The IGF system in patients with inflammatory bowel disease treated with prednisolone or infliximab: potential role of the stanniocalcin-2 / PAPP-A / IGFBP-4 axis
Background Patients with inflammatory bowel disease (IBD) present with reduced serum insulin-like growth factor I (IGF-I). Anti-inflammatory treatment with prednisolone or infliximab ameliorates symptoms and increases circulating IGF-I, but prednisolone induces catabolism, whereas infliximab may pro...
Saved in:
| Published in | BMC gastroenterology Vol. 19; no. 1; pp. 83 - 11 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
BioMed Central
03.06.2019
BioMed Central Ltd BMC |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1471-230X 1471-230X |
| DOI | 10.1186/s12876-019-1000-6 |
Cover
| Abstract | Background
Patients with inflammatory bowel disease (IBD) present with reduced serum insulin-like growth factor I (IGF-I). Anti-inflammatory treatment with prednisolone or infliximab ameliorates symptoms and increases circulating IGF-I, but prednisolone induces catabolism, whereas infliximab may promote protein synthesis. Recently, stanniocalcin-2 (STC2) was discovered as a novel inhibitor of the enzyme pregnancy-associated plasma protein-A (PAPP-A), which modulates IGF-I activity. PAPP-A can cleave IGF binding protein-4 (IGFBP-4), upon which IGF-I is liberated. We hypothesized that prednisolone and infliximab exert different effects on levels of STC2, PAPP-A, and IGFBP-4, thereby explaining the distinct metabolic effects of prednisolone and infliximab.
Methods
Thirty-eight patients with active IBD treated with either prednisolone (
n
= 17) or infliximab (
n
= 21) were examined before and after 7 days of treatment. Circulating levels of IGF-I, IGF-II, IGFBP-3, PAPP-A, and STC2 were measured by immunoassays. Intact IGFBP-4 and two IGFBP-4 fragments were determined by a novel immunoassay. Bioactive IGF was assessed by cell-based IGF receptor activation assay. Concentrations of IGFBP-4, PAPP-A, and STC2 on day 0 and 7 were compared to healthy control subjects.
Results
Following seven days of prednisolone treatment, total and bioactive IGF-I were increased (
p
< 0.001 and
p
< 0.05, respectively). Upon infliximab treatment, total IGF-I levels were augmented (p < 0.05), yet IGF bioactivity remained unaltered. Intact IGFBP-4 and the two IGFBP-4 fragments generated upon cleavage by PAPP-A were all decreased following treatment with either prednisolone or infliximab (all
p
< 0.05). PAPP-A levels were only increased by infliximab (
p
= 0.005), whereas the inhibitor STC2 did not respond to any of the treatments.
Conclusion
IGF-I and IGFBP-4 concentrations were markedly altered in patients with IBD and near-normalized with disease remission following treatment with prednisolone or infliximab. Thus, IGFBP-4 may modulate IGF bioavailability in IBD. The effect of immunosuppression did not appear to extend beyond the regulation of IGF and IGFBP-4, as neither PAPP-A nor STC2 were discernibly affected.
Trial registration
ClinicalTrials.gov:
NCT00955123
. Date of registration: August 7, 2009 (retrospectively registered). |
|---|---|
| AbstractList | Patients with inflammatory bowel disease (IBD) present with reduced serum insulin-like growth factor I (IGF-I). Anti-inflammatory treatment with prednisolone or infliximab ameliorates symptoms and increases circulating IGF-I, but prednisolone induces catabolism, whereas infliximab may promote protein synthesis. Recently, stanniocalcin-2 (STC2) was discovered as a novel inhibitor of the enzyme pregnancy-associated plasma protein-A (PAPP-A), which modulates IGF-I activity. PAPP-A can cleave IGF binding protein-4 (IGFBP-4), upon which IGF-I is liberated. We hypothesized that prednisolone and infliximab exert different effects on levels of STC2, PAPP-A, and IGFBP-4, thereby explaining the distinct metabolic effects of prednisolone and infliximab.
