Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009319 (colitis)
 19,384 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Collagenous colitis is characterized by watery diarrhea and inflammatory infiltration associated with a subepithelial collagen deposit on colonic biopsies despite a normal or subnormal endoscopic appearance. We here describe 5 patients treated with the locally active steroid budesonide. Complete and partial response was observed in 3 and 2 patients, respectively. Budesonide thus seems to be of therapeutic benefit in collagenous colitis. Prospective randomized long-term studies are needed to support this hypothesis.
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PMID:Budesonide in the treatment of collagenous colitis. 969 9

Glucocorticosteroids (GCS) are effective in treatment of inflammatory bowel disease (IBD), but also have unwanted systemic side effects. Here, we describe the effects of budesonide and dexamethasone on acute experimental colitis and on T cells in thymus and spleen, as well as the effect of budesonide treatment on relapsing colitis. Acute colitis was induced by intracolonic administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) in ethanol, and a relapse was induced by an intraperitoneal booster of TNBS. GCS were administered intrarectally on days 1, 4, and 6 after induction of acute colitis or a relapse. Inflammatory cells in the colon were studied on day 7, and in acute colitis also on days 13 and 16. Budesonide treatment in acute and relapsing colitis resulted in reduction of macroscopic damage and decreased the numbers of macrophages and neutrophils in the colon. Dexamethasone was less effective. Dexamethasone, but not budesonide, reduced the number of T cells in the thymus. It is concluded that local budesonide is more effective in treatment of acute experimental colitis than dexamethasone and, in contrast to dexamethasone, did not cause a general suppression of T cells. Although budesonide was very effective in the treatment of relapsing colitis, this effect was not accomplished by affecting the number of T cells in the colon.
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PMID:Effects of local budesonide treatment on the cell-mediated immune response in acute and relapsing colitis in rats. 982 45

Collagenous colitis is a rare cause of chronic watery diarrhea. No effective standard treatment has yet been established. Based upon anecdotal reports some anti-inflammatory and symptomatic drugs seem to have some therapeutic efficacy. Prednisone is widely believed to be the most effective treatment. Here we describe three female patients with histologically confirmed collagenous colitis refractory to therapy with prednisone. Each had received prednisone with a high starting bolus and lower dose maintenance therapy for their disease. However, definite clinical remission could not be achieved. After the administration of 3 x 3 mg/day controlled ileal release (CIR) capsules of budesonide the symptoms resolved immediately. The mean follow-up after beginning budesonide was 11 months (range 7-18). Two patients are still on budesonide. One had had a quick relapse of diarrhea after stopping her treatment. Budesonide therapy was therefore resumed. She has remained symptom-free on a lower daily dose of 2 x 3 mg/day budesonide. One patient has been in remission for more than 1 year after a 3-month course of budesonide. Budesonide is a topically acting steroid with rapid absorption, high receptor affinity, and low systemic bioavailability, thus causing almost no side effects. As yet only few case reports have been published on the use of budesonide for collagenous colitis. We present here the first three cases of prednisone refractory collagenous colitis successfully treated with budesonide.
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PMID:Therapy of prednisone-refractory collagenous colitis with budesonide. 1020 32

Budesonide is a locally acting steroid with a high first-pass metabolism in the liver and low systemic effects. We performed the first pilot study comparing budesonide foam (1 mg/50 ml b.i.d.) with mesalazine enemas (4 g/60 ml o.d.). 33 patients from 3 centres were enrolled in this open randomized clinical trial. 16 patients got budesonide foam and 17 got mesalazine enemas. The drugs were administered for 4 weeks. Histological index (HI) and endoscopic index (EI) were assessed at day 1 and day 28, clinical activity index (CAI) at day 1, 14 and 28. For patients with left-sided colitis and proctosigmoiditis improvement was defined as decrease in CAI of > or = 2 points. For patients with proctitis improvement was defined as decrease in HI of > or = 1 point. The primary efficacy evaluation was performed with the intention to treat population (n = 32). Improvement was found in 67% of the patients in the budesonide group compared to 71% in the mesalazine group. There was no statistically significant difference between the groups. Adverse events were mild and rare in both groups. Both treatments had no significant influence on plasma cortisol. In this pilot study for distal ulcerative colitis budesonide foam is as safe and effective as mesalazine enema.
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PMID:[Budesonide foam as a new therapeutic principle in distal ulcerative colitis in comparison with mesalazine enema. An open, controlled, randomized and prospective multicenter pilot study]. 1082 Aug 60

