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At least 1,063 records · Page 59Linked to original sources
PubMed2005

Glutamine-enriched total parenteral nutrition in patients with inflammatory bowel disease.

BACKGROUND: Studies in animal models of inflammatory bowel disease (IBD) suggest that supplementation of total parenteral nutrition with glutamine (gln), a conditionally essential amino acid in catabolic conditions, increases gln plasma concentrations, reduces intestinal damage, improves nitrogen balance and may improve the course of the disease. However, human data supporting this assumption are missing. METHODS: A total of 24 consecutive patients with an acute exacerbation of IBD (19 Crohn's disease; five ulcerative colitis) and scheduled for total parenteral nutrition (TPN) (>7 days) were randomised. Parallel to a standardised anti-inflammatory therapy, the patients received either a TPN with 1.5 g/kg body weight of a standard amino acid or an isonitrogenic, isocaloric TPN with 1.2 g/kg body weight of a standard amino acid and 0.3 g/kg L-alanine-L-glutamine. Primary end points were gln plasma concentrations and intestinal permeability assessed by urinary lactulose and D-xylose ratio. RESULTS: Gln plasma levels did not differ significantly in either group throughout the study. Intestinal permeability did not change within 7 days either with or without gln supplementation (Delta-lactulose/xylose ratio: 0.01+/-0.05 (gln+) vs 0.02+/-0.1 (gln-)). The observed changes in inflammatory and nutritional parameters, and also disease activity, length of TPN and hospital stay, were independent of glutamine substitution. Five (41%) patients in the gln+ group and three (25%) patients in the gln- group needed surgical intervention. CONCLUSION: Although limited by the sample size, these results do not support the hypothesis that glutamine substitution has an obvious biochemical or clinical benefit in patients with active IBD scheduled for total parenteral nutrition.

Acute Disease↗
PubMed2002

[Biological therapies for treatment of chronic inflammatory bowel diseases. Status update].

BACKGROUND: For the treatment of inflammatory bowel diseases in recent years several antibodies, cytokines and antisense oligonucleotides have been developed using recombinant technology and were tested as so-called "biological therapeutics". EFFECTIVENESS OF BIOLOGICAL THERAPEUTICS: Infliximab, a chimeric TNF-alpha antibody, is the only biological remedy approved for the treatment of refractory and fistulizing Crohn's disease. Because of inherent risks for severe side effects, such as sepsis, the indication should be restricted to truly refractory patients and treated patients must be followed very carefully. In clinical trials other anti-TNF-alpha-effective substances (CDP 571, etanercept, thalidomide), interleukin-10, interleukin-11, ICAM-1-antisense-oligonucleotides and antibodies against alpha 4-integrin were evaluated for the treatment of Crohn's disease. In summary, for all a slight effect was noted but their place in the therapeutical repertoire is not yet defined. None of these substances is approved for patients with inflammatory bowel disease. Future developments are eagerly awaited.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1998

Drug therapy: dose-response relationship of oral mesalazine in inflammatory bowel disease.

Mesalazine is widely used in the treatment of inflammatory bowel disease. Little is known about the dose-response relationship and about possible dose related side effects. In ulcerative colitis higher dosages of mesalazine (3 g) are more effective in maintaining a remission than lower dosages (1.5 g). In mild to moderately active ulcerative colitis, studies also indicate that higher dosages might be more effective in inducing remission. Dose-comparing studies in Crohn's disease are even more sparse, but the available results indicate higher efficacy at higher dose levels. None of the known side effects of mesalazine are clearly dose-related. A pH-dependent release system, however, can cause a sudden release of high doses of mesalazine. Consequent peak levels in serum have been implicated in mesalazine induced nephrotoxicity. In conclusion, despite the current practice of using increasing dosages of mesalazine in inflammatory bowel disease, both efficacy and safety have been established tentatively.

Administration, Oral↗
PubMed1986

[Roentgen diagnosis of inflammatory bowel diseases in the child].

Inflammatory diseases of the bowel, especially of the small bowel, frequently present with vague symptoms in children. In many cases X-ray examination enables diagnosis, differentiation and localization of such diseases, as well as follow up and detection of complications. In the hand of the experienced radiologist the exposure to X-rays is very low. Radiological signs are demonstrated according to the most important inflammatory disease entities.

Child↗
PubMed1973

Circulating carcinoembryonic antigen (CEA): relationship to clinical status of patients with inflammatory bowel disease.

