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An institutional review board-approved retrospective review of the charts of consecutive patients with UC treated with calcineurin inhibitors before undergoing IPAA surgery at a tertiary pediatric center between 1998 and 2003 was performed. The primary endpoint was pouch outcome after at least 2 years of follow-up (healthy pouch, acute pouchitis, chronic refractory pouchitis, or pouch failure); the secondary endpoints were early postoperative complications, number of stages, and time between stages.
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To compare the efficacy of oral mesalazine vs. combined oral and topical mesalazine in mildly to moderately active ulcerative colitis.
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5-Aminosalicylic acid and its metabolite, N-ac-5-ASA, were measured in the plasma, urine, and ileostomy effluent of 24 ileostomates who ingested 750 mg Rowasa I following an overnight fast. Twelve subjects previously had a small-bowel resection or had part of their small bowel out of circuit (mean 95 cm) (Group I) while 12 had an intact small bowel (Group II). The mean peak plasma concentration of N-ac-5-ASA was 1.11 micrograms/ml in Group 1 subjects compared with 2.80 micrograms/ml in Group II subjects (P = N.S.). On average, 53.0 percent of the ingested Rowasa I was detected in the 24-hr ileostomy effluent of Group I subjects compared with 45.3 percent in the Group II subjects (P = N.S.). The mean recovery of 5-ASA and N-ac-5-ASA in urine was 8.5 percent in Group I and 35.6 percent in Group II subjects (P less than 0.001). These studies demonstrate that 5-ASA is released and present in the small bowel following oral ingestion of Rowasa I in patients who have or have not had small bowel resections.
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Final analysis included 117 patients (58 taking 5-ASA and 59 taking placebo; follow-up 9.2 +/- 6.5 months). Cumulative relapse rates at 6 and 12 months were 34% and 58% in 5-ASA patients and 31% and 52% in placebo patients, respectively (rate difference +0.095; 95% CI = -0.085 to +0.274). Subgroups analysis showed that 5-ASA was equally ineffective in patients with ileal, colonic or ileocolonic disease.
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The endoscopic remission rates after 4 weeks in the mesalazine and placebo suppository groups were 81.5% and 29.7%, respectively, and the superiority of mesalazine to placebo was confirmed (P < 0.0001, chi-squared test). For proctitis, the endoscopic remission rates after 4 weeks were 83.8% and 36.1% in the mesalazine and placebo suppository groups, respectively, and the corresponding rates for all other types of UC were 78.6% and 21.4%, respectively. The superiority of mesalazine to placebo was confirmed in both subgroups (P < 0.0001, Fisher's exact test). The percentage of patients without bleeding was significantly higher in the mesalazine group than the placebo group from Day 3 of treatment (P = 0.0001, Fisher's exact test).
Extraintestinal manifestations of inflammatory bowel disease (IBD) is a common clinical problem affecting up to half of all IBD patients; pulmonary disease, however, ranks among less common extraintestinal manifestations of IBD. Pulmonary disease in patients with IBD is most frequently drug induced due to treatment with sulfasalazine or mesalamine leading to eosinophilic pneumonia and fibrosing alveolitis or due to treatment with methotrexate leading to pneumonitis. Recently, various opportunistic infections have been shown to be a further important cause of pulmonary abnormalities in those IBD patients who are treated with immunosuppressants such as anti TNF-α monoclonal antibodies, methotrexate, azathioprine or calcineurin antagonists. In not drug related pulmonary disease a wide spectrum of disease entities ranging from small and large airway dysfunction to obstructive and interstitial lung disorders exist. Patients with lung disorders and inflammatory bowel disease should be evaluated for drug-induced lung disease and opportunistic infections prior to considering pulmonary disease as an extraintestinal manifestation of inflammatory bowel disease.
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Future research should consider managing depression as an essential component of comprehensive care for patients with Crohn's disease. In addition, further research is needed to develop strategies to better improve quality of life among patients with Crohn's disease who are depressed.
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Dysregulation of immune responses to intestinal exogenous antigens contributes to the pathogenesis of inflammatory bowel disease, but the specific antigen responsible for the pathogenesis of inflammatory bowel disease is unknown. We measured serum antibody titers against Caenorhabditis elegans antigens. Immunoglobulin G (IgG) and IgG subclass anti-C. elegans antibodies in serum samples from 29 patients with ulcerative colitis, 30 patients with Crohn's disease, 7 patients with intestinal Behçet's disease, and 11 healthy controls were measured by enzyme-linked immunosorbent assay. Serum IgG and IgG2 antibody titers against C. elegans were significantly higher in patients with inflammatory bowel disease than in controls. Antibody levels were not affected by age, gender, disease activity, extent of disease, or small bowel involvement. The anti-C. elegans antibody titer was significantly lower in patients with Crohn's disease taking mesalazine or sulfasalazine than in patients not taking these drugs. The increased immune responses to C. elegans found in patients with inflammatory bowel disease reflect dysregulated immune responses to enteric antigens, which might play a role in the pathogenesis of inflammatory bowel disease.
