Biomedical subjects

T Andus

Publications and source records attributed to T Andus.

At least 37 records · Page 2Linked to original sources

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↗

PubMed2000

Human intestinal epithelial cells secrete interleukin-1 receptor antagonist and interleukin-8 but not interleukin-1 or interleukin-6.

BACKGROUND: There is growing evidence that intestinal epithelial cells (IECs) are involved in the mucosal immune system. AIM: To assess the pattern of cytokines secreted by IECs and lamina propria mononuclear cells (LPMNCs). To achieve this, the expression and secretion of interleukin (IL)-1, IL-1 receptor antagonist (IL-1ra), IL-6, and IL-8 in human primary colonic and ileal IECs and LPMNCs from the same patient were studied. METHODS: IECs and LPMNCs were isolated from surgical specimens or endoscopic biopsy samples. mRNA expression was investigated by northern blot analysis. Secretion of IL-1beta, IL-6, IL-8, and IL-1ra was measured by enzyme linked immunosorbent assay. RESULTS: IL-1ra mRNA levels were higher in IECs than in LPMNCs in all probands. IL-8 mRNA was only present in low amounts in the IECs from two controls. In none of the specimens were IL-1beta and IL-6 mRNA present in IECs. Transcripts encoding IL-1beta, IL-1ra, IL-6, and IL-8 were identified in LPMNC preparations of all specimens. IECs from normal mucosa produced no detectable amounts of IL-1beta or IL-6, whereas LPMNCs did. IECs secreted some IL-8 (65 (9) pg/10(5) cells) but significantly more was generated by LPMNCs (408 (43) pg/10(5) cells, p<0.0001). However, IECs secreted more IL-1ra than did LPMNCs (120 (12) v 94 (11) pg/10(5) cells). In acute inflammation, IEC IL-1ra secretion was significantly increased. A correlation between secreted IL-1ra and the macroscopical degree of inflammation was found in Crohn's disease (r = 0.64, p<0.0001, n = 36) and ulcerative colitis (r = 0. 76, p<0.0001, n = 24). CONCLUSIONS: IECs from normal mucosa express and secrete IL-1ra and low amounts of IL-8, but no IL-1 or IL-6. In inflamed mucosa the secretion of IL-1ra by IECs is slightly increased but may be not sufficient to antagonise the greatly increased production of proinflammatory cytokines by LPMNCs and the IECs themselves.

Epithelial Cells↗

PubMed2000

Hormone replacement therapy and interrelation between serum interleukin-6 and body mass index in postmenopausal women: a population-based study.

Postmenopausal women are at increased risk to develop osteoporosis, coronary artery disease, heart failure, and hypertension. Interleukin-6 (IL-6) may be a pathogenetic element in these disorders. Serum IL-6 levels increase during aging and seem to be related to increased body fat mass. In the present retrospective study we aimed to investigate the role of hormone replacement therapy (HRT) on serum IL-6 levels and the interrelation of IL-6 and body fat mass. Parameters were assessed in a population-based sample of postmenopausal women (n = 302) and, for comparison, 245 men of the same age. Women with HRT (n = 92) had significantly lower serum IL-6 levels compared to subjects without HRT, which was independent of age, antihypertensive therapy, smoking habits, and blood pressure (1.5 +/- 0.1 vs. 2.9 +/- 0.6 pg/mL; P = 0.017). In women without HRT, the body mass index (BMI) was correlated with serum IL-6 levels (P < 0.001). Multivariate analysis controlling simultaneously for the effects of blood pressure and heart rate confirmed the positive correlation (P = 0.001). However, in subjects with HRT no such correlation between IL-6 and BMI was demonstrated, which was confirmed after controlling covariates. In male subjects, BMI correlated with serum IL-6 (P = 0.009), which was, however, blunted after controlling for blood pressure and heart rate, probably indicating an influence of the sympathetic nervous system on this interrelation. In conclusion, women receiving HRT display lower serum IL-6 levels and a blunted interrelation of IL-6 and BMI. As IL-6 may be a pathogenetic factor in age-related diseases, HRT-related inhibition of IL-6 secretion could be an important element for the favorable effects of HRT in postmenopausal women.