Plasma levels of circulating carcinoembryonic antigen (CEA) were measured by zirconyl phosphate gel radioimmunoassay in 112 patients with chronic inflammatory bowel disease. The levels were then related to category, extent, duration, and severity of disease, as well as to the ages and surgical status of the patients. The distribution of CEA levels and their mean values were significantly raised over the levels in 33 normal control subjects, and were similar among patients with ulcerative colitis compared with those with granulomatous bowel disease. Positive values were defined as those in excess of 2.5 ng/ml. Positive assays occurred in 42% of ulcerative colitis patients, in 38% of Crohn's disease patients, and in 40% of the total group with inflammatory bowel disease. Among normal control subjects, only 3% were positive. Among inflammatory bowel disease patients, positive CEA assays occurred more frequently with more severe disease, more extensive anatomical involvement, younger ages, and shorter duration of disease. Those patients who had undergone total colectomy showed levels of circulating CEA and frequency of CEA positivity similar to those of an age-matched normal control group. Levels of CEA did not correspond with known cancer risk factors in patients with inflammatory bowel disease. Although rising or persisting plasma CEA values unrelated to severity and extent of disease may indicate an unfavourable prognosis in cancer, this study shows that a single CEA value in patients with chronic inflammatory bowel disease is not a reliable indicator of cancer risk.

Age Factors↗
PubMed1994

Cyclosporine and 6-mercaptopurine in pediatric inflammatory bowel disease.

After failure of medical therapy, children with refractory inflammatory bowel disease may require surgical intervention. In this article the authors describe one child in whom, after traditional therapies for refractory ulcerative colitis failed, full remission of the disease occurred after the addition of 6-mercaptopurine and cyclosporine A to her medical regimen. 6-Mercaptopurine has been used with increasing frequency in refractory inflammatory bowel disease; the use of cyclosporine A for this condition is still under investigation.

Child↗
PubMed1999

Clinical applications of technetium Tc 99m hexamethyl propylene amine oxime leukocyte scan in children with inflammatory bowel disease.

BACKGROUND: Labeled leukocyte imaging is a helpful diagnostic tool in the detection of inflammation and sepsis. The technetium Tc 99m hexamethyl propylene amine oxime (99mTc HMPAO)-labeled leukocyte scan has been found to be more sensitive than the Indium-111 labeled leukocyte scan in detecting inflammatory bowel disease, with reported sensitivities of 95% to 100%. Experience with the 99mTc HMPAO-labeled leukocyte scan was examined and its clinical applications evaluated in the immediate treatment of patients with inflammatory bowel disease. METHODS: A retrospective chart review was undertaken that included pediatric patients who underwent 99mTc HMPAO-labeled leukocyte scan at the James Whitcomb Riley Hospital for Children. The disease activity of patients with inflammatory bowel disease was assessed. The leukocyte scan was performed according to the manufacturer's specifications, and images were obtained 30 minutes and 2 hours after administration of the radiopharmaceutical. RESULTS: During the period of July 1996 through November 1997, 41 scans were performed in 35 patients. Twenty-nine patients had histologically proven inflammatory bowel disease: 24 with Crohn's disease, 4 with ulcerative colitis, and 1 with indeterminate colitis. Active inflammatory bowel disease was suspected in 24 patients when the leukocyte scan was performed. Twenty of the 24 patients (83% sensitivity) had abnormal findings in leukocyte scans that prompted more aggressive management in 15 (75%). Six of the 15 who were receiving maximum medical therapy underwent surgical resection of severely affected bowel segments, and medical treatment was intensified in the other 9. The remaining 5 patients were receiving optimal medical therapy, instituted at their recent visit, and did not require further medication adjustments. Four of the 24 patients with active inflammatory bowel disease had normal leukocyte scans (17% false-negative rate), 3 of whom were receiving corticosteroid therapy at the time the scans were performed. All of the 11 patients in whom inflammatory bowel disease was in remission and 6 patients who did not have inflammatory bowel disease had normal findings in leukocyte scans (100% specificity). CONCLUSIONS: Although a tissue diagnosis is still recommended, obtained during upper and lower gastrointestinal endoscopic examinations, and contrast radiography of the small bowel for the initial work-up of patients with suspected inflammatory bowel disease, the 99mTc HMPAO-labeled leukocyte scan is a safe and useful diagnostic adjunct for subsequent evaluation of patients known to have inflammatory bowel disease. The results of 99mTc HMPAO-labeled leukocyte scans directly influenced treatment of 75% of the study patients with active inflammatory bowel disease, which included the decision to refer patients for surgical intervention.

