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Ulcerative Colitis Patients (ulcerative + colitis_patient)
Selected AbstractsUlcerative colitis patients with dysplastic polyps should be advised to undergo colectomyINFLAMMATORY BOWEL DISEASES, Issue 9 2006Jonathan P. Terdiman MD No abstract is available for this article. [source] The effect of 5-aminosalicylic acid,containing drugs on sulfide production by sulfate-reducing and amino acid,fermenting bacteriaINFLAMMATORY BOWEL DISEASES, Issue 1 2003Laurie M. Edmond Abstract The toxic, bacterial metabolite sulfide is implicated in ulcerative colitis. Ulcerative colitis patients taking 5-aminosalicylic acid,containing drugs have lower fecal sulfide levels than those not taking these drugs. The effects of sulfasalazine, balsalazide, olsalazine, and 5-aminosalicylic acid on sulfide production were studied in a three-stage chemostat pulsed on days 1 to 3 with 5 g sulfasalazine (40 mM) and in pure cultures of amino acid,fermenting and sulfate-reducing bacteria. By the third day of sulfasalazine addition to the chemostat, sulfide concentrations in vessels 1 through 3 had dropped from 1.73, 1.78, and 1.43 mM to 0.01, 0.15, and 0.9 mM, respectively. In pure cultures, 50% inhibition of sulfide production from amino acids occurred at 2.5 ± 0.05 mM for sulfasalazine, 5 ± 0.2 mM for olsalazine, 6 ± 1 mM for balsalazide, and more than 20 mM for 5-aminosalicylic acid. Fifty percent inhibition of sulfide production from sulfate occurred at 0.25 ± 0.05 mM for sulfasalazine, 0.7 ± 0.2 mM for balsalazide, and 9.0 ± 1.0 mM for 5-aminosalicylic acid. The order of effectiveness of equimolar concentrations of drugs (most effective first) in this assay was sulfasalazine, then olsalazine (though given clinically at half the dose of other 5-aminosalicylic acid prodrugs) and balsalazide, and lastly 5-aminosalicylic acid. Inhibition of sulfide production by 5-aminosalicylic acid,containing drugs may contribute to their therapeutic effect in ulcerative colitis. [source] ILEITIS AS A MAIN RECURRENT LESION IN A PATIENT WITH ULCERATIVE COLITIS: REPORT OF A CASEDIGESTIVE ENDOSCOPY, Issue 2 2000Shuichi Sano We report a case of ulcerative colitis complicating ileitis that endoscopically and histologically resembled a colonic lesion. Eight years prior to the time of writing, the patient had undergone proctosigmoidectomy and ileocecal resection because of severe hemorrhagic lesions of ulcerative colitis. A month prior to the time of writing, bleeding from the stoma occurred. Endoscopy revealed erosions on easy-bleeding mucosa in the ileum but no active inflammatory lesions in colonic mucosa except for small erosions in the descending colon beneath the stoma. Histologic findings of biopsy specimens from the ileal mucosa showed marked inflammation including neutrophile infiltration and crypt abscesses. This is a rare case of ulcerative colitis showing ileitis as a main recurrent lesion, suggesting that careful observation of the small intestine will be required after ileocecal resection in ulcerative colitis patients. [source] Apoptosis resistance in ulcerative colitis: High expression of decoy receptors by lamina propria T cellsEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 8 2006Raja Fayad Abstract Intestinal mucosa is constantly exposed to normal environmental antigens. A significant number of intestinal mucosal T cells are being deleted through apoptosis. In contrast, T cells from inflamed mucosa of ulcerative colitis patients did not undergo apoptosis. In this study, we determined whether the apoptosis of normal mucosal T cells was induced by antigen receptor stimulation and further determined pathways that mediated the apoptosis. Freshly isolated lamina propria T cells were stimulated with CD3 mAb and apoptosis was determined by Annexin,V staining. Normal mucosal T cells underwent apoptosis upon CD3 mAb stimulation whereas the T cells from inflamed mucosa did not. The apoptosis in normal T cells was blocked by TRAIL-R1:Fc and an inhibiting CD95 antibody. Interestingly, decoy receptor (DcR)1, DcR2, and DcR3 that compete with death receptor (DR)4/5 and CD95 were highly expressed by the T cells from inflamed mucosa, but much lower by T cells from normal mucosa. Our data suggest that normal mucosal T cells are constantly deleted in response to environmental antigens mediated through DR4/5 and CD95 pathways and mucosal T cells from ulcerative colitis resist to undergoing apoptosis due to highly expression of DcR1, DcR2, and DcR3. [source] Both IL-12p70 and IL-23 are synthesized during active Crohn's disease and are down-regulated by treatment with anti-IL-12 p40 monoclonal