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Inflammatory Bowel Disease Questionnaire (IBDQ) data were combined from two double-blind, randomized, multicentre, active-controlled trials assessing 2.4 and 4.8 g/day oral delayed-release mesalazine in 687 patients. Mean score changes from baseline were compared at 3 and 6 weeks and effects of baseline severity, mesalazine dose and response to therapy were examined.
The medical records of 54 patients with gastroduodenal Crohn disease treated between 1958 and 1997 were reviewed.
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Gastroduodenal Crohn disease is a complex and difficult problem that is associated with serious complications and need for reoperation.
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The aim of this prospective research was to compare, in a seven-year follow-up, the clinical outcome of ulcerative pancolitis with that of non-progressive ulcerative colitis. The activity of the disease was evaluated by a Clinical Activity Index and an Endoscopic Index. Of 112 cases of ulcerative colitis observed, 95 showed no change in extent and were studied as examples of non-progressive UC, and in this group the extension of the disease was: pancolitis in 19%, left-sided colitis in 39%, proctosigmoiditis in 17% and proctitis in 25%. A colectomy had to be performed in 5%. None of the enrolled cases developed a cancer during the follow-up. The patients with ulcerative pancolitis or left-sided colitis were treated with 5-ASA 1.6 g/day in a delayed-release formulation, while the cases with proctosigmoiditis or proctitis were treated with 5-ASA enemas 4 g/day. The cases with more than one relapse/year were 39%. The proportion of patients with only one relapse/year was 53%. The patients with steady remission for all the seven years of the trial were only 8%, but with a statistically significant difference between the groups with initial diagnosis of proctosigmoiditis or proctitis and the group with initial diagnosis of pancolitis or left-sided colitis (12% versus 5%). Among the cases with continuous remission, 37% showed colonic alterations, with an endoscopic score higher than 4 but a clinical score less than 6. Side-effects were observed in 6% patients but without treatment withdrawal. Non-progressive ulcerative colitis throughout the colon has a relatively good prognosis which seems to be independent of the location of the disease, even if we have found a statistically significant higher percentage of cases with steady remission among the patients with more distal disease.
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To evaluate the histologic manifestations of collagenous colitis and correlate histologic changes with disease behavior, 14 patients who had undergone sequential evaluations during 33 +/- 6 months of follow-up were studied. Two hundred twelve tissue specimens from all anatomic regions of the colon (mean, 15 +/- 3 samples per patient) were interpretated independently under code by two pathologists. Eight patients (57%) had histologic resolution after 14 +/- 4 months of empiric therapy and in only one of these (12%) did symptoms persist. Four patients (29%) had sequential histologic examinations from the same anatomic region that varied from classical collagenous colitis to inflamed mucosa without a thickened collagen band to normal mucosa. Eight patients (57%) had varying histologic findings from different anatomic regions during the same examination that ranged from classical collagenous colitis to increased inflammation with resolution of the collagen band to normal mucosa. Normal mucosa was found mainly in specimens from the rectosigmoid, and proctosigmoidoscopic examinations alone would have missed the diagnosis of collagenous colitis in 40% of cases. Pathologic interpretations were concordant in 171 of 212 instances (81%). We conclude that histologic resolution of collagenous colitis can occur and it is associated with loss of symptoms. The histologic features of collagenous colitis are distinctive, but they may be patchy and inconsistently sampled. Rectosigmoid biopsies underestimate the diagnosis.
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Only one of four agents tested, namely, 1-glutamine enemas, could decrease the severity of colitis both morphologically and biochemically. Moreover, L-glutamine prevented the colitis-induced oxidant injury in the colonic mucosa. On the other hand, prednisolone and short chain fatty acids seemed to improve only the physiologic changes of colitis.
Budesonide may be an effective therapy for mild-to-moderately active ulcerative colitis (UC). This study aimed to demonstrate non-inferiority for oral 9mg budesonide once daily (OD) versus 3g mesalazine granules OD.