Adolescent↗
PubMed1994

Hepatobiliary manifestations of inflammatory bowel disease.

Several hepatobiliary disorders may be associated with inflammatory bowel disease (IBD). These various disease states can be diagnosed before, concomitant with, or after the diagnosis of IBD is made. This article describes these disorders, clinical features, evaluation, and possible treatment.

Biliary Tract Diseases↗
PubMed2004

[Nutrition and dietary treatment of chronic inflammatory bowel disease].

The relationships between nutrition and chronic inflammatory bowel disease (CIBD) range from a possible involvement in the etiopathogenesis of the disease to dietary intervention in the various disease stages. CIBDs are often associated with dietary depletion. Prevention and treatment of malnutrition are therefore obligatory elements of therapy. The following stepped dietary treatment strategy applies: dietary counseling, supplementary dietary drinks, feeding via a stomach tube, parenteral alimentation. In the case of uncomplicated CIBD, an adequate and balanced diet (light full diet) is the goal. In the event of malnutrition, during an acute attack, and when complications occur, the diet must be adapted accordingly. Total parenteral alimentation is, per se, more likely to be associated with complications, is more expensive that enteral alimentation, and is thus reserved for specific indications.

Adult↗
PubMed1986

Protein metabolism in inflammatory bowel disease.

Major loss of body protein mass in inflammatory bowel disease is much less common than weight loss, which is often attributable to losses of other body, particularly water and fat. It does occur, however, in a few patients, especially in those with compromised food intake. It is due principally to the combined effects of diminished intake and excessive intestinal losses of amino nitrogen. Nitrogen metabolism is influenced not only by protein nutritional state and net nitrogen intake but also by disease activity. There is some evidence for abnormally low secretion of growth hormone in adolescents with inflammatory bowel disease and growth failure. Low serum albumin concentrations are not necessarily related to protein undernutrition and are the combined result of relatively reduced albumin synthesis, increased intestinal losses, and maldistribution between intravascular and extravascular spaces. Concentrations in the plasma of IgG and acute phase reactants may be raised despite increased losses into the bowel lumen. The prevention of total body protein depletion is achieved principally by maintaining adequate and often not supranormal intakes of a balanced source of amino nitrogen in a balanced diet given orally, enterally, or parenterally, combined with a medical or surgical approach to reduce disease activity: supranormal energy intakes are not beneficial.

Adolescent↗
PubMed2003

Oral signs and symptoms in relation to disease activity and site of involvement in patients with inflammatory bowel disease.

OBJECTIVE: An assessment of oral symptoms and signs in patients with inflammatory bowel disease (IBD). METHODS: Fifty-four patients with IBD, 34 with Crohn's disease (CD) and 20 with ulcerative colitis (UC) participated in the study. Forty-two patients without gastrointestinal disease or complaints attending the orthopedic clinic served as controls. Each patient completed a written questionnaire and was subjected to an oral examination. RESULTS: The main findings of this study were the higher prevalence of halitosis (50% vs 10% P < 0.0008), nausea (30% vs 7%, P < 0.017) and reflux (regurgitation) (45% vs 17%, P < 0.017) in patients with UC, and nausea (50% vs 7%, P < 0.026), dry mouth and halitosis (29% vs 10%, P < 0.026) and vomiting (41% vs 5%, P = 0.01) in patients with CD, compared with controls. Patients with active CD had a higher prevalence of dry mouth, nausea and vomiting compared with controls (46, 69 and 54% vs 10, 7 and 5%, respectively, P < 0.001) and of reflux compared with non-active CD (46% vs 5%, P < 0.001). Patients with active UC had a higher prevalence of halitosis and regurgitation (50 and 60% vs 10 and 17%, P < 0.001) compared with controls. CONCLUSIONS: The present study demonstrates increased frequency of oral signs and symptoms in patients with IBD. Patients with active CD had more oral signs compared with non-active CD patients. Manifestations such as nausea, vomiting, regurgitation and dry mouth may have detrimental effects on teeth and soft tissues of the oral cavity. Communication between gastroenterologists and dentists is imperative for success of the overall treatment of their patients.

