The Experts below are selected from a list of 21 Experts worldwide ranked by ideXlab platform

Gijs R. Van Den Brink - One of the best experts on this subject based on the ideXlab platform.

  • intestinal fibrosis is associated with lack of response to infliximab therapy in crohn s disease
    PLOS ONE, 2018
    Co-Authors: Jessica R. De Bruyn, Jessica Steenkamer, Manon E. Wildenberg, Christianne J. Buskens, Willem A. Bemelman, Mark Löwenberg, Cyriel Y. Ponsioen, M Becker, S Meijer, Gijs R. Van Den Brink
    Abstract:

    Overt fibrostenotic disease is a relative contraindication for anti-TNF therapy in Crohn's disease. We hypothesized that subclinical fibrosis may also contribute to an incomplete response to anti-TNF therapy before the onset of symptomatic stenosis. In a previous trial, patients with ileocecal Crohn's disease were randomized to either immediate ileocecal resection or medical treatment with Infliximab. In case of insufficient response to Infliximab, the latter underwent secondary ileocecal resection. We compared specimens from those patients undergoing immediate resection (Infliximab naive, n = 20) to those who failed Infliximab therapy (n = 20). Infliximab naive and Infliximab failure patients had similar severity of inflammation when assessed by CRP levels (median 14 vs 9 mg/L) and histology (Geboes-D'Haens-score, median 10 vs 11 points). On immunohistochemistry, collagen-III and fibronectin depositions were increased in patients previously exposed to Infliximab compared to patients naive to Infliximab. On mRNA level, Procollagen Peptidase showed significantly more mucosal mRNA expression in Crohn's disease patients who failed Infliximab. Infliximab responders showed no increase of this marker after 4 weeks of successful Infliximab treatment. Failure to Infliximab therapy is associated with subclinical fibrosis in Crohn's disease

  • Similar expression of Extra domain A and Procollagen Peptidase in biopsies from Crohn’s disease patients right before Infliximab treatment and after 4 weeks of successful treatment.
    2018
    Co-Authors: Jessica R. De Bruyn, Marte A. Becker, Jessica Steenkamer, Manon E. Wildenberg, Sybren L. Meijer, Christianne J. Buskens, Willem A. Bemelman, Mark Löwenberg, Cyriel Y. Ponsioen, Gijs R. Van Den Brink
    Abstract:

    ED-A: Extra domain A; PCOLN3: Procollagen Peptidase; IFX: Infliximab; 36B4: Acidic Ribosomal Protein 36B4. All gene expressions are normalized against 36B4 as housekeeping gene.

  • Relative expression of different genes of the mucosa and muscularis mucosa (= mucosa), and submucosa and muscularis externa (= submucosa) of Infliximab naïve patients compared to Infliximab failure patients.
    2018
    Co-Authors: Jessica R. De Bruyn, Marte A. Becker, Jessica Steenkamer, Manon E. Wildenberg, Sybren L. Meijer, Christianne J. Buskens, Willem A. Bemelman, Mark Löwenberg, Cyriel Y. Ponsioen, Gijs R. Van Den Brink
    Abstract:

    IFX: Infliximab, 36B4: Acidic Ribosomal Protein 36B4; ED-A: Extra Domain A; PCOLN3: Procollagen Peptidase; ACTA2: alpha smooth muscle actin; TGFB1: transforming growth factor beta 1. *** p =

  • Intestinal fibrosis is associated with lack of response to Infliximab therapy in Crohn's disease
    2018
    Co-Authors: Jessica R. De Bruyn, Marte A. Becker, Jessica Steenkamer, Manon E. Wildenberg, Sybren L. Meijer, Christianne J. Buskens, Willem A. Bemelman, Mark Löwenberg, Cyriel Y. Ponsioen, Gijs R. Van Den Brink
    Abstract:

