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T Andus

Publications and source records attributed to T Andus.

At least 19 recordsLinked to original sources
PubMed2005

Patient education in inflammatory bowel disease does not influence patients knowledge and long-term psychosocial well-being.

BACKGROUND AND AIMS: Patient education is accepted in many disciplines as a valid component of disease management in chronic diseases. The aim of this prospective study was to analyze the effects of an education program in patients with inflammatory bowel disease. METHODS: 145 patients with inflammatory bowel disease were prospectively included: 73 were educated in four sessions, 72 were educated after the one year evaluation period (control group). The following topics were presented: pathogenesis, diagnostic procedures, course of disease, medical and surgical treatment, nutrition, social problems and support, stress management, and coping with the disease. RESULTS: The repeated measurement two-way analysis of variances showed no effects of the patient education program on disease-related knowledge, depression and quality of life. CONCLUSION: This patient education program was not able to increase disease-related knowledge or psychosocial variables in patients with IBD. However, most of the patients were very satisfied with the education program, since as judged by their own assessment it helped them to act responsibly for themselves and their disease.

Adolescent↗
PubMed2005

Severe acute cholestatic hepatitis by infiltration of monoclonal plasma cells in multiple myeloma.

BACKGROUND: Plasma cell infiltration of the liver can be detected in 25 to 40% of patients with multiple myeloma. However, there are only rare cases of multiple myeloma clinically presenting as acute liver disease. CASE REPORT: We report an 88-year-old woman with painless jaundice and abnormal liver function tests, resembling acute cholestatic hepatitis. Viral hepatitis as well as autoimmune hepatitis could be excluded. Liver biopsy revealed a diffuse portal and sinusoidal infiltration of plasma cells with lambda light chain restriction. Serological immune fixation disclosed monoclonal gammopathy of IgG lambda with bone marrow infiltration of 25% plasma cells. After administration of 60 mg prednisolone per day, the elevated liver enzymes declined considerably. CONCLUSION: Hepatic plasma cell infiltration of multiple myeloma can, in rare cases, manifest as acute cholestatic hepatitis, which may respond to treatment with corticosteroids.

Acute Disease↗
PubMed2004

Interferon gamma downregulates IL-8 production in primary human colonic epithelial cells without induction of apoptosis.

BACKGROUND: In acute or chronic inflammatory bowel disease (IBD) interferon gamma (IFNgamma) is still considered to be an important pro-inflammatory mediator. In the present study we investigated the impact of IFNgamma on interleukin-8 (IL-8) production as a read-out for cell activation in intestinal epithelial cell (IEC) lines and primary human colonic epithelial cells (CEC). METHODS: Primary cultures of human CEC were established from the mucosa of patients without inflammatory disease. CEC, HT-29 or Caco-2 cells were incubated with either IFNgamma, tumor necrosis factor (TNF)alpha or IL-10. IL-8 and IL-1Ra secretion was determined by ELISA. Competicon PCR was used for quantification of IL-8mRNA. Apoptosis was quantified by propidium iodine incorporation and fluorescence activated cell sorting (FACS) analysis. RESULTS: In contrast to HT-29 cells in primary human CEC 100 U/ml IFNgamma inhibited IL-8 secretion significantly to 70+/-15% of unstimulated primary CEC (p<0.005) more effectively than IL-10 (87+/-21% versus unstimulated cells, n.s.). In HT-29 cells, IL-8 secretion was induced to 405+/-101% of unstimulated cells. In Caco-2 cells, IFNgamma had no significant effect on IL-8 secretion. The effect in HT-29 and CEC was concentration dependent. In primary CEC, 200 U/ml IFNgamma further reduced IL-8 secretion to 48+/-18% of unstimulated CEC (p<0.05). Whereas IL-8 mRNA was strongly upregulated in HT-29 cells, no upregulation or even a downregulation was found in CEC. Pre-incubation with 100 U/ml IFNgamma did not increase the susceptibility to apoptosis mediated by anti-Fas antibody (CH-11) in primary CEC, whereas HT-29 cells showed increased rates of apoptosis after priming with IFNgamma. CONCLUSION: In contrast to HT-29, IFNgamma downregulated IL-8 secretion and did not induce IL-8 mRNA expression in primary human CEC. This effect was not due to induction of apoptosis.