antibodyINFLAMMATORY BOWEL DISEASES, Issue 1 2006Ivan J Fuss MD Abstract Background: Interleukin (IL)-12p70 and IL-23 are key T helper-1 (TH1) cytokines that drive the inflammation seen in numerous models of intestinal inflammation. These molecules contain an identical p40 chain that is bound to a p35 chain in IL-12 and a p19 chain in IL-23, making both potentially susceptible to modulation by an anti-IL-12p40 monoclonal antibody (mAb). Methods: In the present study, we sought to determine whether active inflammation in Crohn's disease (CD) is associated with the increased synthesis of both of these cytokines and whether patients treated with an anti-IL-12p40 mAb down-regulate IL-23 as well as IL-12p70 as previous reported. Results: To this end we initially determined that IL-12p70 secretion by control and CD antigen-presenting cells (macrophages) in lamina propria mononuclear populations is optimized by stimulation with CD40L and interferon-,. In subsequent studies using these stimulation conditions we found that patients with CD manifested both increased IL-12p70 and IL-23 secretion before anti-IL-12p40 mAb treatment and normal levels of secretion of these cytokines following cessation of treatment. Antigen-presenting cells in lamina propria mononuclear cells from ulcerative colitis patients, in contrast, produced only baseline levels of IL-23. Finally, we found that IL-23-induced T cell production of IL-17 and IL-6 are also greatly reduced after antibody treatment. The latter data are parallel to those from previous studies showing that anti-IL-12p40 down-regulates IFN-, and tumor necrosis factor-, secretion. Conclusions: We conclude that CD but not ulcerative colitis is associated with high levels of both IL-12p70 and IL-23 secretion as well as the secretion of downstream effector cytokines, and that this cytokine production is down-regulated following administration of IL-12p40 mAb. [source] A long-term cohort study of nonsteroidal anti-inflammatory drug use and disease activity in outpatients with inflammatory bowel diseaseINFLAMMATORY BOWEL DISEASES, Issue 6 2004Gregory F. Bonner MD Abstract Background and Aims: We examined whether use of nonsteroidal anti-inflammatory drugs (NSAIDs) in outpatients with inflammatory bowel disease was associated with increased severity of disease activity. Methods: Outpatients with Crohn's disease (CD; n = 426) and with ulcerative colitis (UC; n = 203) were seen between November 1997 and April 2002. Patients were questioned at each visit regarding use of prescription or over-the counter NSAIDs and a clinical disease activity index (modified Harvey Bradshaw [MHB] or Lichtiger score) was obtained. Results: For the Crohn's patients, for 1315 visits no NSAIDs were used, on 215 visits low-dose NSAIDs were used, and for 139 visits high-dose NSAIDs were taken. For UC patient visits, 495 used no NSAIDs, 112 low-dose NSAIDs, and 49 high-dose NSAIDs. Average MHB score was 4.07 for the no-NSAID group, 4.24 for low-dose NSAIDs (P = 0.46), and 4.78 for high-dose (P = 0.0072 versus no NSAIDs). For the ulcerative colitis patients corresponding scores were 5.64, 5.46, and 6.20, respectively (P = not significant). The probability of moderately active disease as defined by crossing a threshold MHB or Lichtiger score, however, was not significantly affected by NSAID use. Subgroup analysis indicated the increase in disease activity among CD patients taking high-dose NSAIDs was limited to patients with colonic involvement. Conclusions: Use of low-dose NSAIDs was not associated with an increase in disease activity for these outpatients with either CD or UC. Use of high-doses of NSAIDs was associated with a higher numerical disease activity index score among CD patients with colonic involvement, but this was not reflected by an increase in significant disease flares. [source] Prospective evaluation of intestinal homing memory T cells in ulcerative colitisINFLAMMATORY BOWEL DISEASES, Issue 5 2004A. L. Hart Abstract Background: Intestinal homing (,7+) memory T cells reflect the mucosal environment in which they were primed. We hypothesized that prospective assessment of cytokine production by intestinal homing (,7+) memory T cells in ulcerative colitis patients followed from remission to early relapse may elucidate shifts in cytokine production relevant to the mucosal environment associated with the early phase of inflammation. Methods: Twelve patients with frequently relapsing ulcerative colitis (,2 relapses in the previous 12 months) were recruited in remission and followed prospectively until relapse. Antibody labeling of whole blood and flow cytometry were used to identify ,7+ cells and ,7, populations within CD3+CD45RA, leukocytes. Production of cytokines (IFN-,, TNF-,, IL-2, IL-10, TGF-,, and IL-4) was determined by intracellular labeling. Results: Early relapse of ulcerative colitis was associated with a shift of T cells from the naive to the memory T cell pool, and further the ratio of ,7+:,7, memory T cells was significantly reduced at relapse (p < 0.01). A greater proportion of intestinal homing ,7+ memory T cells produced IL-4 (p < 0.02) and TNF-, (p < 0.05) at disease relapse compared with remission. Non-intestinal homing ,7,memory T cells also showed a tendency toward an increased production of TH1 and TH2 cytokines. Conclusions: The earliest phase of intestinal inflammation in ulcerative colitis patients is associated with an increase in both TH1 (TNF-, and TH2 (IL-4) cytokines by intestinal homing ,7+ memory T cells. These data support the principles of targeting lymphocyte trafficking as therapies in ulcerative colitis. [source] Dysplasia and carcinoma development in a repeated dextran sulfate sodium-induced colitis modelJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 10 2002Isao Okayasu Abstract Background: As an important mechanism underlying the increased risk of colorectal carcinoma development in patients with long-standing ulcerative colitis, promotion as a result of the regenerative process has been proposed. In the present study, a dysplasia-carcinoma sequence in a novel repeated colitis model in mice is documented. Methods: Repeated colitis was induced by nine administration cycles of 3% dextran sulfate sodium (DSS; molecular weight, 54 000): each administration cycle comprised 3% DSS for 7 days followed by distilled water for the subsequent 14 days, to give conditions similar to the clinically observed active and remission phases in humans. Results: Multiple colorectal tumors (nine low- and four high-grade dysplasias and two carcinomas) developed in 25 mice. These neoplastic lesions consisted of tubular structures, presenting as various types of elevated, flat and depressed tumor, similar to those in ulcerative colitis patients. A time-course study with assessment of the severity of colitis and in vivo bromodeoxyuridine uptake during a single 3% DSS administration cycle revealed a high level of regenerative activity in the colitis-affected mucosal epithelia. Conclusion: Thus, with the present repeated colitis model, regeneration and neoplastic lesions were apparent, the biological features of which provide evidence of a colorectal dysplasia,invasive carcinoma sequence in ulcerative colitis. [source] Antibodies to neutrophil cytoplasma in patients with ulcerative colitis and their first-degree relatives in ThailandJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 8 2001Charkaphan Osangthamnont Abstract Background: The prevalence of perinuclear antineutrophil cytoplasmic antibodies (p-ANCA) does not significantly vary in ethnically diverse populations. The prevalence of p-ANCA is high in ulcerative colitis and primary sclerosing cholangitis. While the prevalence of ulcerative colitis in Asian populations is low, it is interesting to know the prevalence of p-ANCA in such a population. Methods: Sera from 33 cases of ulcerative colitis diagnosed during the last 10 years at the diarrhea clinic, Division of Gastroenterology, Siriraj Hospital, were prospectively compared with case controls consisting of 15 cases of diarrhea from non-inflammatory bowel diseases and 25 non-diarrheic patients. Indirect immunofluorescence assay was used to detect p-ANCA in all the sera. Results: Positive p-ANCA tests were found in 13 of the 33 patients with ulcerative colitis and in one of the 40 controls. Sensitivity of the test was 39.4% and the specificity was 97.5%. The one patient with positive p-ANCA in the control group was the patient with irritable bowel syndrome. Of the 13 p-ANCA-positive ulcerative colitis patients, two cases were found to have proctosigmoiditis, seven cases had left-sided colitis, and four cases had pancolitis. Perinuclear antineutrophil cytoplasmic antibodies was one of the 22 cases of first-degree relatives of ulcerative colitis patients (22 relatives from 12 index ulcerative colitis cases). There was no correlation between the positivity of p-ANCA and disease activity, and extent of the disease. Conclusion: The prevalence of p-ANCA in Thai patients with ulcerative colitis (39.4%) is lower than that in the Western population. Although the prevalence of p-ANCA is low in the Thai population, it should serve as a useful tool in diagnosing ulcerative colitis in this part of the world where the disease is uncommon and difficult