    IntroductionOvert fibrostenotic disease is a relative contraindication for anti-TNF therapy in Crohn’s disease. We hypothesized that subclinical fibrosis may also contribute to an incomplete response to anti-TNF therapy before the onset of symptomatic stenosis.MethodsIn a previous trial, patients with ileocecal Crohn’s disease were randomized to either immediate ileocecal resection or medical treatment with Infliximab. In case of insufficient response to Infliximab, the latter underwent secondary ileocecal resection. We compared specimens from those patients undergoing immediate resection (Infliximab naïve, n = 20) to those who failed Infliximab therapy (n = 20).ResultsInfliximab naïve and Infliximab failure patients had similar severity of inflammation when assessed by CRP levels (median 14 vs 9 mg/L) and histology (Geboes-D’Haens-score, median 10 vs 11 points). On immunohistochemistry, collagen-III and fibronectin depositions were increased in patients previously exposed to Infliximab compared to patients naïve to Infliximab. On mRNA level, Procollagen Peptidase showed significantly more mucosal mRNA expression in Crohn’s disease patients who failed Infliximab. Infliximab responders showed no increase of this marker after 4 weeks of successful Infliximab treatment.DiscussionFailure to Infliximab therapy is associated with subclinical fibrosis in Crohn’s disease.

Jessica R. De Bruyn - One of the best experts on this subject based on the ideXlab platform.

  • intestinal fibrosis is associated with lack of response to infliximab therapy in crohn s disease
    PLOS ONE, 2018
    Co-Authors: Jessica R. De Bruyn, Jessica Steenkamer, Manon E. Wildenberg, Christianne J. Buskens, Willem A. Bemelman, Mark Löwenberg, Cyriel Y. Ponsioen, M Becker, S Meijer, Gijs R. Van Den Brink
    Abstract:

    Overt fibrostenotic disease is a relative contraindication for anti-TNF therapy in Crohn's disease. We hypothesized that subclinical fibrosis may also contribute to an incomplete response to anti-TNF therapy before the onset of symptomatic stenosis. In a previous trial, patients with ileocecal Crohn's disease were randomized to either immediate ileocecal resection or medical treatment with Infliximab. In case of insufficient response to Infliximab, the latter underwent secondary ileocecal resection. We compared specimens from those patients undergoing immediate resection (Infliximab naive, n = 20) to those who failed Infliximab therapy (n = 20). Infliximab naive and Infliximab failure patients had similar severity of inflammation when assessed by CRP levels (median 14 vs 9 mg/L) and histology (Geboes-D'Haens-score, median 10 vs 11 points). On immunohistochemistry, collagen-III and fibronectin depositions were increased in patients previously exposed to Infliximab compared to patients naive to Infliximab. On mRNA level, Procollagen Peptidase showed significantly more mucosal mRNA expression in Crohn's disease patients who failed Infliximab. Infliximab responders showed no increase of this marker after 4 weeks of successful Infliximab treatment. Failure to Infliximab therapy is associated with subclinical fibrosis in Crohn's disease

  • Similar expression of Extra domain A and Procollagen Peptidase in biopsies from Crohn’s disease patients right before Infliximab treatment and after 4 weeks of successful treatment.
    2018
    Co-Authors: Jessica R. De Bruyn, Marte A. Becker, Jessica Steenkamer, Manon E. Wildenberg, Sybren L. Meijer, Christianne J. Buskens, Willem A. Bemelman, Mark Löwenberg, Cyriel Y. Ponsioen, Gijs R. Van Den Brink
    Abstract:

    ED-A: Extra domain A; PCOLN3: Procollagen Peptidase; IFX: Infliximab; 36B4: Acidic Ribosomal Protein 36B4. All gene expressions are normalized against 36B4 as housekeeping gene.

  • Relative expression of different genes of the mucosa and muscularis mucosa (= mucosa), and submucosa and muscularis externa (= submucosa) of Infliximab naïve patients compared to Infliximab failure patients.
    2018
    Co-Authors: Jessica R. De Bruyn, Marte A. Becker, Jessica Steenkamer, Manon E. Wildenberg, Sybren L. Meijer, Christianne J. Buskens, Willem A. Bemelman, Mark Löwenberg, Cyriel Y. Ponsioen, Gijs R. Van Den Brink
    Abstract:

    IFX: Infliximab, 36B4: Acidic Ribosomal Protein 36B4; ED-A: Extra Domain A; PCOLN3: Procollagen Peptidase; ACTA2: alpha smooth muscle actin; TGFB1: transforming growth factor beta 1. *** p =