Aged↗

PubMed1999

[Imitation of an acute exacerbation of established systemic lupus erythematosus caused by parvovirus B19 infection].

HISTORY AND ADMISSION FINDINGS: A 26-year-old woman, for 3 years known to have systemic lupus erythematodes (SLE), was admitted because of fever, muscle and joint pains as well as nausea and vomiting. Maintenance therapy of 50 mg azathioprine, three times daily, had been stopped by the patient several weeks earlier. Physical examination was unremarkable except for pale skin and mucosae as well as pain on pressure over muscle groups of the upper arms and thighs and paravertebrally. DIAGNOSIS, TREATMENT AND COURSE: Laboratory tests showed a pancytopenia with a decrease of the haemoglobin level of 3.0 g/dl. The differential diagnosis included an acute exacerbation of SLE, toxic damage to the bone-marrow by azathioprine or a viral infection involving the bone-marrow. Serological tests and the further course confirmed an acute paravirus B19 infection as the cause. CONCLUSION: Paravirus B19 infection should be included in the differential diagnosis when an acute exacerbation of SLE is suspected.

Acute Disease↗

PubMed1999

Relation between dehydroepiandrosterone sulfate and blood pressure levels in a population-based sample.

Endogenous dehydroepiandrosterone sulfate (DHEAS) levels have been reported to be positively related to blood pressure levels. To further analyze this association, we quantified DHEAS in middle-aged subjects (mean age +/-SEM: 57.8+/-0.1 years) of a population-based sample (n = 646). DHEAS levels were higher in hypertensive as compared with normotensive individuals (1.26+/-0.04 v. 1.09+/-0.03 microg/mL, P = .01). After adjustment for age, gender, and body mass index, DHEAS levels were significantly related to systolic blood pressure (P = .01). In addition, in a subgroup of individuals without antihypertensive medication adjusted DHEAS levels were significantly related to systolic and diastolic blood pressure (n = 461; P<.05, both). DHEAS levels were also related to aldosterone (r = 0.15; P = .002) and androstenedione (its main metabolite; r = 0.66; P<.001) but not to renin levels. Like DHEAS, aldosterone, but not androstenedione, was significantly related to blood pressure levels and hypertension status. In a regression analysis that accounted for aldosterone and renin levels, both DHEAS and aldosterone kept their significant relationships with systolic blood pressure levels. Taken together, we observed a consistent positive association between endogenous DHEAS and systolic blood pressure levels that was independent of other, similarly regulated, adrenal steroids.

Aged↗

PubMed1999

Glucocorticoid receptors are down-regulated in inflamed colonic mucosa but not in peripheral blood mononuclear cells from patients with inflammatory bowel disease.

