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PubMed2006

Disease outcome of inflammatory bowel disease patients: general outline of a Europe-wide population-based 10-year clinical follow-up study.

OBJECTIVE: To give a general outline of a 10-year clinical follow-up study of a population-based European cohort of inflammatory bowel disease (IBD) patients and to present the first results in terms of clinical outcome parameters and risk factors. MATERIALS AND METHODS: A population-based cohort of newly, prospectively, diagnosed cases was initiated between 1991 and 1993. The 2201 patients with IBD (706 had Crohn's disease (CD), 1379 had ulcerative colitis (UC) and 116 had indeterminate colitis) originated from 20 different areas in 11 different European countries and Israel. For the 10-year follow-up of this cohort, electronic data-collecting instruments were made available through an Internet-based website. Data concerning vital status, disease activity, medication use, surgical events, cancer, pregnancy, fertility, quality of life and health-care costs were gathered. A blood sample was obtained from patients and controls to perform genotypic characterization. RESULTS: Thirteen centres from eight European countries and Israel participated. In 958 (316 CD and 642 UC) out of a total of 1505 IBD patients (64%) from these 13 centres, a complete dataset was obtained at follow-up. Even though an increased mortality risk was observed in CD patients 10 years after diagnosis, a benign disease course was observed in this patient group in terms of disease recurrence. A correlation between ASCA and CARD15 variants in CD patients and complicated disease course was observed. A north-south gradient was observed regarding colectomy rates in UC patients. Direct costs were found to be highest in the first year after diagnosis and greater in CD patients than in UC patients, with marked differences between participating countries. CONCLUSIONS: This 10-year clinical follow-up study of a population-based European cohort of IBD patients provides updated information on disease outcome of these patient groups.

Adult↗
PubMed1982

Chronic inflammatory bowel disease in patients with coeliac disease.

Six patients with coeliac disease and inflammatory bowel disease are described. Of special interest were two patients with coeliac disease and dermatitis herpetiformis and ulcerative colitis, one of whom also had sclerosing cholangitis. Three patients had both coeliac disease and ulcerative colitis, and one of them also had sclerosing cholangitis. In one patient with coeliac disease Crohn's disease of the small bowel was diagnosed. There seems to be association between coeliac disease without dermatitis herpetiformis, and ulcerative colitis. The possible combination of coeliac disease and inflammatory bowel disease deserves more attention than it has hitherto received.

Adult↗
PubMed1984

Search for evidence of a viral aetiology for inflammatory bowel disease.

The aetiology of the inflammatory bowel diseases. Crohn's disease, and ulcerative colitis, is still obscure. A viral aetiology has been proposed, based in part on reports that filtrates prepared from tissues of patients with inflammatory bowel disease induce cytopathic effects in tissue culture cells. Our attempts to culture viruses in many cell lines from filtrates prepared from the tissue of 95 patients have been negative, except for one case in which cytomegalovirus was isolated from the tissue of a Crohn's disease patient. Our studies confirm previous reports that intestinal tissue filtrates induce cytopathic effects in inoculated cell cultures, but the effect we observed is non-specific; cytopathic effects were induced in most cell lines tested and with similar frequency irrespective of whether the intestinal filtrates were prepared from Crohn's disease patients, ulcerative colitis patients, or non-inflammatory bowel disease controls. Electron microscopy studies of tissue culture cells exhibiting cytopathic effects have not revealed virus particles. Characterisation of the cytopathic effect inducing factor showed that it was incapable of serial passage in tissue culture, too small to be a conventional virus, resistant to inactivation by ultraviolet light, and heat stable. Our results suggest that the observed cytopathic effect was caused by a non-replicating cytotoxic factor, or factors, released from intestinal tissues of both inflammatory bowel disease and non-inflammatory bowel disease patients.

Animals↗
PubMed2006

New genes in inflammatory bowel disease: lessons for complex diseases?

The chronic inflammatory bowel diseases Crohn's disease and ulcerative colitis are common causes of gastrointestinal disease in northern Europe, affecting as many as one in 250 people. Although mortality is low, morbidity associated with these diseases is substantial. We review the recent advances in the genetics of inflammatory bowel disease, with particular emphasis on the data that have been generated since the discovery of the CARD15 (NOD2) gene in 2001.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2006

Correlated expression of high-sensitivity C-reactive protein in relation to disease activity in inflammatory bowel disease: lack of differences between Crohn's disease and ulcerative colitis.