Thirty-eight patients with active IBD treated with either prednisolone (n = 17) or infliximab (n = 21) were examined before and after 7 days of treatment. Circulating levels of IGF-I, IGF-II, IGFBP-3, PAPP-A, and STC2 were measured by immunoassays. Intact IGFBP-4 and two IGFBP-4 fragments were determined by a novel immunoassay. Bioactive IGF was assessed by cell-based IGF receptor activation assay. Concentrations of IGFBP-4, PAPP-A, and STC2 on day 0 and 7 were compared to healthy control subjects.
Following seven days of prednisolone treatment, total and bioactive IGF-I were increased (p < 0.001 and p < 0.05, respectively). Upon infliximab treatment, total IGF-I levels were augmented (p < 0.05), yet IGF bioactivity remained unaltered. Intact IGFBP-4 and the two IGFBP-4 fragments generated upon cleavage by PAPP-A were all decreased following treatment with either prednisolone or infliximab (all p < 0.05). PAPP-A levels were only increased by infliximab (p = 0.005), whereas the inhibitor STC2 did not respond to any of the treatments.
IGF-I and IGFBP-4 concentrations were markedly altered in patients with IBD and near-normalized with disease remission following treatment with prednisolone or infliximab. Thus, IGFBP-4 may modulate IGF bioavailability in IBD. The effect of immunosuppression did not appear to extend beyond the regulation of IGF and IGFBP-4, as neither PAPP-A nor STC2 were discernibly affected.
ClinicalTrials.gov: NCT00955123 . Date of registration: August 7, 2009 (retrospectively registered). Abstract Background Patients with inflammatory bowel disease (IBD) present with reduced serum insulin-like growth factor I (IGF-I). Anti-inflammatory treatment with prednisolone or infliximab ameliorates symptoms and increases circulating IGF-I, but prednisolone induces catabolism, whereas infliximab may promote protein synthesis. Recently, stanniocalcin-2 (STC2) was discovered as a novel inhibitor of the enzyme pregnancy-associated plasma protein-A (PAPP-A), which modulates IGF-I activity. PAPP-A can cleave IGF binding protein-4 (IGFBP-4), upon which IGF-I is liberated. We hypothesized that prednisolone and infliximab exert different effects on levels of STC2, PAPP-A, and IGFBP-4, thereby explaining the distinct metabolic effects of prednisolone and infliximab. Methods Thirty-eight patients with active IBD treated with either prednisolone (n = 17) or infliximab (n = 21) were examined before and after 7 days of treatment. Circulating levels of IGF-I, IGF-II, IGFBP-3, PAPP-A, and STC2 were measured by immunoassays. Intact IGFBP-4 and two IGFBP-4 fragments were determined by a novel immunoassay. Bioactive IGF was assessed by cell-based IGF receptor activation assay. Concentrations of IGFBP-4, PAPP-A, and STC2 on day 0 and 7 were compared to healthy control subjects. Results Following seven days of prednisolone treatment, total and bioactive IGF-I were increased (p < 0.001 and p < 0.05, respectively). Upon infliximab treatment, total IGF-I levels were augmented (p < 0.05), yet IGF bioactivity remained unaltered. Intact IGFBP-4 and the two IGFBP-4 fragments generated upon cleavage by PAPP-A were all decreased following treatment with either prednisolone or infliximab (all p < 0.05). PAPP-A levels were only increased by infliximab (p = 0.005), whereas the inhibitor STC2 did not respond to any of the treatments. Conclusion IGF-I and IGFBP-4 concentrations were markedly altered in patients with IBD and near-normalized with disease remission following treatment with prednisolone or infliximab. Thus, IGFBP-4 may modulate IGF bioavailability in IBD. The effect of immunosuppression did not appear to extend beyond the regulation of IGF and IGFBP-4, as neither PAPP-A nor STC2 were discernibly affected. Trial registration ClinicalTrials.gov: NCT00955123. Date of registration: August 7, 2009 (retrospectively registered). Patients with inflammatory bowel disease (IBD) present with reduced serum insulin-like growth factor I (IGF-I). Anti-inflammatory