Budesonide (BDS) is a potent corticosteroid that has important implications in the pharmacotherapy of inflammatory bowel disease, especially in the treatment of ulcerative colitis and Crohn's disease. BDS is available on the market in the form of enteric-coated preparations. However these products, similar to other available site-specific dosage forms, are not sufficiently selective to treat colonic inflammatory bowel disease. The objective of this study was to evaluate the efficacy of a new microparticulate system containing BDS, to treat experimentally induced colitis in rats. This microparticulate system consisted of BDS-containing hydrophobic cores, microencapsulated within an enteric polymer, which solubilizes at above pH 7, thus combining pH-sensitive and controlled-release properties. Colonic injury and inflammation were assessed by measuring colon/bodyweight ratio, myeloperoxidase (MPO) activity, and by scoring macroscopic and histological damage in colitic rats. Rats were treated orally with BDS, included in the developed system, once a day for 4 days after the induction of inflammation. A BDS suspension and BDS-containing enteric microparticles were included as control formulations in the experimental design. The administration of the new BDS delivery system significantly reduced the colon/bodyweight ratio compared with the administration of control formulations. Similarly, MPO activity and macroscopic and histological damage of the inflamed colonic segments decreased significantly when the BDS formulation was administered, compared with the results obtained after oral administration of the drug suspension. There were no significant differences, however, when the new treatment was compared with the control formulation consisting of simple enteric microparticles.
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PMID:Colon-specific delivery of budesonide from microencapsulated cellulosic cores: evaluation of the efficacy against colonic inflammation in rats. 1157 3

Budesonide modified-release capsule is an effective form of therapy for the treatment of Crohn's disease located in the distal ileum, ileocecal region, and ascending colon. Because some of the benefit of budesonide therapy results from local effects, this agent will not be very effective in the treatment of patients with extensive colitis or left-side colitis. Budesonide is equal to less effective than prednisolone or prednisone therapy in the treatment of active Crohn's disease, but is associated with fewer glucocorticoids adverse reactions.
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PMID:Budesonide modified-release capsules. 1212 Jan 82

Budesonide, a topical corticosteroid, has proven useful for the management of Crohn's disease. Its efficacy is similar to prednisone but it has fewer side effects. A new pH-modified release capsule (Budenofalk) is probably efficacious in distal ulcerative colitis. The aim of the present study was to establish the pharmacokinetics, pharmacodynamics, and safety of two dosage regimens of budesonide capsules and to obtain efficacy information. Budenofalk 9 mg daily was administered as a single dose 9 mg in 8 patients and as three 3 mg doses in 7 patients with active distal ulcerative colitis for 8 weeks. Symptoms were assessed at three timepoints during the study: baseline, 4 and 8 weeks after start of treatment. Endoscopic evaluation and budesonide concentration in mucosal biopsy specimens was performed at 0 and 8 weeks. A pharmacokinetic profile and pharmacodynamic profile (cortisol, lymphocytes and neutrophils) was performed at day 5. In the 9 mg o.d. group, higher peak concentrations and systemic availability was found compared to the 3 mg t.i.d. group. Cortisol suppression was more pronounced after 9 mg o.d. than after 3 mg t.i.d. Lag-time, AUC and pharmacodynamic effects were comparable (14% mean decrease lymphocyte count and 26% mean increase neutrophil count). Mucosal biopsy specimens in the distal colon revealed significant budesonide levels with both regimens. After 8 weeks, 71% in the 9 mg o.d. group and 38% in the 3 t.i.d. group responded. The endoscopic index improved from 10 +/- 2 to 2 +/- 3 (p <0.001) with 9 mg o.d. and from 9 +/- 2 to 4 +/- 4.7 (p = 0.02) with 3 mg t.i.d. The pharmacokinetic and pharmacodynamic profiles found in this study indicate that Budenofalk reaches the distal part of colon and rectum, but further studies to validate the budesonide assay in the mucosa and comparison with a control group are necessary. This limited study suggests that Budenofalk is effective in distal colitis and side effects are rare. Based on these observations a large clinical trial using 9 mg o.d. is indicated to confirm efficacy and assess further possible side effects.
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PMID:Evaluation of oral budesonide in the treatment of active distal ulcerative colitis. 1551 Feb 33