Antineoplastic Agents↗
PubMed2003

Analysis of the therapeutic efficacy of different doses of budesonide in patients with active Crohn's ileocolitis depending on disease activity and localization.

BACKGROUND AND AIMS: The nonsystemic steroid budesonide has been used to treat active ileocecal and ileocolonic Crohn's disease (CD). This study investigated the optimal budesonide dose using a pH-dependent release formulation. The goal of treatment was the remission of CD (CDAI <150) within 6 weeks of treatment. PATIENTS AND METHODS: The study was of randomized, double-blind, dose-finding design. Patients with active CD ileocolitis without steroid pretreatment were treated with 3x2 mg ( n=39), 3x3 mg ( n=33), or 3x6 mg ( n=32) oral pH-modified released budesonide daily. RESULTS: The remission rates after 6 weeks were 36% with 3x2 mg, 55% with 3x3 mg, and 66% with 3x6 mg. Significantly more patients were in remission while treated with 3x6 mg than with 3x2 mg budesonide/day. Subgroup analyses revealed that patients with high disease activity (CDAI >/= 300) or ileocolonic disease with disease manifestation distal to the transverse colon responded better to the highest budesonide dose. CONCLUSION: Oral pH-modified released budesonide shows a dose-dependent effectiveness in patients with active ileocolonic CD. In the majority of patients 9 mg budesonide per day is sufficient. However, in patients with highly active disease or ileal disease with distal colonic manifestation higher doses of budesonide could increase the therapeutic response

Adult↗
PubMed2003

[Value of abdominal ultrasound screening in patients with benign diseases of the skin].

OBJECTIVE: We investigated the value of abdominal ultrasound screening of abdominal foci in patients with benign diseases of the skin. PATIENTS AND METHODS: The data of 151 patients (age (mean) 56,6 years; male n = 79, female n = 72) from the department of dermatology were retrospectively analysed. The patients were sent for ultrasound evaluation of abdominal foci as cause of benign diseases of the skin. RESULTS: In these 151 patients 3 potential foci were found (2 yen suspicion of a liver tumor, 1 yen thickened bowel wall). The liver tumors could not be confirmed by computed tomography, in the patient with a thickened bowel wall, a Crohńs disease was newly diagnosed. Abdominal ultrasound led to clinically relevant findings in fewer than 1 % of cases. We diagnosed 142 abnormal findings, mostly without clinical relevance. These abnormal findings caused follow-up examinations in 30 of the cases (19 computed tomographies; 2 magnetic resonance tomographies). CONCLUSION: Abdominal ultrasound does not seem useful in the primary screening of patients with benign diseases of the skin. Perhaps a more restrictive and selective use of ultrasound could be valuable.

Abdomen↗
PubMed2003

Replacement of conventional glucocorticoids by oral pH-modified release budesonide in active and inactive Crohn's disease: results of an open, prospective, multicenter trial.

Glucocorticosteroids (GCS) are established in the treatment of active Crohn's ileitis and ileocolitis. Recently, the topical steroid budesonide was found to be effective in untreated patients with Crohn's disease (CD) causing less side effects than conventional GCS. No clinical data have been reported about the effects of switching from conventional GCS to budesonide in terms of side effects and disease activity. The primary aim of this study was to evaluate the development of side effects after switching from conventional GCS treatment to Eudragit L-coated budesonide (pH-modified release formulation) in patients taking 5-30 mg prednisolone equivalent per day for at least two weeks. In all, 178 patients with active CD (N = 88) or CD in remission during GCS treatment (N = 90) were included. Conventional GCS treatment was tapered down during a maximum of three weeks, with simultaneous intake of 3 x 3 mg budesonide. Thereafter, patients received 3 x 3 mg budesonide alone for six weeks. GCS-related side effects, disease activity and adverse events were documented at study entry and after 0, 2, 4, and 6 weeks of budesonide treatment. The percentage of patients with GCS-related side effects decreased from 65.2% (intention-to-treat-population) at entry to 43.3% (P < 0.0001) at the end of the trial. The total number of GCS-related side effects decreased significantly from 269 to 90. Of the patients who entered the study with active disease under conventional GCS therapy, 38.6% were in remission at the end of the study. Of the patients who entered the study with CD in remission, 78% stayed in remission after switching from conventinal GCS to budesonide. In conclusion, switching from conventional GCS treatment to budesonide leads to a significant reduction of GCS related side effects in patients with CD without causing rapid deterioration of the disease.