treatment with prednisolone or infliximab ameliorates symptoms and increases circulating IGF-I, but prednisolone induces catabolism, whereas infliximab may promote protein synthesis. Recently, stanniocalcin-2 (STC2) was discovered as a novel inhibitor of the enzyme pregnancy-associated plasma protein-A (PAPP-A), which modulates IGF-I activity. PAPP-A can cleave IGF binding protein-4 (IGFBP-4), upon which IGF-I is liberated. We hypothesized that prednisolone and infliximab exert different effects on levels of STC2, PAPP-A, and IGFBP-4, thereby explaining the distinct metabolic effects of prednisolone and infliximab.BACKGROUNDPatients with inflammatory bowel disease (IBD) present with reduced serum insulin-like growth factor I (IGF-I). Anti-inflammatory treatment with prednisolone or infliximab ameliorates symptoms and increases circulating IGF-I, but prednisolone induces catabolism, whereas infliximab may promote protein synthesis. Recently, stanniocalcin-2 (STC2) was discovered as a novel inhibitor of the enzyme pregnancy-associated plasma protein-A (PAPP-A), which modulates IGF-I activity. PAPP-A can cleave IGF binding protein-4 (IGFBP-4), upon which IGF-I is liberated. We hypothesized that prednisolone and infliximab exert different effects on levels of STC2, PAPP-A, and IGFBP-4, thereby explaining the distinct metabolic effects of prednisolone and infliximab.Thirty-eight patients with active IBD treated with either prednisolone (n = 17) or infliximab (n = 21) were examined before and after 7 days of treatment. Circulating levels of IGF-I, IGF-II, IGFBP-3, PAPP-A, and STC2 were measured by immunoassays. Intact IGFBP-4 and two IGFBP-4 fragments were determined by a novel immunoassay. Bioactive IGF was assessed by cell-based IGF receptor activation assay. Concentrations of IGFBP-4, PAPP-A, and STC2 on day 0 and 7 were compared to healthy control subjects.METHODSThirty-eight patients with active IBD treated with either prednisolone (n = 17) or infliximab (n = 21) were examined before and after 7 days of treatment. Circulating levels of IGF-I, IGF-II, IGFBP-3, PAPP-A, and STC2 were measured by immunoassays. Intact IGFBP-4 and two IGFBP-4 fragments were determined by a novel immunoassay. Bioactive IGF was assessed by cell-based IGF receptor activation assay. Concentrations of IGFBP-4, PAPP-A, and STC2 on day 0 and 7 were compared to healthy control subjects.Following seven days of prednisolone treatment, total and bioactive IGF-I were increased (p < 0.001 and p < 0.05, respectively). Upon infliximab treatment, total IGF-I levels were augmented (p < 0.05), yet IGF bioactivity remained unaltered. Intact IGFBP-4 and the two IGFBP-4 fragments generated upon cleavage by PAPP-A were all decreased following treatment with either prednisolone or infliximab (all p < 0.05). PAPP-A levels were only increased by infliximab (p = 0.005), whereas the inhibitor STC2 did not respond to any of the treatments.RESULTSFollowing seven days of prednisolone treatment, total and bioactive IGF-I were increased (p < 0.001 and p < 0.05, respectively). Upon infliximab treatment, total IGF-I levels were augmented (p < 0.05), yet IGF bioactivity remained unaltered. Intact IGFBP-4 and the two IGFBP-4 fragments generated upon cleavage by PAPP-A were all decreased following treatment with either prednisolone or infliximab (all p < 0.05). PAPP-A levels were only increased by infliximab (p = 0.005), whereas the inhibitor STC2 did not respond to any of the treatments.IGF-I and IGFBP-4 concentrations were markedly altered in patients with IBD and near-normalized with disease remission following treatment with prednisolone or infliximab. Thus, IGFBP-4 may modulate IGF bioavailability in IBD. The effect of immunosuppression did not appear to extend beyond the regulation of IGF and IGFBP-4, as neither PAPP-A nor STC2 were discernibly affected.CONCLUSIONIGF-I and IGFBP-4 concentrations were markedly altered in patients with IBD and near-normalized with disease remission following