BACKGROUND/AIMS: As opposed to regular C-reactive protein (CRP) assays, the introduction of high-sensitivity ones has enabled us to detect low grade inflammation in patients with inflammatory bowel disease (IBD). We addressed the subject of the degree of correlation between the concentration of high-sensitivity CRP (hs-CRP) and the inflammatory IBD activity score. METHODS: Included were 90 patients with Crohn's disease (CD), 70 with ulcerative colitis (UC) and 160 controls. Disease activity was determined using CD activity index (CDAI) for CD and Mayo score for UC. The Dade Boering BNII Nephelometer was used to determine the hs-CRP concentrations. RESULTS: The coefficient of correlation between hs-CRP and the disease activity score was similar for both UC (0.26) and CD (0.36). CONCLUSIONS: These findings are relevant for therapeutic intervention in which a greater absolute reduction in the hs-CRP concentration in CD patients (who generally present higher CRP concentrations than those found in UC) might be interpreted as a better response compared to the same absolute reduction in UC patients. This information is needed for clinicians using the hs-CRP assay to estimate IBD disease activity in daily practice.

Adult↗
PubMed1997

[Increased urea synthesis in patients with active inflammatory bowel disease].

Patients with active inflammatory bowel disease are often reported to be in negative nitrogen balance. Therefore, we examined basal and amino acid stimulated urea synthesis in 11 patients with active inflammatory bowel disease and in 10 patients with non-active disease. A primed continuous infusion of an amino acid mixture was given from t = 1 h to t = 5 h; during the first and the last two hours no amino acid infusion was given. Urea nitrogen synthesis rate was quantified independently of changes in blood amino acid concentration by means of the functional hepatic nitrogen clearance, i.e. the linear slope of the regression of urea nitrogen synthesis rate on blood amino acid concentration. Basal and amino acid stimulated urea nitrogen synthesis rate as well as functional hepatic nitrogen clearance were elevated twofold in the patients with active disease. No differences between the two groups were observed as regards basal or stimulated plasma glucagon, cortisol, catecholamines and serum levels of interleukin-1 alpha, interleukin-1 beta, tumor necrosis factor-alpha and interleukin-6. The results show that liver function related to conversion of amino-nitrogen to urea is increased and may contribute to the less efficient nitrogen economy in patients with active inflammatory bowel disease.

Adult↗
PubMed2004

[Inflammatory bowel diseases and lymphoma].

The aims of this review are to precise the incidence of non-Hodgkin's lymphoma and Hodgkin's disease in inflammatory bowel disease and to assess the relationship between immunosuppressive therapy and lymphoma in inflammatory bowel disease. Population-based data show that incidence of lymphoma is not increased in patients with Crohn's disease or ulcerative colitis. There is an increased incidence of non-Hodgkin's lymphoma in inflammatory bowel disease patients on immunosuppressive therapy but overall risk is low in all cohort studies. Relationship between immunosuppression and lymphoma in inflammatory bowel disease is confirmed by frequency of cerebral lymphoma and association with Epstein-Barr virus.

Epstein-Barr Virus Infections↗
PubMed1985

Nephrolithiasis in childhood inflammatory bowel disease.

Six children with inflammatory bowel disease and nephrolithiasis are reported. Their mean age at the passage of the first stone was 12.5 years and the mean duration of active inflammatory bowel disease was 34.5 months. Four had ulcerative colitis and two had Crohn's disease. In three patients, the onset of stone disease was associated with a flare in the bowel disease. Stone passage in four patients was accompanied by an increase in abdominal pain; three experienced gross hematuria. Stones from four of the patients were composed primarily of calcium phosphate; stones from the remaining patients contained uric acid and/or calcium oxalate. The pathogenesis of nephrolithiasis as it relates to inflammatory bowel disease is considered and an approach to therapy offered.

Adolescent↗
PubMed2000

Defining new pathogens and nonculturable infectious agents associated with inflammatory bowel disease.

The causes of inflammatory bowel disease remain uncertain, but increasing evidence supports roles for two pathogenic processes: genetic susceptibility in the host and an aberrant host response to enteric bacteria. Here, we review studies showing that the pathogenesis of inflammatory bowel disease involves both bacterial agents and genetic susceptibilities. We discuss the roles of known and novel commensal intestinal bacteria in the pathogenesis of inflammatory bowel disease and the various recombinant approaches used to identify these pathogens.

Journal Article↗
PubMed1995

Metabolic bone assessment in patients with inflammatory bowel disease.