BACKGROUND: Growing evidence indicates that the immune system and the hypothalamic-pituitary-adrenal system are linked by several mechanisms, for example intracellular glucocorticoid receptors (hGR). Glucocorticoids are the standard treatment of acute attacks of inflammatory bowel disease (IBD). Binding of glucocorticoids to hGR down-regulates the transcription of inflammatory genes that can propagate IBD. PATIENTS AND METHODS: IBD patients were either treated with 5-60 mg of prednisolone for more than 1 week or were without glucocorticoid treatment for more than 4 weeks. hGR levels were determined from isolated cytosol of peripheral blood mononuclear cells (PBMCs) or mucosal biopsies using a radioassay with [3H]-dexamethasone. Interleukin (IL) 6 levels were determined by enzyme-linked immunosorbent assay (ELISA). RESULTS: The systemic (PBMC) hGR levels of corticosteroid-treated IBD patients were significantly lower than those of control subjects (59.6 +/- 57.1 dpm mg-1 cytosol protein vs. 227.0 +/- 90.8 dpm mg-1 cytosol protein, P = 0.007) and IBD patients not receiving glucocorticoid treatment (179.7 +/- 171.3 dpm mg-1 cytosol protein, P = 0.002). Systemic hGR levels in untreated IBD patients did not differ significantly from those in control subjects. In patients with connective tissue diseases, systemic hGR levels were also found to be decreased in the absence of glucocorticoid treatment. Systemic hGR levels in patients with Crohn's disease (CD) treated with steroids (66.6 +/- 61.0 dpm mg-1 cytosol protein) were not different from those in patients with ulcerative colitis (UC) (56.1 +/- 51.6 dpm mg-1 cytosol protein). In contrast to these findings, mucosal hGR levels were significantly decreased in both steroid-treated (18.0 +/- 15.5) and not steroid-treated (37.8 +/- 30.5) patients compared with control subjects (125.6 +/- 97.1; P = 0.00009 and P = 0.0008 respectively). IL-6 levels in all IBD groups with and without steroids were significantly different from those in control subjects. CONCLUSION: In IBD there is no difference in systemic hGR levels between not steroid-treated patients and control subjects, in spite of inflammatory activity (IL-6). Mucosal hGR levels were decreased independently of treatment, probably leading to a decreased protection against NF-kappaB action in the intestinal mucosa.

Binding, Competitive↗

PubMed1999

T-cell co-stimulatory molecules are upregulated on intestinal macrophages from inflammatory bowel disease mucosa.

BACKGROUND AND AIMS: Macrophages play an important role during mucosal inflammation in inflammatory bowel disease (IBD). As the co-stimulatory molecules B7-1 (CD80) and B7-2 (CD86) play an integral role in the activation of T cells by antigen-presenting cells (APC) we investigated the surface expression of B7-1 and B7-2 on colonic macrophages from normal and IBD mucosa. METHODS: Intestinal macrophages were isolated from biopsies of 13 control persons and 14 patients with IBD (seven with Crohn's disease (CD); and seven with ulcerative colitis (UC)). Cells were characterized by triple fluorescence flow cytometrical analysis using CD33 as macrophage marker. RESULTS: The expression of B7-1 (CD80) (9.2% +/- 4.2%) and B7-2 (CD86) (15.1% +/- 7.3%) was low on colonic macrophages from normal mucosa, indicating only a low antigen presenting potential. However, on macrophages from IBD colon there was a significant increase in the expression of co-stimulatory molecules (CD80, 33.8% +/- 8.9%, P = 0.00005 vs. control; CD86, 39.9% +/- 8.8%, P = 0.00002). There was no significant difference between CD and UC in the expression of CD80 (CD, 31.3% +/- 6.7%; UC, 34.4% +/- 13.3%) and CD86 (CD, 41.9% +/- 3.8%; UC, 35.6% +/- 13.8%). While in normal mucosa only 10.6% +/- 4.9% of the macrophages expressed CD14, more than 90% of the CD86/CD80 positive cells of the inflamed mucosa were positive for CD14. CONCLUSION: Colonic macrophages from normal mucosa rarely express the co-stimulatory molecules CD80 and CD86. In IBD a new macrophage population is found with high expression of co-stimulatory molecules presumably responsible for the perpetuated immune response.

Antigens, CD↗

PubMed1999

Lack of clinical efficacy of additional factor XIII treatment in patients with steroid refractory colitis. The Factor XIII Study Group.

