References of "Gastroenterology"
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See detailGenetic markers and the risk of complicated disease behaviour in Crohn's disease patients
Henckaerts, L.; Verstreken, I.; Van Steen, Kristel ULg et al

in Gastroenterology (2007), 132(4), 17-18

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See detailMixed IBD families: A distinct entity within IBD
Pierik, M.; Van Steen, Kristel ULg; Joossens, M. et al

in Gastroenterology (2007), 132(4), 450-450

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See detailGene expression profiling to predict the response of infliximab in patients with UC
Arijs, Ingrid; Van lommel, Leertje; Van Steen, Kristel ULg et al

in Gastroenterology (2007), 132(4), 174-174

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See detailFaecal bacterial dgge profiles of Crohn's disease patients are different from those of their healthy first degree relatives and matched healthy controls
Joossens, M.; Vanhoutte, T.; De Preter, V. et al

in Gastroenterology (2007), 132(4), 704-704

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See detailTransmission of CARD15 (NOD2) variants in families with Crohns disease
Vermeire, S.; Esters, N.; Pierik, M. et al

in Gastroenterology (2003), 124(4 (Suppl I)), 368

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See detailThe value of serologic markers in indeterminate colitis: A prospective follow-up study - Reply
Joossens, S.; Van Steen, Kristel ULg; Vermeire, S. V. et al

in Gastroenterology (2003), 125(3), 999-1000

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See detailAutoimmunity associated with anti-tumor necrosis factor alpha treatment in Crohn's disease: A prospective cohort study
Vermeire, S.; Noman, M.; Van Assche, G. et al

in Gastroenterology (2003), 125(1), 32-39

Background & Aims: Infliximab therapy is an effective approach to treating Crohn's disease. Development of antinuclear antibodies has been described in patients treated, but the size of the problem and ... [more ▼]

Background & Aims: Infliximab therapy is an effective approach to treating Crohn's disease. Development of antinuclear antibodies has been described in patients treated, but the size of the problem and the relationship with autoimmunity have not been investigated. We investigated the occurrence of antinuclear antibodies in 125 consecutive Crohn's disease patients and studied the relationship with symptoms of autoimmunity. Methods: Autoantibodies and clinical data were investigated before and 1, 2, and 3 months after infliximab infusion. If antinuclear antibodies were greater than or equal to1:80, further study of double-stranded DNA, single-stranded DNA, histones, and ENA was performed. Results: Cumulative antinuclear antibody incidence at 24 months was 71 of 125 (56.8%). Almost half of these patients developed antinuclear antibodies after the first infusion, and >75% became antinuclear antibody positive after fewer than 3 infusions. So far, only :15 of 71 patients have become seronegative, after a median of 12 months. Of 43 antinuclear antibody-positive patients who were further subtyped, 14 of 43 (32.6%) had double-stranded DNA, 17 (39.5%) had single-stranded DNA, 9 (20.9%) had antihistone, and 0% were ENA positive. Two patients (both antihistone and double-stranded DNA positive) developed drug-induced lupus without major organ damage, and I developed autoimmune hemolytic anemia. Antinuclear antibodies were associated with the female sex (odds ratio, 3.166; 95% confidence interval, 1.167-8.585; P = 0.024) and with papulosquamous or butterfly rash (odds ratio, 10.016; 95% confidence interval, 1.708-58.725; P = 0.011). Conclusions: The cumulative incidence of antinuclear antibodies was 56.8% after 24 months in this cohort of infliximab-treated Crohn's disease patients. Antinuclear antibodies persisted up to I year after the last infusion, and only a few patients became seronegative. Two patients developed drug-induced lupus erythematosus. Antinuclear antibodies were associated with the female sex and skin manifestations. [less ▲]