Adult↗
PubMed2005

Systemic administration of the chemokine macrophage inflammatory protein 1alpha exacerbates inflammatory bowel disease in a mouse model.

INTRODUCTION: Exacerbations of inflammatory bowel disease are thought to be related to concurrent infections. As infections are associated with elevated local and serum concentrations of chemokines, we have determined whether systemic administration of the CC chemokine macrophage inflammatory protein 1alpha (MIP-1alpha) exacerbates colitis in a mouse model. METHODS: Colitis was induced in Balb/c mice using trinitrobenzene sulfonic acid (TNBS). Starting four days later, animals received daily intraperitoneal injections of recombinant MIP-1alpha. On day 7, mice were killed and pieces of colon taken for immunohistology and polymerase chain reaction analysis. The direct effects of MIP-1alpha on mucosal T cells and fibroblasts in vitro were also investigated. RESULTS: Systemic administration of MIP-1alpha markedly enhanced colitis with mice developing large transmural ulcers filled with granulation tissue. Treatment resulted in increased numbers of CD4 cells infiltrating the colonic lamina propria, increased interferon gamma (IFN-gamma) levels, and increased transcripts for tumour necrosis factor alpha (TNF-alpha) and matrix metalloproteinase 3 (MMP3). Isolated lamina propria lymphocytes from mice with TNBS colitis contained increased numbers of IFN-gamma and TNF-alpha transcripts when stimulated with MIP-1alpha in vitro. Colonic lamina propria fibroblasts also responded to MIP-1alpha with increased proliferation and decreased collagen 1 synthesis but fibroblast proliferation was not seen in vivo. CONCLUSIONS: These experiments show that increasing serum concentrations of a chemokine, MIP-1alpha, exacerbates immune mediated colitis. The effect seems to be due to the ability of MIP-1alpha to boost Th1 responses in the gut wall. Our findings also suggest a potential pathway by which peripheral infections can exacerbate inflammatory bowel disease.

Animals↗
PubMed1998

Bone mineral density and nutritional status in children with chronic inflammatory bowel disease.

BACKGROUND: Osteoporosis has been reported in adult patients with inflammatory bowel disease. AIMS: To evaluate bone mineral density (BMD), nutritional status, and determinants of BMD in children with inflammatory bowel disease. PATIENTS: Fifty five patients (34 boys and 21 girls, age range 4-18) were studied; 22 had Crohn's disease and 33 ulcerative colitis. METHODS: Lumbar spine and total body BMD, and body composition were assessed by dual energy x ray absorptiometry (DXA). Results were expressed as standard deviation scores (SDS). Lean body mass was also assessed by bioelectrical impedance analysis (BIA). Yearly measurements during two years were performed in 21 patients. RESULTS: The mean SDS of lumbar spine BMD and total body BMD were significantly lower than normal (-0.75 and -0.95, both p < 0.001). Height SDS and body mass index SDS were also decreased. The decrease in BMD SDS could not be explained by delay in bone maturation. The cumulative dose of prednisolone correlated negatively with lumbar spine BMD SDS (r = -0.32, p < 0.02). Body mass index SDS correlated positively with total body BMD SDS (r = 0.36, p < 0.02). Patients with Crohn's disease had significantly lower lumbar spine and total body BMD SDS than patients with ulcerative colitis, even after adjustment for cumulative dose of prednisolone. In the longitudinal data cumulative dose of prednisolone between the measurements correlated negatively with the change in lumbar spine and total body BMD SDS. Lean tissue mass measured by DXA had a strong correlation with lean body mass measured by BIA (r = 0.98). CONCLUSIONS: Children with inflammatory bowel disease have a decreased BMD. Children with Crohn's disease have a higher risk of developing osteopaenia than children with ulcerative colitis. Corticosteroid therapy and nutritional status are important determinants of BMD in these patients.

Absorptiometry, Photon↗
PubMed2000

Clinical features of inflammatory bowel disease.