Patients with active ulcerative colitis have decreased levels of factor XIII (FXIII) activity, which is important for woundhealing. Recent uncontrolled studies claimed a beneficial effect of Factor XIII on clinical symptoms of ulcerative colitis, in particular intestinal bleeding. The objective of this trial was to evaluate the benefits of additional FXIII treatment in steroid-refractory patients with ulcerative colitis in a prospective, double blind, placebo-controlled study. A total of 28 patients were enrolled between October 1994 and January 1997. Primary objective of this study was the time until cessation of visible intestinal bleeding with 14 days after the start of treatment. Patients were treated for ten days either by i.v. application of FXIII concentrate or by placebo. The analysis of the primary efficacy criterion, cessation of intestinal bleeding, by a planned interim analysis showed no significant differences between the treatment groups (p = 0.8). This resulted in the termination of the study. The same applied to the CAI score. No patient in both treatment groups reached remission according to the colo-/-sigmoidoscopy score. Due to the high number of patients (16 of 28) who had to be excluded from the per-protocol analysis (e.g. changes to the concomitant medication) only the intention-to-treat population was analyzed. Overall the study showed no beneficial effect of additional FXIII treatment on active steroid-refractory ulcerative colitis. These results do not confirm previous open label studies which had reported a significant improvement of clinical symptoms.

Adolescent↗

PubMed1998

[Initial symptoms, extra-intestinal manifestations and course of pregnancy in chronic inflammatory bowel diseases].

BACKGROUND: In many cases inflammatory bowel disease is accompanied by extraintestinal manifestations. This results in lowering of live quality. The aim of this study was to gather data retrospectively about initial symptoms, extraintestinal manifestations and course of pregnancy in a large unselected population with inflammatory bowel disease in South Germany. PATIENTS AND METHODS: Data from 1975 to 1989 (392 patients) were analyzed and partially compared with data from 1992 to 1995 (211 patients). RESULTS: Patients with Crohn's disease in average have been 25 years old at the time point of initial symptoms, whereas the age of ulcerative colitis patients was 30 years (p < 0.0001). The number of Crohn's disease patients with a long interval between initial symptoms and diagnosis (> 1 year) was significantly decreased in the second population (50% vs 38%; p < 0.05). Dominant initial symptoms in Crohn's disease were indisposition, abdominal pain and nonbloody diarrhea in contrast to ulcerative colitis which manifested mostly with bloody diarrhea. Extraintestinal manifestations occurred in 76% of patients with Crohn's disease and 64.6% with ulcerative colitis. Complications during the course of pregnancy have been detected in 40.5% in Crohn's disease and 60% in ulcerative colitis. CONCLUSION: A better knowledge of initial symptoms and extraintestinal manifestations in inflammatory bowel disease can help to decrease the interval between initial symptoms and the diagnosis. Pregnancy in patients with inflammatory bowel disease needs to be treated with special care.

Adolescent↗

PubMed1998

Cytokines in inflammatory bowel disease.

Cytokines play a central role in the modulation of the intestinal immune system. They are produced by lymphocytes (especially T cells of the Th1 and Th2 phenotypes), monocytes, intestinal macrophages, granulocytes, epithelial cells, endothelial cells, and fibroblasts. They have proinflammatory functions [interleukin-1 (IL-1), tumor necrosis factor (TNF), IL-6, IL-8, IL-12] or antiinflammatory functions [interleukin-1 receptor antagonist (IL-1ra), IL-4, IL-10, IL-11, transforming growth factor beta (TGF beta)]. Mucosal and systemic concentrations of many pro- and antiinflammatory cytokines are elevated in inflammatory bowel disease (IBD). An imbalance between proinflammatory and antiinflammatory cytokines was found for the IL-1/IL-1ra ratio in the inflamed mucosa of patients with Crohn's disease, ulcerative colitis, diverticulitis, and infectious colitis. Furthermore, the inhibition of proinflammatory cytokines and the supplementations with antiinflammatory cytokines reduced inflammation in animal models, such as the dextran sulfate colitis (DSS) model, the trinitrobenzene sulfonic acid (TNBS) model, or the genetically engineered model of IL-10 knockout mice. Based on these findings a rationale for cytokine treatment was defined. The first clinical trials using neutralizing monoclonal antibodies against TNF alpha (cA2) or the antiinflammatory cytokine IL-10 have shown promising results. However, many questions must be answered before cytokines can be considered standard therapy for IBD.