Administration, Oral↗
PubMed2003

Patients with refractory Crohn's disease or ulcerative colitis respond to dehydroepiandrosterone: a pilot study.

BACKGROUND: Dehydroepiandrosterone is a steroid hormone used as an 'over-the-counter' drug in the USA. Treatment with dehydroepiandrosterone was effective in randomized controlled trials in patients with systemic lupus erythematosus. Dehydroepiandrosterone sulphate concentrations are decreased in patients with inflammatory bowel disease. Dehydroepiandrosterone inhibits nuclear factor-kappaB and the secretion of interleukin-6 and interleukin-12 via the peroxisome proliferator-activated receptor alpha. AIM: A phase II pilot trial was started to evaluate the effect of dehydroepiandrosterone in active inflammatory bowel disease. METHODS: Twenty patients with chronic active inflammatory bowel disease [seven Crohn's disease (Crohn's disease activity index, 242 +/- 51; mean +/- s.d.); 13 ulcerative colitis (clinical activity index, 7.8 +/- 2.1)] took 200 mg dehydroepiandrosterone per day orally for 56 days. RESULTS: Six of the seven patients with Crohn's disease and eight of the 13 patients with ulcerative colitis responded to treatment, with a decrease in the Crohn's disease activity index of > 70 points and a decrease in the clinical activity index of > 4 points, respectively. Six Crohn's disease patients and six ulcerative colitis patients went into remission (Crohn's disease activity index < 150; clinical activity index <or= 4). No patient withdrew from the study because of side-effects. CONCLUSIONS: In a pilot study, dehydroepiandrosterone was effective and safe in patients with refractory Crohn's disease or ulcerative colitis. Adjustment of the dehydroepiandrosterone dosage may further improve the treatment success.

Adjuvants, Immunologic↗
PubMed2003

Treatment of pouchitis with dehydroepiandrosterone (DHEA) - a case report.

BACKGROUND: Dehydroepiandrosterone (DHEA) inhibits activation of nuclear factor kappa B (NF-kappaB), which is known to be activated in inflammatory lesions of ulcerative colitis, via PPARalpha. In a pilot trial DHEA was effective for the treatment of active ulcerative colitis. Pouchitis is a common complication after proctocolectomy for ulcerative colitis and still a therapeutical challenge. CASE: DHEA 200 mg/d was tested in chronic active pouchitis in a 35-year-old female patient. DHEA was given for eight weeks, and follow up for further eight weeks was performed. The number of stools dropped from 15-18/d to 8/d, the addition of mucus, which was observed initially, was absent during treatment. The consistence of stools improved from liquid/soft to soft/solid. Abdominal pain resolved and endoscopical signs of inflammation improved. Eight weeks after termination of treatment with DHEA, the patient again suffered from 12 to 18 soft to liquid stools per day and mild abdominal pain. CONCLUSION: Therapeutic effects of DHEA in pouchitis should be evaluated systematically.

Adjuvants, Immunologic↗
PubMed2002

Induction and maintenance of clinical remission by interferon-beta in patients with steroid-refractory active ulcerative colitis-an open long-term pilot trial.