BACKGROUND/AIMS: Patients with inflammatory bowel disease are at risk for osteopenia. To study the metabolic bone status of these patients, a cross-sectional study was conducted. METHODS: Eighty-four patients (49 women, 35 men) with inflammatory bowel disease, 34 of whom had Crohn's disease and 50 ulcerative colitis (including 18 with prior coloproctectomy and ileoanal anastomosis), underwent clinical, dietary, and spine radiological assessments. Bone metabolism was assessed by measuring serum levels of calcium, phosphate, parathyroid hormone (1-84), 25-hydroxyvitamin D3, 1,25-dihydroxyvitamin D3, and osteocalcin. Lumbar and femoral neck bone mineral densities were measured by dual energy X-ray absorptiometry. RESULTS: Serum osteocalcin level was decreased in 29 patients (34%), 12 of whom had never undergone steroid therapy. The other biochemical markers of bone metabolism were in the normal range. Thirty-six patients (43%) had osteopenia, and 6 patients (7%) had vertebral crush fractures. Osteopenia was observed in 27 patients (52%) and 9 patients (28%) with and without corticosteroid therapy, respectively. No patient had clinical or biological signs of osteomalacia. Analysis of bone density (lumbar Z score) by a multiple regression analysis showed a statistically significant correlation with age, cumulative corticosteroid doses, sedimentation rate, and osteocalcin level (R2 = 0.76; P = 0.05). CONCLUSIONS: The results suggest that bone turnover in inflammatory bowel disease is characterized by low bone formation in the presence of normal levels of calcium-regulating hormones.

Adolescent↗
PubMed1999

Metabolic bone disease in adults with inflammatory bowel disease.

Bone loss is seen frequently in those with inflammatory bowel disease (IBD). It appears to be more common in those with Crohn's disease than in those with ulcerative colitis. Corticosteroids play an important role in the development of osteoporosis. The prevalence of osteoporosis in IBD, the effects of corticosteroids on bone metabolism, and treatment options are reviewed.

Adult↗
PubMed2005

[Circumstances of the diagnosis and clinical course of inflammatory bowel disease].

The diagnosis of inflammatory bowel disease is sometimes difficult. The cardinal symptom of ulcerative colitis is bloody diarrhoea. The clinical characteristics of Crohn's disease are more heterogeneous, but typically include abdominal pain in the right lower quadrant, diarrhoea, weight loss and/or perianal disease. Extra intestinal (joint, cutaneaous and eye) manifestations can precede digestive symptoms and lead to the diagnosis of inflammatory bowel disease. The clinical course of these two diseases is unpredictable. The risk of colorectal cancer is significantly increased 8 years after diagnosis of pancolitis. Thus, regular surveillance by colonoscopy with random biopsies is recommended.

Colorectal Neoplasms↗
PubMedDate not supplied

Inflammatory bowel diseases: principles of nutritional therapy.

Inflammatory Bowel Diseases - ulcerative colitis and Crohn's disease- are chronic gastrointestinal inflammatory diseases of unknown etiology. Decreased oral intake, malabsorption, accelerated nutrient losses, increased requirements, and drug-nutrient interactions cause nutritional and functional deficiencies that require proper correction by nutritional therapy. The goals of the different forms of nutritional therapy are to correct nutritional disturbances and to modulate inflammatory response, thus influencing disease activity. Total parenteral nutrition has been used to correct and to prevent nutritional disturbances and to promote bowel rest during active disease, mainly in cases of digestive fistulae with high output. Its use should be reserved for patients who cannot tolerate enteral nutrition. Enteral nutrition is effective in inducing clinical remission in adults and promoting growth in children. Due to its low complication rate and lower costs, enteral nutrition should be preferred over total parenteral nutrition whenever possible. Both present equal effectiveness in primary therapy for remission of active Crohn's disease. Nutritional intervention may improve outcome in certain individuals; however, because of the costs and complications of such therapy, careful selection is warranted, especially in patients presumed to need total parenteral nutrition. Recent research has focused on the use of nutrients as primary treatment agents. Immunonutrition is an important therapeutic alternative in the management of inflammatory bowel diseases, modulating the inflammation and changing the eicosanoid synthesis profile. However, beneficial reported effects have yet to be translated into the clinical practice. The real efficacy of these and other nutrients (glutamine, short-chain fatty acids, antioxidants) still need further evaluation through prospective and randomized trials.

Colitis, Ulcerative↗
PubMed1995

Increased leucocyte adhesiveness/aggregation is a most useful indicator of disease activity in patients with inflammatory bowel disease.