Animals↗

PubMed1998

Nuclear factor kappaB is activated in macrophages and epithelial cells of inflamed intestinal mucosa.

BACKGROUND & AIMS: Transcription factors of the nuclear factor kappaB (NF-kappaB) family play an important role in the regulation of genes involved in inflammation. In inflammatory bowel diseases, proinflammatory cytokines known to be regulated by NF-kappaB are involved. The aim of this study was to investigate the role of NF-kappaB activation during mucosal inflammation in situ. METHODS: A monoclonal antibody, alpha-p65mAb, was applied for immunofluorescence and immunohistochemical analysis that recognizes activated NF-kappaB. Electrophoretic mobility shift assay was used to directly demonstrate the presence of active DNA-binding NF-kappaB. RESULTS: Using the alpha-p65mAb antibody, activated NF-kappaB could be found in biopsy specimens from inflamed mucosa but was almost absent in uninflamed mucosa. The number of cells showing NF-kappaB activation correlated with the degree of mucosal inflammation but was not significantly different between inflamed mucosa from patients with Crohn's disease, ulcerative colitis, and nonspecific colitis or diverticulitis. NF-kappaB activation was localized in macrophages and in epithelial cells as identified by double-labeling techniques. Electrophoretic mobility shift assay with isolated lamina propria mononuclear cells and epithelial cells confirmed these results. CONCLUSIONS: This study shows for the first time the activation of NF-kappaB during human mucosal inflammation in situ. In addition to macrophages, epithelial cells contained activated NF-kappaB, indicating an involvement in the inflammatory process.

Adult↗

PubMed1998

Isolation and phenotypic characterization of colonic macrophages.

Macrophages play an important role in the intestinal mucosal immune system. However, they are a poorly defined cell population. We therefore determined their phenotype in normal colonic mucosa. Macrophages were isolated from colonic biopsies and surgical specimens by collagenase digestion. Colonic macrophages were positively sorted by anti-CD33 magnetic beads. Flow cytometric triple fluorescence analysis was applied to study CD14, CD16, CD33, CD44, CD11b, CD11c, CD64, HLA-DR, CD80, CD86 and CD3/CD19 expression. CD33 was evaluated as a positive marker for intestinal macrophages. CD33+ cells isolated from normal colonic mucosa showed co-expression of the established intracellular macrophage marker CD68 in FACS analysis. CD33+ cells were capable of phagocytosis. Isolation of this cell population by magnetic anti-CD33 beads and culture resulted in a 4.2-40-fold increase in IL-1beta and 4.5-44-fold increase in tumour necrosis factor-alpha (TNF-alpha) secretion compared with unsorted lamina propria mononuclear cells (LPMC). Of the CD33+ cells, 90.9 +/- 6.9% (mean +/- s.d.) were CD44+. However, macrophages from colonic mucosa showed only a low expression of CD14 (10.5 +/- 3.8%), CD16 (10.1 +/- 3.9%), HLA-DR (27.3 +/- 9.2%), CD11b (17.4 +/- 6.8%), CD11c (17.8 +/- 10.4%). Furthermore, expression of CD80 (9.2 +/- 4.2%) and CD86 (15.1 +/- 7.3%) was low, suggesting a low ability of normal intestinal macrophages to activate T cells and T cell-mediated immune responses. We conclude that CD33 is useful for the isolation and flow cytometric characterization of colonic macrophages. These cells exhibit a single phenotype in normal mucosa (CD33++, CD44++, CD14-, CD16-, CD11b-, CD11c-, HLA-DRlow, CD80-, CD86-) lacking lipopolysaccharide (LPS) receptor and costimulatory molecules.

Antigen-Presenting Cells↗

PubMed1998

Effect of programmed endoscopic follow-up examinations on the rebleeding rate of gastric or duodenal peptic ulcers treated by injection therapy: a prospective, randomized controlled trial.