to diagnose. The negativity of p-ANCA in almost all first-degree relatives of Thai ulcerative colitis patients should be further elucidated. [source] Treatment of ulcerative colitis with adalimumab or infliximab: long-term follow-up of a single-centre cohortALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 4 2010N. Gies Aliment Pharmacol Ther 2010; 32: 522,528 Summary Background, Randomized, controlled trials have demonstrated that anti-TNF agents are efficacious in inducing remission in cases of Crohn's disease and ulcerative colitis. However, response rates for anti-TNF agents in ,real life' clinical practice are less well-defined. Aims, To examine the response rates and long-term outcomes of infliximab and adalimumab treatment for out-patients with ulcerative colitis and to study the variables associated with response rates. Methods, In a prospective study, a single-centre out-patient cohort was treated and followed up according to a structured protocol of clinical care. Response to treatment was assessed using a physician's global assessment that focused on normalization of bowel frequency, absence of blood with defecation and tapering of corticosteroids to zero. Results, Fifty-three ulcerative colitis patients were included in the study. Responses to induction therapy were 96.4% (27/28) for infliximab and 80% (20/25) for adalimumab (P = 0.0889). Responses to maintenance therapy were similar: infliximab 77.8% (14/18) and adalimumab 70.0% (14/20) (P = 0.7190). Multivariate analyses of the induction and maintenance responses did not reveal confounding elements. No new safety signals were identified. Conclusions, This long-term follow-up of a single-centre cohort of ulcerative colitis patients demonstrates that ,real-life' out-patient treatment with infliximab and adalimumab is effective in induction and maintenance of response. [source] Meta-analysis: pre-operative infliximab treatment and short-term post-operative complications in patients with ulcerative colitisALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 4 2010Z. YANG Aliment Pharmacol Ther,31, 486,492 Summary Background, Infliximab was approved for use in ulcerative colitis in recent years. It has been debated if infliximab increases the risk of post-operative complications in patients with ulcerative colitis. Aim, To perform a meta-analysis that examines the relationship between preoperative infliximab treatment and short-term post-operative complications in patients with ulcerative colitis. Methods, We searched the PubMed and MEDLINE databases to identify observational studies on the impact of pre-operative infliximab use on short-term post-operative complications in ulcerative colitis. Infectious complications mainly included wound infection, sepsis and abscess, whereas non-infectious complications included intestinal obstruction, thromboembolism and gastrointestinal haemorrhage. Pooled odds ratios (ORs) were calculated for each relationship. Results, A total of 5 studies and 706 patients were included in our meta-analysis. Overall, we did not find a strong association between pre-operative treatment of infliximab and short-term infectious [OR 2.24, 95% confidence interval (CI) 0.63,7.95] or non-infectious (OR 0.85, 95% CI 0.50,1.45) post-operative complications in ulcerative colitis patients. On the contrary, we discovered that pre-operative infliximab use increased short-term total post-operative complications (OR 1.80, 95% CI 1.12,2.87). Conclusions, Pre-operative infliximab use increased the risk of short-term post-operative complications. Subgroup analysis is underpowered to assess the nature of these complications but shows a trend towards increased post-operative infection. [source] Clinical trial: comparison of alendronate and alfacalcidol in glucocorticoid-associated osteoporosis in patients with ulcerative colitisALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 4 2009S. KITAZAKI Summary Background, Bone loss is often observed in patients with ulcerative colitis, particularly if they require glucocorticoids. Aim, To determine whether the bisphosphonate, alendronate, is safe and effective in preserving bone mass compared to the active vitamin D3, alfacalcidol, in ulcerative colitis patients receiving glucocorticoids. Methods, Thirty-nine patients with ulcerative colitis and treated with glucocorticoids were randomized to receive alendronate (5 mg/day) or alfacalcidol (1 ,g/day) daily for 12 months. Loss of bone mass was evaluated by bone mineral density, bone resorption by urinary N -telopeptide for type I collagen, and bone formation by serum bone alkaline phosphatase. Results, Alendronate, but not