The aim of the study was to determine the comparative usefulness of inflammatory markers, in evaluating disease activity in patients with inflammatory bowel disease. Disease activity was assessed by the Mayo Clinic score for ulcerative colitis, and Harvey-Bradshaw score for Crohn's disease. Five hundred normal blood donors who had no underlying inflammatory condition served as controls. The erythrocyte sedimentation rate, platelet and white blood cell count, C reactive protein, and the leucocyte adhesiveness/aggregation test (LAAT) were determined in each patient. One hundred and twenty four patients with inflammatory bowel disease were tested while in remission and 128 in relapse. Their mean (SD) per cent of aggregated white blood cells in the peripheral blood was 8 (5) and 17 (10) respectively compared with controls 6 (4) (p < 0.0001). Moreover, the LAAT could effectively discriminate between various grades of disease activity, the values in patients with active disease being 13 (6)% in mild, 17 (10)% in moderate, and 26 (10)% in severe disease (p < 0.0001). Other acute phase reactants including the erythrocyte sedimentation rate, the white blood cell count, the platelet count, neutrophil count, as well as, the C reactive protein concentration did not differentiate as well between the various groups. Using logistic regression analysis to differentiate between inflammatory bowel disease patients in remission or relapse, the LAAT was the single best indicator. The addition of any other test did not contribute to the discrimination. Among the different laboratory variables tested only the LAAT significantly discriminated between the five different subgroups of controls, remission and mild, moderate or severe disease activity.

Adolescent↗
PubMed2006

Toll-like receptor-1, -2, and -6 polymorphisms influence disease extension in inflammatory bowel diseases.

BACKGROUND: Evidence that a deficient innate immune response toward the bacterial flora of the gut plays a role in the pathogenesis of inflammatory bowel disease (IBD) is growing. This is underscored by the finding of the association between CARD15 variants and Crohn's disease (CD) and D299G in Toll-like receptor (TLR) 4 and IBD. Our aims were to study nonsynonymous polymorphisms in other TLR genes in IBD. METHODS: Thirty-five single nucleotide polymorphisms (SNP) in TLR1-10 were identified from public databases. 284 IBD parent-child trios and a second independent cohort of 285 IBD patients and 191 healthy controls were genotyped with polymerase chain reaction-restriction fragment length polymorphisms. Patients were pooled for genotype-phenotype analyses. RESULTS: Although none of the SNPs was involved in disease susceptibility, a number of variants influenced the disease phenotype. A positive association between TLR1 R80T and pancolitis in UC (P = .045, OR [95% CI] 2.844 [1.026-7.844]) was found. The TLR2 R753G SNP was also associated with pancolitis (P = .027, OR [95% CI] 4.741 [1.197-18.773]). The relative risks for heterozygous patients to develop pancolitis were 5.8 and 3.3 for R80T and R753G, respectively. There was a negative association between TLR6 S249P and ulcerative colitis with proctitis only (P = .026, OR [95% CI] 0.223 [0.096-0.705]). In CD, we found a negative association between ileal disease involvement and TLR1 S602I (P = .03, OR [95% CI] 0.522 [0.286-0.950]). CONCLUSION: TLR2 and its cofactors TLR1 and TLR6 are involved in the initial immune response to bacteria by recognizing peptidoglycan. An association between nonsynonymous variants in the TLR1, -2, and -6 genes and extensive colonic disease in UC and CD was found. Our findings further highlight the role of an abnormal innate immune response in the pathogenesis of IBD.

Adult↗
PubMed1996

Inflammatory bowel disease in children.

Pediatric inflammatory bowel disease is a complex area of pediatric gastrointestinal imaging. Multiple causative factors are discussed with emphasis upon disorders without known or presumed infectious etiology. Conditions discussed include Henoch-Schönlein purpura, Kawasaki disease, Behçet's disease, Crohn's disease, and ulcerative colitis with their respective clinical and radiological findings, differential diagnosis features, plus pertinent extraintestinal manifestations of inflammatory bowel disease.

Child↗
PubMed2006

Isotretinoin-induced inflammatory bowel disease.

Three case reports on inflammatory bowel disease associated with use of isotretinoin are described. All three patients were male adolescents, in good health when starting isotretinoin (for acne treatment for about six months). Several weeks after discontinuation of isotretinoin the patients developed severe symptoms requiring hospitalisation. The diagnosis of ulcerative colitis was made in two of these patients, while in the third patient Crohn's disease was diagnosed. Although inflammatory bowel disease is described as an adverse drug reaction in the product information of isotretinoin, few cases have been described so far. The link with prior isotretinoin use may not be recognised by the patient or the physician, since the diagnosis of inflammatory bowel disease is often preceded by several years of vague symptoms. On the other hand, spontaneous onset of inflammatory bowel disease (not related to isotretinoin) cannot be excluded. We appeal to the readers for a reaction to this, to shed more light on the likeliness of this alleged association.

Adolescent↗