  • Intestinal fibrosis is associated with lack of response to Infliximab therapy in Crohn's disease
    2018
    Co-Authors: Jessica R. De Bruyn, Marte A. Becker, Jessica Steenkamer, Manon E. Wildenberg, Sybren L. Meijer, Christianne J. Buskens, Willem A. Bemelman, Mark Löwenberg, Cyriel Y. Ponsioen, Gijs R. Van Den Brink
    Abstract:

    IntroductionOvert fibrostenotic disease is a relative contraindication for anti-TNF therapy in Crohn’s disease. We hypothesized that subclinical fibrosis may also contribute to an incomplete response to anti-TNF therapy before the onset of symptomatic stenosis.MethodsIn a previous trial, patients with ileocecal Crohn’s disease were randomized to either immediate ileocecal resection or medical treatment with Infliximab. In case of insufficient response to Infliximab, the latter underwent secondary ileocecal resection. We compared specimens from those patients undergoing immediate resection (Infliximab naïve, n = 20) to those who failed Infliximab therapy (n = 20).ResultsInfliximab naïve and Infliximab failure patients had similar severity of inflammation when assessed by CRP levels (median 14 vs 9 mg/L) and histology (Geboes-D’Haens-score, median 10 vs 11 points). On immunohistochemistry, collagen-III and fibronectin depositions were increased in patients previously exposed to Infliximab compared to patients naïve to Infliximab. On mRNA level, Procollagen Peptidase showed significantly more mucosal mRNA expression in Crohn’s disease patients who failed Infliximab. Infliximab responders showed no increase of this marker after 4 weeks of successful Infliximab treatment.DiscussionFailure to Infliximab therapy is associated with subclinical fibrosis in Crohn’s disease.

Willem A. Bemelman - One of the best experts on this subject based on the ideXlab platform.

  • intestinal fibrosis is associated with lack of response to infliximab therapy in crohn s disease
    PLOS ONE, 2018
    Co-Authors: Jessica R. De Bruyn, Jessica Steenkamer, Manon E. Wildenberg, Christianne J. Buskens, Willem A. Bemelman, Mark Löwenberg, Cyriel Y. Ponsioen, M Becker, S Meijer, Gijs R. Van Den Brink
    Abstract:

    Overt fibrostenotic disease is a relative contraindication for anti-TNF therapy in Crohn's disease. We hypothesized that subclinical fibrosis may also contribute to an incomplete response to anti-TNF therapy before the onset of symptomatic stenosis. In a previous trial, patients with ileocecal Crohn's disease were randomized to either immediate ileocecal resection or medical treatment with Infliximab. In case of insufficient response to Infliximab, the latter underwent secondary ileocecal resection. We compared specimens from those patients undergoing immediate resection (Infliximab naive, n = 20) to those who failed Infliximab therapy (n = 20). Infliximab naive and Infliximab failure patients had similar severity of inflammation when assessed by CRP levels (median 14 vs 9 mg/L) and histology (Geboes-D'Haens-score, median 10 vs 11 points). On immunohistochemistry, collagen-III and fibronectin depositions were increased in patients previously exposed to Infliximab compared to patients naive to Infliximab. On mRNA level, Procollagen Peptidase showed significantly more mucosal mRNA expression in Crohn's disease patients who failed Infliximab. Infliximab responders showed no increase of this marker after 4 weeks of successful Infliximab treatment. Failure to Infliximab therapy is associated with subclinical fibrosis in Crohn's disease

  • Similar expression of Extra domain A and Procollagen Peptidase in biopsies from Crohn’s disease patients right before Infliximab treatment and after 4 weeks of successful treatment.
    2018
    Co-Authors: Jessica R. De Bruyn, Marte A. Becker, Jessica Steenkamer, Manon E. Wildenberg, Sybren L. Meijer, Christianne J. Buskens, Willem A. Bemelman, Mark Löwenberg, Cyriel Y. Ponsioen, Gijs R. Van Den Brink
    Abstract:

    ED-A: Extra domain A; PCOLN3: Procollagen Peptidase; IFX: Infliximab; 36B4: Acidic Ribosomal Protein 36B4. All gene expressions are normalized against 36B4 as housekeeping gene.

