin in carefully defined subsets of patients with idiopathic inflammatory bowel disease.
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PMID:Intravenous immunoglobulin therapy for active, extensive, and medically refractory idiopathic ulcerative or Crohn's colitis. 172 32

Nine patients with lymphoma occurring in association with inflammatory bowel disease were admitted to The Mount Sinai Hospital between 1960 and 1983. Five (two men and three women) occurred among 1156 patients (0.43%) with ulcerative colitis (UC) and four (men), among 1480 patients (0.27%) with Crohn's disease (CD), a strong male preponderance in the latter group. In all four of the patients with CD and in four of the five patients with UC, the lymphomas were extraintestinal. The mean age of onset of UC in these patients was late (46 years, 19 years older than in our overall series), with lymphomas occurring a mean of only 12 years later. By contrast, patients with CD had bowel disease much younger (mean age, 26 years), and their lymphomas appeared after a longer disease duration (mean, 24 years). The risk factors for the one patient with colonic lymphoma were similar to those with colitis-associated colorectal carcinoma: extensive and long-standing colitis and relatively young age when malignant disease developed. Four of the patients with lymphoma had associated colonic carcinoma; in three of them, the carcinoma appeared within the first decade of colitis, an unusual occurrence. A second malignant lesion also occurred in three patients with UC.
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PMID:Lymphoma in inflammatory bowel disease. 173 11


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