BACKGROUND: The imbalance of pro- and anti-inflammatory cytokines plays an important role in the pathogenesis of inflammatory bowel disease. Shifting this disturbed ratio by means of TNF-antibodies or interferon has been shown to be helpful in treating Crohn's disease and multiple sclerosis, respectively. AIM: This pilot study investigated whether interferon-beta can induce clinical remission in corticoid-refractory ulcerative colitis. METHODS: Twenty-five patients with steroid-refractory active ulcerative colitis (Clinical activity index according to Rachmilewitz: 13.5 +/- 5.2) were treated in an open pilot trial with 0.5 MIU human natural interferon-beta (hn-IFN-beta) i.v. (n=18) or 1 MIU recombinant interferon-beta-1a (r-IFN-beta-1-a) s.c. (n=7) daily with the goal of induction of remission. Subsequent maintenance treatment was carried out for 52.0 +/- 78.8 weeks (range 4-336 weeks) with the same dose, three times per week. RESULTS: Twenty-two of 25 patients (88%) went into remission during induction treatment (hn-IFN-beta 16/18, r-IFN-beta-1a 6/7). Mean time to response was 3.0 +/- 1.3 weeks. Mean length of remission was 13.0 +/- 19.7 months. Only eight of 22 patients in remission relapsed during maintenance treatment. Five of these went into remission again after increasing the dose. Adverse events consisted of slight to moderate flu-like symptoms and slight to moderate hair loss in five of 15 female patients. CONCLUSION: Although this open pilot study included only a small number of patients, the high response rate suggests that interferon-beta may be a safe and effective treatment for steroid-refractory active ulcerative colitis.

Adjuvants, Immunologic↗
PubMed2002

Toll-like receptors 2 and 4 are up-regulated during intestinal inflammation.

BACKGROUND & AIMS: Bacterial wall products play an important role in the activation of immune and nonimmune cells of the intestinal mucosa. Toll-like receptors (TLRs) TLR2 and TLR4 have been identified as signaling receptors activated by bacterial wall components. METHODS: Expression of TLRs in human intestinal mucosa obtained by endoscopy and surgery was analyzed by immunohistochemistry. Intestinal macrophages were isolated by immunomagnetic beads armed with a CD33 antibody. Reverse-transcription polymerase chain reaction was performed for TLR1-5. Results were confirmed by Northern blot and flow cytometry. Interleukin-1beta messenger RNA (mRNA) was quantified by a polymerase chain reaction-enzyme-linked immunosorbent assay-kit. RESULTS: Immunohistochemistry revealed a significant increase in the TLR2 and TLR4 antigen expression on submucosal cells in inflamed intestinal mucosa compared with non-inflamed mucosa. TLR expression was localized in intestinal macrophages by double-labeling techniques. No TLR-polymerase chain reaction product could be obtained with mRNA from CD33-positive macrophages from normal mucosa. We observed an induction of mRNA for TLR2, TLR4, and TLR5 in inflammation-associated macrophages. TLR1 and TLR3 were only detectable in blood monocytes. Monocytes reacted to lipopolysaccharide stimulation with a 3-fold and in vitro differentiated macrophages with a 16-fold increase of cellular interleukin-1beta mRNA. Macrophages from normal mucosa did not respond to lipopolysaccharide showing the functional relevance of TLR expression. CONCLUSIONS: This study shows the inflammation-dependent induction of TLR2 and TLR4 expression in intestinal macrophages. The absence of TLRs abolishes the reactivity of mucosal macrophages to bacterial wall products. Presence of TLRs may thereby contribute to the inflammatory process.

Blood Cells↗
PubMed2001

Subtractive screening reveals up-regulation of NADPH oxidase expression in Crohn's disease intestinal macrophages.