treatment with prednisolone or infliximab. Thus, IGFBP-4 may modulate IGF bioavailability in IBD. The effect of immunosuppression did not appear to extend beyond the regulation of IGF and IGFBP-4, as neither PAPP-A nor STC2 were discernibly affected.ClinicalTrials.gov: NCT00955123 . Date of registration: August 7, 2009 (retrospectively registered).TRIAL REGISTRATIONClinicalTrials.gov: NCT00955123 . Date of registration: August 7, 2009 (retrospectively registered). Thirty-eight patients with active IBD treated with either prednisolone (n = 17) or infliximab (n = 21) were examined before and after 7 days of treatment. Circulating levels of IGF-I, IGF-II, IGFBP-3, PAPP-A, and STC2 were measured by immunoassays. Intact IGFBP-4 and two IGFBP-4 fragments were determined by a novel immunoassay. Bioactive IGF was assessed by cell-based IGF receptor activation assay. Concentrations of IGFBP-4, PAPP-A, and STC2 on day 0 and 7 were compared to healthy control subjects. Following seven days of prednisolone treatment, total and bioactive IGF-I were increased (p < 0.001 and p < 0.05, respectively). Upon infliximab treatment, total IGF-I levels were augmented (p < 0.05), yet IGF bioactivity remained unaltered. Intact IGFBP-4 and the two IGFBP-4 fragments generated upon cleavage by PAPP-A were all decreased following treatment with either prednisolone or infliximab (all p < 0.05). PAPP-A levels were only increased by infliximab (p = 0.005), whereas the inhibitor STC2 did not respond to any of the treatments. IGF-I and IGFBP-4 concentrations were markedly altered in patients with IBD and near-normalized with disease remission following treatment with prednisolone or infliximab. Thus, IGFBP-4 may modulate IGF bioavailability in IBD. The effect of immunosuppression did not appear to extend beyond the regulation of IGF and IGFBP-4, as neither PAPP-A nor STC2 were discernibly affected. Background Patients with inflammatory bowel disease (IBD) present with reduced serum insulin-like growth factor I (IGF-I). Anti-inflammatory treatment with prednisolone or infliximab ameliorates symptoms and increases circulating IGF-I, but prednisolone induces catabolism, whereas infliximab may promote protein synthesis. Recently, stanniocalcin-2 (STC2) was discovered as a novel inhibitor of the enzyme pregnancy-associated plasma protein-A (PAPP-A), which modulates IGF-I activity. PAPP-A can cleave IGF binding protein-4 (IGFBP-4), upon which IGF-I is liberated. We hypothesized that prednisolone and infliximab exert different effects on levels of STC2, PAPP-A, and IGFBP-4, thereby explaining the distinct metabolic effects of prednisolone and infliximab. Methods Thirty-eight patients with active IBD treated with either prednisolone (n = 17) or infliximab (n = 21) were examined before and after 7 days of treatment. Circulating levels of IGF-I, IGF-II, IGFBP-3, PAPP-A, and STC2 were measured by immunoassays. Intact IGFBP-4 and two IGFBP-4 fragments were determined by a novel immunoassay. Bioactive IGF was assessed by cell-based IGF receptor activation assay. Concentrations of IGFBP-4, PAPP-A, and STC2 on day 0 and 7 were compared to healthy control subjects. Results Following seven days of prednisolone treatment, total and bioactive IGF-I were increased (p < 0.001 and p < 0.05, respectively). Upon infliximab treatment, total IGF-I levels were augmented (p < 0.05), yet IGF bioactivity remained unaltered. Intact IGFBP-4 and the two IGFBP-4 fragments generated upon cleavage by PAPP-A were all decreased following treatment with either prednisolone or infliximab (all p < 0.05). PAPP-A levels were only increased by infliximab (p = 0.005), whereas the inhibitor STC2 did not respond to any of the treatments. Conclusion IGF-I and IGFBP-4 concentrations were markedly altered in patients with IBD and near-normalized with disease remission following treatment with prednisolone or infliximab. Thus, IGFBP-4 may modulate IGF bioavailability in IBD. The effect of immunosuppression did not appear