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See detailNOD2/CARD15 does not influence response to infliximab in Crohn's disease
Vermeire, S.; Louis, Edouard ULg; Rutgeerts, P. et al

in Gastroenterology (2002), 123(1), 106-111

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See detailThe value of serologic markers in indeterminate colitis: A prospective follow-up study
Joossens, S.; Van Steen, Kristel ULg; Vermeire, S. V. et al

in Gastroenterology (2002), 122(5), 1242-1247

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See detailBudesonide in Collagenous colitis: A Double-Blind Placebo-Controlled Trial With Histologic Follow-Up
Baert, Filip; Schmit, Alain; D'Haens, Geert et al

in Gastroenterology (2002), 122

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See detailAcute pancreatitis attributed to the use of interferon alfa-2b
Eland, I. A.; Rasch, M. C.; Sturkenboom, M. J. et al

in Gastroenterology (2000), 119(1), 230-233

Two patients experienced episodes of acute pancreatitis shortly after starting treatment with interferon alfa-2b (IFN-alpha) for a chronic hepatitis C infection. The first patient was a 40-year-old man ... [more ▼]

Two patients experienced episodes of acute pancreatitis shortly after starting treatment with interferon alfa-2b (IFN-alpha) for a chronic hepatitis C infection. The first patient was a 40-year-old man who developed acute pancreatitis after 15 weeks of treatment with 3 MU IFN-alpha subcutaneously (SC) 3 times weekly and 1200 mg ribavirin. After disappearance of symptoms and normalization of laboratory values, oral intake of solid foods and IFN-alpha therapy were restarted. Within hours, a relapse of acute pancreatitis occurred. A rechallenge with IFN-alpha 4 days later was followed by a prompt increase in serum lipase level, and IFN-alpha therapy was discontinued. The second patient was a 38-year-old man who developed acute pancreatitis 2 hours after SC administration of 5 MU IFN-alpha. Ultrasound endoscopy showed sludge in the gallbladder. The patient was rechallenged 5 weeks later with 3 MU IFN-alpha SC. Although serum amylase and lipase levels increased after readministration of IFN-alpha, treatment was continued. The patient was readmitted 2 weeks later with severe abdominal pain, and IFN-alpha administration was discontinued. Considering the temporal relationship between the start of IFN-alpha treatment and development of acute pancreatitis, the absence of other clear etiologic factors for acute pancreatitis, disappearance of symptoms after discontinuation of IFN-alpha, and positive reactions to rechallenge, IFN-alpha is the most probable cause for development of acute pancreatitis in these patients. [less ▲]

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See detailPrognostic factors in patients with Zollinger-Ellison syndrome and multiple endocrine neoplasia type 1. Groupe d'Etude des Neoplasies Endocriniennes Multiples (GENEM and groupe de Recherche et d'Etude du Syndrome de Zollinger-Ellison (GRESZE).
Cadiot, G.; Vuagnat, A.; Doukhan, I. et al

in Gastroenterology (1999), 116(2), 286-293

BACKGROUND & AIMS: Risk factors of metachronous liver metastases and death are not well known in patients with the Zollinger-Ellison syndrome and multiple endocrine neoplasia type 1. These factors were ... [more ▼]

BACKGROUND & AIMS: Risk factors of metachronous liver metastases and death are not well known in patients with the Zollinger-Ellison syndrome and multiple endocrine neoplasia type 1. These factors were retrospectively determined in 77 patients. METHODS: Data chart review was performed. RESULTS: Median follow-up was 102 months (range, 12-366). Surgery was performed on 48 patients, including 9 of the 10 patients with large pancreatic tumors (>/=3 cm). Liver metastases developed in 4 patients (40%) with large pancreatic tumors, in 3 (4.8%) without, and in 1 of the 4 patients with pancreatic tumors of unknown size; all had previously undergone surgery. The only independent factor associated with development of liver metastases identified by multivariate analysis was large pancreatic tumors (risk ratio, 29.0; 95% confidence interval [CI], 3. 2-260.7). Surgery was not selected. The probability of being free of liver metastases in the 63 patients without large pancreatic tumors was 96% (95% CI, 88-100) at 10 and 15 years. Thirteen (16.9%) patients died. The only independent factors of death selected by multivariate analysis were Zollinger-Ellison syndrome diagnosis before 1980 (risk ratio, 8.2; 95% CI, 1.7-40.6) and age at diagnosis (risk ratio/year, 1.08; 95% CI, 1.03-1.14). CONCLUSIONS: Large pancreatic tumors are predictive of the development of metachronous liver metastases, and surgery does not seem to prevent them. [less ▲]