Microscopic colitis, encompassing collagenous and lymphocytic colitis, is a fairly common cause of chronic watery diarrhoea, especially in elderly women. In recent epidemiological studies the annual incidence of each disorder was 4-6/100.000 inhabitants. The aetiology is unknown. The main clinical symptoms are watery diarrhoea, weight loss and abdominal pain. Laboratory analyses are nondiagnostic, and the diagnoses rely on histopathological examination of colonic mucosal biopsies. There is an association to autoimmune diseases such as thyroid disorders, diabetes mellitus, celiac disease and arthritis. Budesonide is the best-documented treatment of collagenous colitis. It is superior to placebo in short-term therapy, but the long-term efficacy is not well studied. The evidence for other therapeutic alternatives such as loperamide, cholestyramine, bismuth subsalicylate, or 5-aminosalicylates is weak. In unresponsive severe disease azathioprine or methotrexate may be tried. There are at present no controlled data on the treatment of lymphocytic colitis. The long-term prognosis of microscopic colitis is good, serious complications are rare and there is no increased mortality.
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PMID:[Microscopic colitis--more common cause of diarrhea than believed. Biopsies are the only way to diagnosis, drug treatment is effective]. 1614 78

The ideal chemopreventative agent, in addition to being efficacious in the prevention of cancer, must be easily administered, affordable, safe, and well tolerated, with minimal side effects. In the past decade, a growing body of literature has emerged on the prevention of CRC in patients with long-standing CD and UC. The data are not definitive and consist almost exclusively of retrospective case-control and cohort studies rather than the more rigorous prospective RCTs. 5-ASA compounds have been most thoroughly studied, and most of the existing data support the use of 5-ASA in the prevention of CRC. Although the precise dose and duration are unclear, studies suggest that chronic systemic administration of 5-ASA at a dose of at least 1.2 g/d is most likely to be effective. A beneficial effect of folate, albeit not statistically significant, has been consistently shown in every study performed for this purpose. Folate supplementation, which is safe and affordable, should also be recommended for all patients with IBD, especially those taking sulfasalazine. UDCA has been shown to exert a protective effect in most studies on patients with UC and concomitant PSC. Because this patient population is at particularly high risk for CRC, it is advisable to consider UDCA in all patients with colitis complicated by PSC. For patients without PSC, sufficient data do not exist to recommend it for the purpose of cancer prevention. Five of the six corticosteroid studies have found a beneficial effect of systemic steroids, although most did not reach statistical significance. Regardless, given the frequent and serious adverse effects associated with chronic steroid use, systemic corticosteroids should not be prescribed for this indication. Budesonide, an oral corticosteroid with minimal systemic absorption, is a potential alternative, although it has not yet been studied as a chemopreventative agent. Similarly, until the long-term safety of chronic NSAID use can be demonstrated in patients with IBD, the role of NSAIDs in chemoprevention remains undefined. Although the data are conflicting, immune-modulating medications, such as AZA, do not seem to confer any reduction in the risk of dysplasia or CRC. The data on calcium supplementation and statin use are still too limited to endorse their use for the prevention of colitis-related CRC. Chemoprevention is an area that holds great promise in the reduction of morbidity and mortality associated with IBD. Further studies, including prospective trials when possible and cost-effectiveness analyses, need to be performed to develop an optimal strategy for the reduction of cancer risk in patients with IBD.
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PMID:Chemoprevention: risk reduction with medical therapy of inflammatory bowel disease. 1695 46

As the diagnosis of microscopic colitis (MC) is made on the basis of histologic criteria, it is crucial to render an accurate microscopic interpretation. Features include 20 or more lymphocytes per 100 epithelial cells, mixed lamina propria inflammatory infiltrate, and preservation of crypt architecture for both lymphocytic and collagenous colitis (CC). CC is further characterized by a collagen band at least 10 mum thick. Although the pathogenesis of MC is poorly understood, medication-induced toxicity to the colonic mucosa is important to recognize, as medication cessation leads to prompt improvement. If MC is mild, symptomatic treatment is all that is needed, because some cases are self-limiting. Budesonide, 9 mg daily for at least 8 weeks, is the best documented treatment of choice for more severe or protracted cases. A 75% response rate has been reported; however, when treatment is discontinued, relapse is common, and longer-term tapering dose therapy often is necessary. There are disadvantages and no advantage to other forms of steroid therapy. Cholestyramine, bismuth, and 5-aminosalicylate derivatives appear to be less efficacious but are reasonable therapeutic options for less severe cases. Use of immunosuppressant therapy such as azathioprine or 6-mercaptopurine should be highly restricted because MC is a benign condition that does not result in other complications. Probiotic therapy with Lactobacillus acidophilus and Bifidobacterium animalis has not been shown to be effective in reducing bowel frequency. Surgical diversion of the fecal stream can control diarrhea and improve histology but is very rarely indicated and should be reserved for highly selected cases of severely symptomatic steroid-refractory MC.
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PMID:Microscopic colitis. 1754 61


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