alfacalcidol, significantly increased bone mineral density in the lumbar spine. Alendronate decreased serum bone alkaline phosphatase levels, but alfacalcidol did not. Urinary N -telopeptide for type I collagen levels decreased in both groups, but were significantly lower in the alendronate group. There were no significant differences in the adverse events in the two groups. Conclusion, Our study indicates that alendronate is a safe, well-tolerated and more effective therapy than alfacalcidol for preventing glucocorticoid-associated bone loss in patients with ulcerative colitis. [source] Age at onset of inflammatory bowel disease and the risk of surgery for non-neoplastic bowel diseaseALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 12 2007W. J. TREMAINE Summary Background, There is conflicting data regarding the response to medical and surgical therapy for inflammatory bowel disease with respect to age at disease onset. Aim, To determine if the age at onset of Crohn's disease and ulcerative colitis is a risk factor for surgery for non-neoplastic bowel disease. Methods, This was a case,control study of patients evaluated between 1998 and 2001. Cases had undergone an initial operation for bowel disease. Controls were matched 1:1 for gender, disease subtype, date of first visit (±2 years), time from diagnosis prior to first visit (±3 years) and duration of follow-up. Association with age, disease extent, smoking history, medication use and co-morbidities vs. case/control status was assessed using multiple variable conditional logistic regression to estimate the odds ratio (OR) and 95% confidence intervals (CI) for undergoing surgery. Results, Among 132 Crohn's patients, older patients had lower odds for surgery (OR per 5 years, 0.86; 95% CI: 0.75,0.98). The rate of surgery for non-neoplastic bowel disease was not significantly associated with disease distribution, co-morbidities or cigarette smoking. Among 234 ulcerative colitis patients, the rate of surgery was unrelated to age, disease extent, co-morbidities or cigarette smoking, Conclusions, For Crohn's disease, but not ulcerative colitis, the risk of surgery for non-neoplastic bowel disease decreases with increasing age at diagnosis, irrespective of disease distribution and history of cigarette smoking. [source] Efficacy of Lactobacillus GG in maintaining remission of ulcerative colitisALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 11 2006M. A. ZOCCO Summary Background Aminosalicylates are the mainstay of therapy to prevent relapse of quiescent ulcerative colitis. The rationale for using probiotics is based on the evidence implicating intestinal bacteria in the pathogenesis of this disorder. Aim To evaluate the efficacy of Lactobacillus GG alone or in combination with mesalazine vs. mesalazine as maintenance treatment in ulcerative colitis. Patients and methods 187 ulcerative colitis patients with quiescent disease were randomized to receive Lactobacillus GG 18 × 109 viable bacteria/day (65 patients), mesalazine 2400 mg/day (60 patients) or Lactobacillus GG + mesalazine (62 patients). Disease activity index, endoscopic and histological scores were determined at 0, 6 and 12 months and in case of relapse. The primary end point was to evaluate sustained remission. Results Overall analysis showed no difference in relapse rate at 6 (P = 0.44) and 12 months (P = 0.77) among the three treatment groups. However, the treatment with Lactobacillus GG seems to be more effective than standard treatment with mesalazine in prolonging the relapse-free time (P < 0.05). Conclusions Lactobacillus GG seems to be effective and safe for maintaining remission in patients with ulcerative colitis, and it could represent a good therapeutic option for preventing relapse in this group of patients. [source] Azathioprine without oral ciclosporin in the long-term maintenance of remission induced by intravenous ciclosporin in severe, steroid-refractory ulcerative colitisALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 12 2002E. Domènech Summary Background : Intravenous ciclosporin is considered to be the only alternative to avoid surgery in severe, steroid-refractory ulcerative colitis. In responders, some authors recommend a switch to oral ciclosporin to act as a ,bridge' until the therapeutic action of azathioprine is achieved for maintenance treatment. Aim : To report the short- and long-term outcome of intravenous ciclosporin-responsive ulcerative colitis patients treated with oral azathioprine without oral ciclosporin. Methods : The records of all patients treated with intravenous ciclosporin for severe, steroid-refractory ulcerative colitis were