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We searched MEDLINE, the Cochrane Library, and EMBASE. The primary endpoints, and clinical and endoscopic recurrence, were analysed using the Mantel-Haenszel and DerSimonian and Laird methods.
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5-Aminosalicylates are the standard treatment for induction and maintenance of remission in mild-to-moderate ulcerative colitis. In recent years, the 5-aminosalicylic acid-containing pro-drug balsalazide has been the focus of attention.
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Ulcerative colitis (UC) is associated with an increased risk for colorectal cancer (CRC) and possibly also increased risk for cancers outside the intestinal tract. We followed-up a population-based cohort of 1160 patients with UC diagnosed in Copenhagen County between 1962 and 1987 for up to 36 years to analyze the overall and site-specific cancer risk.
Patients with inflammatory bowel disease (IBD) are a high risk population for bacteremia. Derangement in the mucosal architecture of the gastrointestinal (GI) tract and frequent endoscopic interventions in immunocompromised individuals are considered primary causes. Isolation of opportunistic microorganisms from the bloodstream of IBD patients has been increasingly reported in recent years. Leclercia adecarboxylata is a ubiquitous, aerobic, motile, gram-negative bacillus. The human GI tract is known to harbor this rarely pathogenic microorganism. There are only a few case reports of bacteremia with this microorganism; the majority are either polymicrobial or associated with immunocompromised patients. We describe a case of monomicrobial L. adecarboxylata bacteremia in a 43-year-old female who presented with bloody diarrhea. Colonoscopy revealed diffuse colonic mucosal inflammation with numerous ulcers, and histopathology revealed crypt abscesses. Following an episode of rectal bleeding, two sets of blood cultures grew L. adecarboxylata, which was treated with intravenous ceftriaxone. After a complicated hospital course, she was eventually diagnosed with ulcerative colitis and enteropathic arthritis, treated with intravenous methylprednisolone, mesalamine, and infliximab which resulted in resolution of her symptoms. In our previously immunocompetent patient, derangement of the gut mucosal barrier was the likely cause of bacteremia, yet performing endoscopic intervention may have contributed to bacterial translocation.
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Patients with ulcerative colitis (UC) and Crohn's disease (CD) are at increased risk for developing colorectal cancer (CRC), and this is believed to be a result of chronic inflammation. Although conclusive evidence is still missing, both epidemiological and experimental observations suggest that certain drugs used to treat inflammation, such as mesalazine, can reduce the incidence of colitis-associated CRC. Therefore, in recent years, several studies have been conducted to dissect the mechanisms by which mesalazine interferes with CRC cell growth and survival. This review summarizes the current information on the molecular mechanisms that underlie the antineoplastic action of mesalazine.
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Based on adherence to intestinal mucosa, intralumenally administered liposomal formulations of 5-aminosalicylate (5-ASA) and 6-mercaptopurine (6-MP) were studied for their potential to enhance local drug delivery to intestinal tissue for the treatment of inflammatory bowel disease.
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The purpose of this work was to study the solubility of two drugs with different physicochemical properties in luminal fluids obtained from various regions of the human gastrointestinal (GI) tract and to determine the most important luminal parameters influencing their solubility. Jejunal fluids were aspirated from healthy volunteers via an oral intubation tube. Ileal and colonic fluids were obtained from patients undergoing GI surgery. Stoma fluids were also retrieved from patients. pH and buffer capacity of all fluids were determined. Saturation solubility of prednisolone (unionisable) and mesalamine (5-aminosalicylic acid) (zwitterionic) was measured. Mean solubility of prednisolone in the different luminal fluids was 0.50 mg/mL (±0.05) and did not vary significantly between the different regions of the GI tract (ANOVA, p > 0.05). No correlation between prednisolone solubility and jejunal bile salt content was found. Mesalamine solubility increased down the GI tract: 1.97 (±0.25), 3.26 (±0.08), 6.24 (±1.13) and 7.95 (±0.21) mg/mL in jejunal, ileal, ascending and transverse/descending colonic fluids respectively. Buffer capacity also increased and in one patient was observed to range from 6.4 to 28.6 reaching 44.4 mM/L/pH unit in ileal, ascending and transverse/descending colon fluids respectively. Mesalamine solubility was found to be dependent on both buffer capacity and pH, with buffer capacity being the most important (standardized coefficient β = 0.849, p < 0.0001) compared to pH (β = 0.219, p < 0.05). For drugs delivered as modified release formulations it is important to consider solubility in different regions of the GI tract as significant differences can arise which will ultimately influence drug bioavailability.