BACKGROUND AND STUDY AIMS: A second-look endoscopy is often performed to evaluate the efficacy of a prior injection therapy in patients with bleeding peptic gastric or duodenal ulcers. Although this strategy is widely established, it does not rely on unequivocal data from controlled studies. In a prospective, randomized, controlled multicenter trial we assessed the effect of programmed endoscopic follow-up examinations with eventual retreatment on the outcome of bleeding ulcers in these patients. PATIENTS AND METHODS: One hundred and five patients with gastric or duodenal peptic ulcers presenting with active (Forrest type I) or recent (Forrest type IIa and IIb) bleeding upon endoscopy within four hours after admission were included in the study. Emergency treatment consisted of the sequential injection of both epinephrine (1:10,000 v/v) and up to 2 ml of fibrin/thrombin around the ulcer base. Fifty-two patients were randomized to receive programmed endoscopic monitoring with eventual retreatment in cases of Forrest type I, IIa, or IIb ulcers beginning within 16-24 hours after the index bleed. Follow-up endoscopies were continued until the macroscopic appearance revealed a Forrest type IIc or III ulcer. Fifty-three patients in the control group were closely monitored, and only received a second endoscopy when there was clinical or biochemical evidence of recurrent bleeding. The groups did not differ with respect to age, sex, site and severity of bleeding. RESULTS: The numbers of patients with recurrent bleeding were similar whether they were endoscopically monitored or not (21% versus 17%, P=0.80 chi-squared test). In addition, there was no statistically significant difference between the two groups with respect to the number of blood units transfused, need for surgical intervention, hospital stay or number of deaths (Mann-Whitney U-test). Improving local ulcer stigmata was not related to a better outcome. CONCLUSIONS: Programmed endoscopic follow-up examinations with eventual retreatment in patients locally injected for an acute or recent hemorrhage from a gastric or duodenal ulcer did not influence their outcome when compared to patients receiving only a second endoscopic intervention upon evidence for recurrent hemorrhage. Scheduled control endoscopies cannot be recommended after an initial successful endoscopic treatment of peptic ulcer bleeding when selection of the patients for second-look endoscopy is directed by the Forrest criteria.

Aged↗

PubMed1998

The accuracy of abdominal ultrasound in the assessment of bowel disorders.

BACKGROUND: Little is known about the sensitivity, specificity, and predictive values of transabdominal ultrasonographic (US) findings in a teaching hospital setting. METHODS: We carried out a prospective study including 227 patients with symptoms suggestive of inflammatory bowel disorder. The Picker 9200 CS equipment (5-mHz curved-array probe) was used to obtain bowel images. Gastrointestinal endoscopy, enteroclysis, bowel enema, computed tomography scan, or bowel surgery was used as reference. RESULTS: Of 227 patients, 168 had pathologic findings of the bowel as final diagnosis. The overall sensitivity of US was 76%, whereas the positive predictive value was 98%. Overall specificity was 95%. The negative predictive value for bowel disorders was only 58%, since US missed pathologic findings in 48 patients. Subgroup analysis showed a sensitivity of 84% for Crohn's disease, 66% for ulcerative colitis, 46% for bowel tumors, and 60% for diverticulitis. Topographic comparisons showed that US detected inflammatory bowel-wall alterations preferentially in the terminal ileum and colon, whereas abnormalities in the duodenum, jejunum, and rectum were frequently missed (sensitivity, 10%-20%). CONCLUSIONS: Positive US findings are useful for the diagnosis of bowel processes. US is highly predictive albeit not disease-specific. Negative US examinations, however, do not exclude pathologic bowel processes. A topographic location of pathologic US findings is mostly confined to the colon.

Adult↗

PubMed1998

Association of humoral markers of inflammation and dehydroepiandrosterone sulfate or cortisol serum levels in patients with chronic inflammatory bowel disease.