Macrophages play a central role during the pathogenesis of inflammation. In normal intestinal mucosa surface expression of typical macrophage markers such as CD14, CD16, CD11b or T-cell co-stimulatory molecules such as CD80 or CD86 is low indicating anergy and low pro-inflammatory activity of these cells. During inflammatory bowel disease (IBD) the mucosa is invaded by a population of macrophages displaying these markers, secreting higher cytokine levels and representing an activated cell population. CD33(+) cells (macrophages) were isolated from normal and Crohn's disease mucosa and mRNA was isolated by polyT magnetic beads. A subtractive screening was performed subtracting mRNA from normal macrophages from those of Crohn's disease macrophages. Oxidative burst activity was determined by flow cytometry. Seventy clones were obtained by the subtractive mRNA screening. Sequencing showed > 99% homology to mRNA of monocyte chemoattractant protein-1 (MCP-1) for three clones. Five clones obtained by subtraction revealed > 99% homology to mRNA of cytochrome b (subunit gp91). Differential expression of the cytochrome b subunit gp91 and the cytosolic NADPH oxidase subunit p67 was confirmed by RT-PCR and 'virtual' Northern blots. The fluorescence ratio of stimulated versus unstimulated cells was 0.9 +/- 0.16 in control macrophages indicating a lack of oxidative burst activity. In Crohn's disease this ratio was significantly increased to 1.80 +/- 0.8 (P = 0.004) confirming the molecular data. In conclusion NADPH oxidase mRNA is down-regulated or absent in macrophages from normal mucosa correlating with a lack of oxidative burst activity. In IBD macrophage-oxidative burst activity is increased and NADPH oxidase mRNA induced. Inhibition of NADPH oxidase could be a new therapeutical target in IBD and reduce mucosal tissue damage in active IBD.

Chemokine CCL2↗
PubMed2001

Differential activation of cytokine secretion in primary human colonic fibroblast/myofibroblast cultures.

BACKGROUND: Fibroblasts and myofibroblasts are known to secrete a wide spectrum of cytokines, but the individual spectrum is tissue-specific. We investigated the effect of cell activation on cytokine secretion of isolated human colonic fibroblasts/myofibroblasts from control patients and patients with mucosal inflammation. METHODS: Primary cultures of human colonic submucosal fibroblasts/myofibroblasts were incubated with IL-1alpha (100 U/ml), IL-Ibeta (10 ng/ml), IL-10 (10 ng/ml), TNF (10 ng/ml), PMA (10 ng/ml), LPS (50 ng/ml), IL-4 (10 ng/ml), or a combination of IL-1 and TNF. Secreted cytokines were determined by ELISA. NF-kappaB activation was demonstrated by electrophoretic mobility-shift assays (EMSA). RESULTS: Incubation of colonic fibroblasts/myofibroblasts with IL-1, LPS, TNF and PMA induced secretion of IL-6, IL-8, M-CSF and GM-CSF. IL-8 and IL-6 secretion could be stimulated by IL-1alpha, IL-1beta, TNF, PMA and LPS within 6 h of incubation. IL-6 secretion was stimulated from 0.5 +/- 0.01 pg/h x microg fibroblast protein to 18.5 +/- 2.6 pg/h x microg fibroblast protein with IL-1beta (P < 0.01). IL-8 secretion was stimulated from 1.0 +/- 0.1 pg/h x microg fibroblast protein to 41.1 +/- 3.6 pg/h x microg (P < 0.005). IL-4 and IL-10 did not change cytokine secretion significantly. No significant differences between cultures from normal and inflamed mucosa were observed. TNF and IL-1 induced NF-kappaB activation. ALLN, a proteasome and NF-kappaB activation inhibitor, reduced TNF-mediated IL-8, GM-CSF and M-CSF induction significantly, whereas induction of IL-6 secretion remained unchanged. CONCLUSION: Human colonic myofibroblasts can secrete large amounts of IL-6, IL-8, M-CSF and GM-CSF upon stimulation. The induction of IL-8, M-CSF and GM-CSF, but not of IL-6 secretion, is mediated mainly by NF-kappaB activation. The cytokine profile and the total amounts of cytokines released suggest that colonic myofibroblasts can play a role in leukocyte recruitment and during mucosal inflammation. They therefore have to be regarded as an important part of the mucosal immune system.

Adult↗
PubMed2001

Association of HLA-DR genotypes and IL-1ra gene polymorphism with treatment failure of budesonide and disease patterns in Crohn's disease.