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See detailDifferential expression of galectin 3 and galectin 1 in colorectal cancer progression.
Sanjuan, X.; Fernandez, P. L.; Castells, A. et al

in Gastroenterology (1997), 113(6), 1906-15

BACKGROUND & AIMS: Galectins are beta-galactoside-binding proteins possibly involved in tumor progression. The aim of this study was to determine the pattern of galectin 3 and galectin 1 expression and ... [more ▼]

BACKGROUND & AIMS: Galectins are beta-galactoside-binding proteins possibly involved in tumor progression. The aim of this study was to determine the pattern of galectin 3 and galectin 1 expression and involvement in colorectal cancer progression. METHODS: Galectin 3 expression was examined immunohistochemically in 39 samples of normal mucosae, 25 adenomas, 87 carcinomas, and 39 lymph node metastases. Galectin 1 was analyzed in 25 samples of mucosae, 15 adenomas, 25 carcinomas, and 11 metastases. Western blot analysis was also performed. RESULTS: All normal mucosae showed strong nuclear galectin 3 expression, which was down-regulated in the neoplastic progression, because only 60% of adenomas, 48% of carcinomas, and 44% of metastases were strongly positive (P < 0.0001). Cytoplasmic expression was down-regulated in adenomas (16%) but increased again in carcinomas (64%) (P < 0.0001). Galectin 1 expression was mainly detected in stromal cells and correlated with tumor progression from normal mucosae to adenomas and carcinomas (P < 0.0001). CONCLUSIONS: Galectin 3 expression is down-regulated in the initial stages of neoplastic progression, whereas a dissociated cytoplasmic expression increases in later phases of tumor progression. Galectin 1 in colorectal mucosa is predominantly a stromal product whose overexpression is associated with the neoplastic progression of colorectal cancer. [less ▲]

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See detailGenetic markers may predict disease behavior in patients with ulcerative colitis.
Roussomoustakaki, M.; Satsangi, J.; Welsh, K. et al

in Gastroenterology (1997), 112(6), 1845-53

BACKGROUND & AIMS: Recent studies have suggested that HLA DRB1*0103 and allele 2 of the interleukin 1 receptor antagonist (IL-1RA) gene predict severe and extensive ulcerative colitis, respectively. The ... [more ▼]

BACKGROUND & AIMS: Recent studies have suggested that HLA DRB1*0103 and allele 2 of the interleukin 1 receptor antagonist (IL-1RA) gene predict severe and extensive ulcerative colitis, respectively. The aim of this study was to test these hypotheses in patients undergoing surgery for their colitis. METHODS: HLA DRB1 and DQB1 genotyping was performed in 99 patients and 472 controls. Genotyping for polymorphisms of genes encoding tumor necrosis factor alpha and IL-1RA was performed in 107 patients and 89 controls. Measurement of antineutrophil cytoplasmic antibody (ANCA) was performed in 72 patients and 58 healthy subjects by fixed neutrophil enzyme-linked immunosorbent assay and indirect immunofluorescence. RESULTS: The DRB1*0103 allele was increased in patients (14.1% vs. 3.2% in controls; P < 1 x 10[-5]). This association was greatest in patients with extensive disease (15.8%; P < 0.0001) or extraintestinal manifestations (22.8%; P < 0.0001): mouth ulcers (25.8%; P < 0.0001), arthritis (27.2%; P < 0.0001), and uveitis (35.7%; P < 0.0001). The DRB1*04 alleles were reduced in patients (P = 0.005). Differences were noted between extensive and distal disease in the frequency of allele 2 of IL-1RA (10.9% in distal vs. 28.6% in extensive; P = 0.01) and allele 2 homozygosity. ANCA was detected in 76.4% of patients. Carriage of IL-1RA allele 2 and tumor necrosis factor 2 allele was increased in ANCA-positive patients. CONCLUSIONS: Genetic markers may predict disease behavior in ulcerative colitis. [less ▲]

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