  • Relative expression of different genes of the mucosa and muscularis mucosa (= mucosa), and submucosa and muscularis externa (= submucosa) of Infliximab naïve patients compared to Infliximab failure patients.
    2018
    Co-Authors: Jessica R. De Bruyn, Marte A. Becker, Jessica Steenkamer, Manon E. Wildenberg, Sybren L. Meijer, Christianne J. Buskens, Willem A. Bemelman, Mark Löwenberg, Cyriel Y. Ponsioen, Gijs R. Van Den Brink
    Abstract:

    IFX: Infliximab, 36B4: Acidic Ribosomal Protein 36B4; ED-A: Extra Domain A; PCOLN3: Procollagen Peptidase; ACTA2: alpha smooth muscle actin; TGFB1: transforming growth factor beta 1. *** p =

  • Intestinal fibrosis is associated with lack of response to Infliximab therapy in Crohn's disease
    2018
    Co-Authors: Jessica R. De Bruyn, Marte A. Becker, Jessica Steenkamer, Manon E. Wildenberg, Sybren L. Meijer, Christianne J. Buskens, Willem A. Bemelman, Mark Löwenberg, Cyriel Y. Ponsioen, Gijs R. Van Den Brink
    Abstract:

    IntroductionOvert fibrostenotic disease is a relative contraindication for anti-TNF therapy in Crohn’s disease. We hypothesized that subclinical fibrosis may also contribute to an incomplete response to anti-TNF therapy before the onset of symptomatic stenosis.MethodsIn a previous trial, patients with ileocecal Crohn’s disease were randomized to either immediate ileocecal resection or medical treatment with Infliximab. In case of insufficient response to Infliximab, the latter underwent secondary ileocecal resection. We compared specimens from those patients undergoing immediate resection (Infliximab naïve, n = 20) to those who failed Infliximab therapy (n = 20).ResultsInfliximab naïve and Infliximab failure patients had similar severity of inflammation when assessed by CRP levels (median 14 vs 9 mg/L) and histology (Geboes-D’Haens-score, median 10 vs 11 points). On immunohistochemistry, collagen-III and fibronectin depositions were increased in patients previously exposed to Infliximab compared to patients naïve to Infliximab. On mRNA level, Procollagen Peptidase showed significantly more mucosal mRNA expression in Crohn’s disease patients who failed Infliximab. Infliximab responders showed no increase of this marker after 4 weeks of successful Infliximab treatment.DiscussionFailure to Infliximab therapy is associated with subclinical fibrosis in Crohn’s disease.

Cyriel Y. Ponsioen - One of the best experts on this subject based on the ideXlab platform.

  • intestinal fibrosis is associated with lack of response to infliximab therapy in crohn s disease
    PLOS ONE, 2018
    Co-Authors: Jessica R. De Bruyn, Jessica Steenkamer, Manon E. Wildenberg, Christianne J. Buskens, Willem A. Bemelman, Mark Löwenberg, Cyriel Y. Ponsioen, M Becker, S Meijer, Gijs R. Van Den Brink
    Abstract:

    Overt fibrostenotic disease is a relative contraindication for anti-TNF therapy in Crohn's disease. We hypothesized that subclinical fibrosis may also contribute to an incomplete response to anti-TNF therapy before the onset of symptomatic stenosis. In a previous trial, patients with ileocecal Crohn's disease were randomized to either immediate ileocecal resection or medical treatment with Infliximab. In case of insufficient response to Infliximab, the latter underwent secondary ileocecal resection. We compared specimens from those patients undergoing immediate resection (Infliximab naive, n = 20) to those who failed Infliximab therapy (n = 20). Infliximab naive and Infliximab failure patients had similar severity of inflammation when assessed by CRP levels (median 14 vs 9 mg/L) and histology (Geboes-D'Haens-score, median 10 vs 11 points). On immunohistochemistry, collagen-III and fibronectin depositions were increased in patients previously exposed to Infliximab compared to patients naive to Infliximab. On mRNA level, Procollagen Peptidase showed significantly more mucosal mRNA expression in Crohn's disease patients who failed Infliximab. Infliximab responders showed no increase of this marker after 4 weeks of successful Infliximab treatment. Failure to Infliximab therapy is associated with subclinical fibrosis in Crohn's disease