reviewed. Responders following treatment with azathioprine but without oral ciclosporin as maintenance therapy were included. Patients with colonic cytomegalovirus infection and/or follow-up of less than 1 year were excluded. Results : Twenty-seven patients were included. Steroids were discontinued in 24 (89%). The median follow-up was 36 months. Eighteen (75%) patients presented mild or moderate relapses, which were easily managed with salicylates or steroids. Cumulative probabilities of relapse were 42%, 72% and 77% at 1, 3 and 5 years, respectively. Eleven (40.7%) patients underwent elective colectomy. Cumulative probabilities of colectomy were 29%, 35% and 42% at 1, 3 and 5 years, respectively. No opportunistic infections were observed. Conclusions : Oral azathioprine seems to be enough to maintain long-term remission induced by intravenous ciclosporin in patients with steroid-refractory ulcerative colitis. The ,bridging step' with oral ciclosporin may not be necessary in this subset of patients, although a randomized controlled trial is warranted to confirm this hypothesis. [source] Minimal renal dysfunction in inflammatory bowel disease is related to disease activity but not to 5-ASA useALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 3 2001K. R. Herrlinger Background: Conflicting data exist about proteinuria in inflammatory bowel diseases. It is still unclear whether the occurrence of proteinuria in inflammatory bowel disease patients is an extra-intestinal manifestation of disease or the result of adverse effects to medication, especially to aminosalicylates (ASA). Methods: A total of 95 patients (51 with Crohn's disease and 44 with ulcerative colitis) were enrolled in the study. Disease activity was assessed by Crohn's Disease Activity Index (CDAI) or the Truelove index, respectively. Urine was collected over 24 h and protein excretion of specific marker proteins for tubular (,1-microglobulin-,1-MG) and glomerular (albumin-Alb, Immunoglobulin G-IgG) dysfunction was measured using a highly sensitive immunoluminometric assay. Results: Out of 51 Crohn's disease patients, 20 showed elevated urinary ,1-MG. The amount of ,1-MGuria was strongly correlated to the CDAI (r=0.6, P < 0.001). Only four Crohn's disease patients showed slightly elevated values for glomerular proteins in urine. Similar results were obtained for ulcerative colitis: whereas only two ulcerative colitis patients showed albuminuria, tubular proteinuria was detected in 28 out of 44 ulcerative colitis patients. Proteinuria was strongly dependent on disease activity (P < 0.01) but was not related to ASA treatment. Conclusions: Proteinuria of tubular marker proteins occurs in the majority of inflammatory bowel disease patients and is related to disease activity rather than to ASA treatment. Tubular proteinuria seems to reflect a renal extra-intestinal manifestation of inflammatory bowel disease and may serve as a new relevant marker of disease activity. [source] Diminished cytokine signalling against bacterial components in mononuclear leucocytes from ulcerative colitis patients after leukocytapheresisCLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 1 2005K. Mitsuyama Summary Infiltration by circulating inflammatory cells is a prominent local inflammatory feature of ulcerative colitis (UC). Several trials have suggested that leukocytapheresis by filtration can benefit patients with active UC. We investigated how this therapy might modulate the inflammatory response. Patients with active UC who were beginning repeated filtration leukocytapheresis were studied. Mononuclear cell preparations were obtained from blood before and after the first treatment, and expression of cytokine signalling components and the cell-proliferative response were analysed in vitro. Leukocytapheresis reduced lipopolysaccharide-induced production of proinflammatory cytokines (interleukin-1, -6, -8 and tumour necrosis factor-,, P < 0·05 for all) and activation of intracellular signalling components (nuclear factor-,B, mitogen-activated protein kinases, and signal transducer and activator of transcription-3), as well as surface expression of toll-like receptor-4 (P < 0·05) in mononuclear cells. The therapy also reduced the cell-proliferative response by mononuclear cells stimulated with sonicated bacterial preparations from autologous intestine (P < 0·05). These results indicate that activated mononuclear cells in the peripheral blood of patients with active UC are removed by leukocytapheresis and replaced by cells with a lower activation status. This replacement may partly explain the therapeutic benefit. [source] | ||||||||||||||||||||||