OBJECTIVE: Associations between HLA-DR genotypes and susceptibility to Crohn's disease (CD) have been reported. However, it is not known whether certain HLA-DR genotypes or IL-1ra gene polymorphism are associated with responsiveness to treatment or different clinical patterns of disease. DESIGN/SETTING: In a large, randomized, controlled multicentre trial, 318 patients with CD were treated with daily doses of 6, 9 or 18 mg budesonide. Patients were stratified into two groups: patients without steroid pretreatment and with active CD (CDAI > 150) and patients with conventional steroid pretreatment of < or= 30 mg prednisolone per day, which was replaced by oral budesonide within 3 weeks. MAIN OUTCOME MEASURES: The HLA-DRB1 genotypes 1-16 and the IL-1ra gene polymorphism were examined for an association with budesonide treatment failure. RESULTS: Only HLA-DR 8 was associated with treatment failure of budesonide. HLA-DR 8 is not very common. Only 17/243 patients who could be evaluated expressed this genotype, and 13 of these 17 patients did not respond to budesonide (P < 0.00067). Neither the other HLA-DR genotypes nor the IL-1ra gene polymorphism had an influence on treatment outcome of budesonide therapy. No significant association of fistulas, perianal disease, need for bowel resections, and disease localization with certain HLA-DRB1 genotypes or the IL-1ra gene polymorphism were found. CONCLUSIONS: This is the first description of an association of a certain HLA-DR genotype (HLA-DR 8) with treatment failure in inflammatory bowel disease (IBD).

Adult↗
PubMed2001

Monocyte differentiation in intestine-like macrophage phenotype induced by epithelial cells.

Macrophages in normal colonic mucosa show a specific and distinct phenotype with low expression of the typical monocyte/macrophage surface antigens CD14, CD16, and CD11b and T-cell costimulatory molecules. A method for the in vitro induction of a macrophage phenotype similar to this intestinal phenotype is presented. Multicellular spheroids (MCSs) of intestinal epithelial cell (IEC) and control cell lines were cocultured with elutriated monocytes. Surface antigen expression was analyzed by immunohistochemistry and flow cytometry. Interleukin (IL)-1beta mRNA was measured by quantitative PCR. Monocytes adhered and infiltrated the MCSs within 24 h. In the MCSs of all IEC lines, the typical monocyte/macrophage surface antigens CD14, CD16, CD11b, and CD11c, which are detectable after 24 h of coculture by immunohistochemistry and flow cytometry, were down-regulated after 7 days (e.g., for CD14 at 24 h, expression was 86% of CD33+ cells; at day 7, it was 11%). A clear decrease of lipopolysaccharide (LPS)-stimulated IL-1beta transcription in monocytes cocultured with IEC MCSs could be observed during the 7-day period. For the first time an intestine-like macrophage-phenotype could be induced in vitro. Interactions with IECs play an essential role during this differentiation, which is of functional relevance, e.g., for LPS-induced cytokine secretion.

Antigens, CD↗
PubMed2000

[Pulmonary metastasis of extranodal high malignancy B-cell non-Hodgkin lymphoma of the bulbus duodeni and pylorus of the stomach].

We report a 71-year-old female patient with repeated vomitus, meteorism, epigastric pain and reflux for more than four month. She had a palpable mass in the upper abdomen and lost 7 kg of weight during the last four months. Chest X-ray showed two masses, 2 cm and 3 cm in diameter, in the left and right lower lung. A stenosing polypoid mucosal swelling in the antrum and the duodenal bulb. The pulmonal masses were biopsied under CT-guidance. Biopsy proved a high malignant B-cell non-Hodgkin's lymphoma of the stomach. The masses in the lung were identified as metastases of the gastrointestinal lymphoma. In conclusion on this tumor was an extranodal non-Hodgkin's lymphoma stadium BE IV according to Musshoff. A CHOP-chemotherapy was initiated. Restaging after three cycles of CHOP revealed a complete remission. Primary gastrointestinal non-Hodgkin's lymphomas are relatively rare neoplasms of the abdomen. Unusual and interesting in this case ist the metastatic pattern involving the lung periphery without local lymph node metastases.

Aged↗