The purpose of this review is to highlight new developments during the past year regarding diagnosis and clinical features of inflammatory bowel disease. Endoscopy remains the cornerstone for diagnosis and evaluation of ileocolonic inflammatory bowel disease. In ulcerative colitis, recent studies have challenged the concept of a continuous and homogeneous inflammatory process with constant rectal involvement: patchy inflammation and rectal sparing were reported in treated ulcerative colitis, and frequent cecum and appendiceal orifice skip lesions were confirmed. Cross-sectional imaging techniques usefully complement endoscopy by assessing whole-bowel thickness and detecting abscesses and fistulae. Furthermore, echo Doppler ultrasound is able to measure mesenteric blood flow, which is increased in active inflammatory bowel disease and seems to parallel inflammatory disease activity. Osteopenia, which affects approximately half of patients with inflammatory bowel disease, can be detected by dual-energy x-ray absorptiometry and prevented. Hyperhomocysteinemia, a predisposing factor for thrombosis, seems to be more frequent in inflammatory bowel disease, and can be corrected by folate supplementation. The concept of an aggressive, penetrating form of Crohn disease with early postoperative recurrence as opposed to a more indolent, nonpenetrating form of the disease, with later recurrence, was recently challenged. The most significant predictor of the risk of malignancy in inflammatory bowel disease remains the presence of dysplasia in colonic biopsy specimens. A dysplastic polypoid lesion or mass is a strong predictor of cancer but should be distinguished from the dysplasia inherent in a coincident sporadic adenoma.

Journal Article↗
PubMed1997

Cytokine gene deleted mice in the study of gastrointestinal inflammation.

The major experimental and intellectual advance in gastroenterology in recent years has been the observation that mice with deletions in specific cytokine genes develop a spontaneous inflammatory bowel disease. Inflammatory bowel disease has also been seen in a number of other mouse strains with perturbed immune responses. The driving force for disease in a number of these models is the normal bacterial flora. These studies show that the gut immune system is in homeostasis with the antigens of the flora, but inappropriate T-helper 1 (Th1)-type responses to the flora cause severe gut injury and since the antigenic stimulus persists, the consequence is chronic inflammation.

Animals↗
PubMed1991

Geographic variation of inflammatory bowel disease within the United States.

One approach to learn about possible environmental risks in inflammatory bowel disease relates to studying its geographic pattern of occurrence. The geographic variation of inflammatory bowel disease within the United States was analyzed using the accumulated 17.5 million hospital discharges of all U.S. Medicare beneficiaries during two consecutive years. To validate the geographic pattern shown by the Medicare data, hospitalization was compared with mortality from inflammatory bowel disease among different states. Mortality and hospitalization statistics both suggested that the occurrence of inflammatory bowel disease was determined by environmental factors that had a marked geographic variation within the United States. Both Crohn's disease and ulcerative colitis appeared to be more frequent in northern parts of the United States than in southern and in urban more than rural parts. These trends were observed for men and women and for blacks and whites alike. Similar geographic patterns of Crohn's disease and ulcerative colitis suggested the influence of one or more identical risk factors for both diseases.

Aged↗
PubMed2001

Inflammatory bowel disease is not associated with an increased risk of lymphoma.

BACKGROUND & AIMS: Previous studies of the risk of lymphoma in inflammatory bowel disease patients have provided conflicting results. This study examines the risk of Hodgkin's and non-Hodgkin's lymphoma among patients with inflammatory bowel disease. METHODS: The authors performed a retrospective cohort study using the General Practice Research Database. Inflammatory bowel disease patients were matched to randomly selected controls on age, sex, and primary care practice. Lymphoma rates were also compared with published age- and sex-specific rates. RESULTS: The study included 6605 patients with Crohn's disease, 10,391 with ulcerative colitis, and 60,506 controls followed for an average of 3.7, 3.9, and 4.4 years, respectively. The incidence of lymphoma was not increased in patients with inflammatory bowel disease (relative risk = 1.20; 95% CI, 0.67-2.06). In subgroup analyses, an increased risk was not observed among patients with Crohn's disease (relative risk = 1.39; 95% CI, 0.50-3.40) or ulcerative colitis (relative risk = 1.11; 95% CI, 0.51-2.19). Compared with inflammatory bowel disease patients not treated with azathioprine or 6-MP, the relative risk of lymphoma among the 1465 inflammatory bowel disease patients treated with these medications (average, 106 mg/day for 2.0 years) was 1.27 (95% CI 0.03-8.20). CONCLUSIONS: Patients with inflammatory bowel disease do not have an increased risk of lymphoma as compared with the general population. Although we cannot completely rule out a modest increased risk of lymphoma with azathioprine or 6-MP therapy, an increased risk was not observed in this cohort.

Adult↗