OBJECTIVES: Dehydroepiandrosterone sulfate (DHEAS) and cortisol are multifunctional adrenal hormones with immunomodulating properties. DHEAS levels were found to be very low in chronic inflammatory diseases. This study aimed to shed more light on the interrelation between DHEAS and cortisol (and humoral markers of inflammation) in chronic inflammatory bowel disease. METHODS: DHEAS and cortisol serum levels were measured by ELISA in the serum of 66 normal subjects, 115 patients with Crohn's disease (CD) and 64 patients with ulcerative colitis (UC). Humoral markers of inflammation and disease activity scores were assessed by standard techniques. RESULTS: DHEAS was lower in patients with CD (p < 0.005) and UC (p < 0.005) than in controls, which was, in part, dependent on previous corticosteroid treatment (p < 0.01). In CD patients, z-normalized DHEAS was inversely correlated with blood sedimentation rate (p = 0.017). Z-normalized DHEAS was negatively correlated with interleukin-6 (IL-6) in the form of a trend (p = 0.068), and z-normalized DHEAS was significantly positively correlated with hemoglobin (p = 0.001) but not with the Crohn's disease activity index. Cortisol, however, was positively correlated with blood sedimentation rate (p = 0.034) and C-reactive protein (p = 0.006). In contrast, in UC patients no such correlation of z-normalized DHEAS or cortisol and parameters of humoral inflammatory activity or Rachmilewitz index exist. CONCLUSIONS: DHEAS as a marker of inflammation was low in CD and UC. In CD patients, low DHEAS and high cortisol serum levels were associated with higher humoral inflammatory activity. With respect to humoral inflammatory activity in CD patients, DHEAS and cortisol seem to be inversely regulated, which may have an impact on several immune functions, such as IL-6 secretion.

Adolescent↗

PubMed1998

Low dose oral pH modified release budesonide for maintenance of steroid induced remission in Crohn's disease. The Budesonide Study Group.

BACKGROUND: The relapse rate after steroid induced remission in Crohn's disease is high. AIMS: To test whether oral pH modified release budesonide (3 x 1 mg/day) reduces the relapse rate and to identify patient subgroups with an increased risk of relapse. METHODS: In a multicentre, randomised, double blind study, 179 patients with steroid induced remission of Crohn's disease received either 3 x 1 mg budesonide (n = 84) or placebo (n = 95) for one year. The primary study aim was the maintenance of remission of Crohn's disease for one year. RESULTS: Patient characteristics at study entry were similar for both groups. The relapse rate was 67% (56/84) in the budesonide group and 65% (62/95) in the placebo group. The relapse curves in both groups were similar. The mean time to relapse was 93.5 days in the budesonide group and 67.0 days in the placebo group. No prognostic factors allowing prediction of an increased risk for relapse or definition of patient subgroups who derived benefit from low dose budesonide were found. Drug related side effects were mild and no different between the budesonide and the placebo group. CONCLUSION: Oral pH modified release budesonide at a dose of 3 x 1 mg/day is not effective for maintaining steroid induced remission in Crohn's disease.

Administration, Oral↗

PubMed1998

[Standards, perspectives and limits of conservative therapy of chronic inflammatory bowel diseases].

Improvement and standardization of the conservative therapy of inflammatory bowel disease has lead to a better prognosis for the patients. During the acute flare of Crohn's disease steroids are still the standard therapy, whereas 5-aminosalicylic acid (5-ASA) preparations are used for maintenance therapy during remission. In contrast ulcerative colitis may be treated with 5-ASA also for acute exacerbations. The development of new drugs as for example the topical steroids helps to improve life quality of the patients by reducing adverse side effects. Potent immunosuppressants as azathioprine and methotrexate are useful in chronic active and refractory disease. Cyclosporin A plays a role in severe steroid refractory colitis. In the future immunomodulation by application of antiinflammatory cytokines or antibodies to inflammatory cytokines may have its place in the treatment of IBD patients. In some cases, however, the conservative therapy reaches its limits. Mistakes in the therapy are made, when these limits are not recognized and complications are not discovered in time.

Anti-Inflammatory Agents↗