  • Similar expression of Extra domain A and Procollagen Peptidase in biopsies from Crohn’s disease patients right before Infliximab treatment and after 4 weeks of successful treatment.
    2018
    Co-Authors: Jessica R. De Bruyn, Marte A. Becker, Jessica Steenkamer, Manon E. Wildenberg, Sybren L. Meijer, Christianne J. Buskens, Willem A. Bemelman, Mark Löwenberg, Cyriel Y. Ponsioen, Gijs R. Van Den Brink
    Abstract:

    ED-A: Extra domain A; PCOLN3: Procollagen Peptidase; IFX: Infliximab; 36B4: Acidic Ribosomal Protein 36B4. All gene expressions are normalized against 36B4 as housekeeping gene.

  • Relative expression of different genes of the mucosa and muscularis mucosa (= mucosa), and submucosa and muscularis externa (= submucosa) of Infliximab naïve patients compared to Infliximab failure patients.
    2018
    Co-Authors: Jessica R. De Bruyn, Marte A. Becker, Jessica Steenkamer, Manon E. Wildenberg, Sybren L. Meijer, Christianne J. Buskens, Willem A. Bemelman, Mark Löwenberg, Cyriel Y. Ponsioen, Gijs R. Van Den Brink
    Abstract:

    IFX: Infliximab, 36B4: Acidic Ribosomal Protein 36B4; ED-A: Extra Domain A; PCOLN3: Procollagen Peptidase; ACTA2: alpha smooth muscle actin; TGFB1: transforming growth factor beta 1. *** p =

  • Intestinal fibrosis is associated with lack of response to Infliximab therapy in Crohn's disease
    2018
    Co-Authors: Jessica R. De Bruyn, Marte A. Becker, Jessica Steenkamer, Manon E. Wildenberg, Sybren L. Meijer, Christianne J. Buskens, Willem A. Bemelman, Mark Löwenberg, Cyriel Y. Ponsioen, Gijs R. Van Den Brink
    Abstract:

    IntroductionOvert fibrostenotic disease is a relative contraindication for anti-TNF therapy in Crohn’s disease. We hypothesized that subclinical fibrosis may also contribute to an incomplete response to anti-TNF therapy before the onset of symptomatic stenosis.MethodsIn a previous trial, patients with ileocecal Crohn’s disease were randomized to either immediate ileocecal resection or medical treatment with Infliximab. In case of insufficient response to Infliximab, the latter underwent secondary ileocecal resection. We compared specimens from those patients undergoing immediate resection (Infliximab naïve, n = 20) to those who failed Infliximab therapy (n = 20).ResultsInfliximab naïve and Infliximab failure patients had similar severity of inflammation when assessed by CRP levels (median 14 vs 9 mg/L) and histology (Geboes-D’Haens-score, median 10 vs 11 points). On immunohistochemistry, collagen-III and fibronectin depositions were increased in patients previously exposed to Infliximab compared to patients naïve to Infliximab. On mRNA level, Procollagen Peptidase showed significantly more mucosal mRNA expression in Crohn’s disease patients who failed Infliximab. Infliximab responders showed no increase of this marker after 4 weeks of successful Infliximab treatment.DiscussionFailure to Infliximab therapy is associated with subclinical fibrosis in Crohn’s disease.

Mark Löwenberg - One of the best experts on this subject based on the ideXlab platform.

  • intestinal fibrosis is associated with lack of response to infliximab therapy in crohn s disease
    PLOS ONE, 2018
    Co-Authors: Jessica R. De Bruyn, Jessica Steenkamer, Manon E. Wildenberg, Christianne J. Buskens, Willem A. Bemelman, Mark Löwenberg, Cyriel Y. Ponsioen, M Becker, S Meijer, Gijs R. Van Den Brink
    Abstract:

    Overt fibrostenotic disease is a relative contraindication for anti-TNF therapy in Crohn's disease. We hypothesized that subclinical fibrosis may also contribute to an incomplete response to anti-TNF therapy before the onset of symptomatic stenosis. In a previous trial, patients with ileocecal Crohn's disease were randomized to either immediate ileocecal resection or medical treatment with Infliximab. In case of insufficient response to Infliximab, the latter underwent secondary ileocecal resection. We compared specimens from those patients undergoing immediate resection (Infliximab naive, n = 20) to those who failed Infliximab therapy (n = 20). Infliximab naive and Infliximab failure patients had similar severity of inflammation when assessed by CRP levels (median 14 vs 9 mg/L) and histology (Geboes-D'Haens-score, median 10 vs 11 points). On immunohistochemistry, collagen-III and fibronectin depositions were increased in patients previously exposed to Infliximab compared to patients naive to Infliximab. On mRNA level, Procollagen Peptidase showed significantly more mucosal mRNA expression in Crohn's disease patients who failed Infliximab. Infliximab responders showed no increase of this marker after 4 weeks of successful Infliximab treatment. Failure to Infliximab therapy is associated with subclinical fibrosis in Crohn's disease

  • Similar expression of Extra domain A and Procollagen Peptidase in biopsies from Crohn’s disease patients right before Infliximab treatment and after 4 weeks of successful treatment.
    2018
    Co-Authors: Jessica R. De Bruyn, Marte A. Becker, Jessica Steenkamer, Manon E. Wildenberg, Sybren L. Meijer, Christianne J. Buskens, Willem A. Bemelman, Mark Löwenberg, Cyriel Y. Ponsioen, Gijs R. Van Den Brink
    Abstract:

    ED-A: Extra domain A; PCOLN3: Procollagen Peptidase; IFX: Infliximab; 36B4: Acidic Ribosomal Protein 36B4. All gene expressions are normalized against 36B4 as housekeeping gene.

  • Relative expression of different genes of the mucosa and muscularis mucosa (= mucosa), and submucosa and muscularis externa (= submucosa) of Infliximab naïve patients compared to Infliximab failure patients.
    2018
    Co-Authors: Jessica R. De Bruyn, Marte A. Becker, Jessica Steenkamer, Manon E. Wildenberg, Sybren L. Meijer, Christianne J. Buskens, Willem A. Bemelman, Mark Löwenberg, Cyriel Y. Ponsioen, Gijs R. Van Den Brink
    Abstract:

    IFX: Infliximab, 36B4: Acidic Ribosomal Protein 36B4; ED-A: Extra Domain A; PCOLN3: Procollagen Peptidase; ACTA2: alpha smooth muscle actin; TGFB1: transforming growth factor beta 1. *** p =

  • Intestinal fibrosis is associated with lack of response to Infliximab therapy in Crohn's disease
    2018
    Co-Authors: Jessica R. De Bruyn, Marte A. Becker, Jessica Steenkamer, Manon E. Wildenberg, Sybren L. Meijer, Christianne J. Buskens, Willem A. Bemelman, Mark Löwenberg, Cyriel Y. Ponsioen, Gijs R. Van Den Brink
    Abstract:

    IntroductionOvert fibrostenotic disease is a relative contraindication for anti-TNF therapy in Crohn’s disease. We hypothesized that subclinical fibrosis may also contribute to an incomplete response to anti-TNF therapy before the onset of symptomatic stenosis.MethodsIn a previous trial, patients with ileocecal Crohn’s disease were randomized to either immediate ileocecal resection or medical treatment with Infliximab. In case of insufficient response to Infliximab, the latter underwent secondary ileocecal resection. We compared specimens from those patients undergoing immediate resection (Infliximab naïve, n = 20) to those who failed Infliximab therapy (n = 20).ResultsInfliximab naïve and Infliximab failure patients had similar severity of inflammation when assessed by CRP levels (median 14 vs 9 mg/L) and histology (Geboes-D’Haens-score, median 10 vs 11 points). On immunohistochemistry, collagen-III and fibronectin depositions were increased in patients previously exposed to Infliximab compared to patients naïve to Infliximab. On mRNA level, Procollagen Peptidase showed significantly more mucosal mRNA expression in Crohn’s disease patients who failed Infliximab. Infliximab responders showed no increase of this marker after 4 weeks of successful Infliximab treatment.DiscussionFailure to Infliximab therapy is associated with subclinical fibrosis in Crohn’s disease.