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We identified 171 subjects ranging in age from 1.5 to 17.7 years at diagnosis (mean 11.2 years). Mean follow-up was 5.1 years. Of these subjects, 43% had mild disease at presentation and 57% had disease that was classified as moderate or severe. After treatment 90% of the former group and 81% of the latter group had resolution of symptoms by 6 months. During any subsequent yearly follow-up interval, approximately 55% of the entire study population was symptom free, 38% had chronic intermittent symptoms, and 7% had continuous symptoms. A significantly lower risk of colectomy was noted for those with initially mild disease compared with those with moderate/severe disease. At 1-year the risk of colectomy was 1% among those with mild disease versus 8% with moderate/severe disease; at 5 years, the risk of colectomy was 9% in the mild disease group versus 26% in the moderate/severe disease group (p <0.03).
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All reported randomised controlled trials were retrieved by searching the Medline and EMBASE databases and the bibliographies of relevant studies. Trials which met inclusion criteria were assessed for scientific rigour. Data were extracted by two independent observers according to predetermined criteria.
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A computer-assisted literature search for relevant studies (1981-2002) was performed using MEDLINE, BIOS, the Cochrane Controlled Trials Register, the Cochrane IBD Group Specialized Trials Register, and the Science Citation Index, followed by a manual search of reference lists from previously retrieved articles, review articles, symposia proceedings, and abstracts from major gastrointestinal conferences.
One hundred twelve children were ≤ 5 years of age with no child enrolled at <1 year of age. Of those, 42.9% had Crohn's disease (CD), 46.4% ulcerative colitis (UC), and 10.7% had IBD-unclassified. Among the children with CD, children 1-5 years of age had more isolated colonic disease (39.6%) compared with 6- to 10-year-olds (25.3%, P = .04), and 11- to 16-year-olds (22.3%, P < .01). The change from a presenting colon-only phenotype to ileocolonic began at 6-10 years. Children 1-5 years of age with CD had milder disease activity (45.8%) at diagnosis compared with the oldest group (28%, P = .01). Five years postdiagnosis, there was no difference in disease activity among the 3 groups. However, compared with the oldest group, a greater proportion of 1- to 5-year-olds with CD were receiving corticosteroids (P < .01) and methotrexate (P < .01), and a greater proportion of 1- to 5-year-olds with UC were receiving mesalamine (P < .0001) and thiopurine immunomodulators (P < .0002).
Autonomic function in inflammatory bowel disease has not yet been studied by means of analysis of 24-hour heart rate variability.
Mesalazine represents effective and well-tolerated first-line therapy for mildly to moderately acute disease as well as for the long-term maintenance treatment in the patient with ulcerative colitis.
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5-Aminosalicylic acid (5-ASA) suppressed nitrite-stimulated oxidation of the fatty acid n-butyrate in a dose-dependent manner in isolated human and rat colonic epithelial cells. 4-ASA had one-sixth of the capacity of 5-ASA and sulphapyridine (SP) little of the capacity of 5-ASA to suppress fatty acid oxidation in human colonic epithelial cells. Sulphasalazine (SASP), azodisalicylic acid (ADS), acetyl-5-ASA and acetyl salicylic acid (ASA) did not suppress fatty acid oxidation in rat colonocytes. The suppression index of fatty acid oxidation (SIFO) of respective salicylic acids correlated with the reported clinical effectiveness of each drug against ulcerative colitis (UC). The capacity of 5-ASA to affect nitrite-stimulated oxidation of fat in the colonic mucosa suggests that nitrite ions and control of fatty acid oxidation play a central role in the development and therapy of active UC.
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IL-8 response of HT29 cells was greater with Crohn's disease (689 +/- 298 [mean +/- SD] pg IL-8/mL at 4 hours, n = 7) and colon cancer isolates (532 +/- 415 pg/mL, n = 14) than with ulcerative colitis (236 +/- 58 pg/mL, n = 6) or control isolates (236 +/- 100 pg/mL, n = 6, P < 0.0001). Bacterial supernatants contained shed flagellin that triggered IL-8 release. For whole bacteria the IL-8 response to E. coli that agglutinate red blood cells (548 +/- 428 pg IL-8/mL, n = 16), a function that correlates with epithelial invasion, was greater than for nonhemagglutinators (281 +/- 253 pg/mL, n = 17; P < 0.0001). This was particularly marked among E. coli that, although flagellate, could not release IL-8 from TLR5-transfected HEK293 cells. IL-8 release was mediated by extracellular-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK) and inhibited by mesalamine, but not hydrocortisone, at therapeutic concentrations.