to extend beyond the regulation of IGF and IGFBP-4, as neither PAPP-A nor STC2 were discernibly affected. Trial registration ClinicalTrials.gov: NCT00955123. Date of registration: August 7, 2009 (retrospectively registered). Background Patients with inflammatory bowel disease (IBD) present with reduced serum insulin-like growth factor I (IGF-I). Anti-inflammatory treatment with prednisolone or infliximab ameliorates symptoms and increases circulating IGF-I, but prednisolone induces catabolism, whereas infliximab may promote protein synthesis. Recently, stanniocalcin-2 (STC2) was discovered as a novel inhibitor of the enzyme pregnancy-associated plasma protein-A (PAPP-A), which modulates IGF-I activity. PAPP-A can cleave IGF binding protein-4 (IGFBP-4), upon which IGF-I is liberated. We hypothesized that prednisolone and infliximab exert different effects on levels of STC2, PAPP-A, and IGFBP-4, thereby explaining the distinct metabolic effects of prednisolone and infliximab. Methods Thirty-eight patients with active IBD treated with either prednisolone (n = 17) or infliximab (n = 21) were examined before and after 7 days of treatment. Circulating levels of IGF-I, IGF-II, IGFBP-3, PAPP-A, and STC2 were measured by immunoassays. Intact IGFBP-4 and two IGFBP-4 fragments were determined by a novel immunoassay. Bioactive IGF was assessed by cell-based IGF receptor activation assay. Concentrations of IGFBP-4, PAPP-A, and STC2 on day 0 and 7 were compared to healthy control subjects. Results Following seven days of prednisolone treatment, total and bioactive IGF-I were increased (p < 0.001 and p < 0.05, respectively). Upon infliximab treatment, total IGF-I levels were augmented (p < 0.05), yet IGF bioactivity remained unaltered. Intact IGFBP-4 and the two IGFBP-4 fragments generated upon cleavage by PAPP-A were all decreased following treatment with either prednisolone or infliximab (all p < 0.05). PAPP-A levels were only increased by infliximab (p = 0.005), whereas the inhibitor STC2 did not respond to any of the treatments. Conclusion IGF-I and IGFBP-4 concentrations were markedly altered in patients with IBD and near-normalized with disease remission following treatment with prednisolone or infliximab. Thus, IGFBP-4 may modulate IGF bioavailability in IBD. The effect of immunosuppression did not appear to extend beyond the regulation of IGF and IGFBP-4, as neither PAPP-A nor STC2 were discernibly affected. Trial registration ClinicalTrials.gov: NCT00955123. Date of registration: August 7, 2009 (retrospectively registered). Keywords: IGF binding protein-4, Inflammatory bowel disease, Infliximab, Prednisolone, Pregnancy-associated plasma protein-a, Stanniocalcin-2 Background Patients with inflammatory bowel disease (IBD) present with reduced serum insulin-like growth factor I (IGF-I). Anti-inflammatory treatment with prednisolone or infliximab ameliorates symptoms and increases circulating IGF-I, but prednisolone induces catabolism, whereas infliximab may promote protein synthesis. Recently, stanniocalcin-2 (STC2) was discovered as a novel inhibitor of the enzyme pregnancy-associated plasma protein-A (PAPP-A), which modulates IGF-I activity. PAPP-A can cleave IGF binding protein-4 (IGFBP-4), upon which IGF-I is liberated. We hypothesized that prednisolone and infliximab exert different effects on levels of STC2, PAPP-A, and IGFBP-4, thereby explaining the distinct metabolic effects of prednisolone and infliximab. Methods Thirty-eight patients with active IBD treated with either prednisolone ( n = 17) or infliximab ( n = 21) were examined before and after 7 days of treatment. Circulating levels of IGF-I, IGF-II, IGFBP-3, PAPP-A, and STC2 were measured by immunoassays. Intact IGFBP-4 and two IGFBP-4 fragments were determined by a novel immunoassay. Bioactive IGF was assessed by cell-based IGF receptor activation assay. Concentrations of IGFBP-4, PAPP-A, and STC2 on day 0 and 7 were compared to healthy control subjects. Results Following seven days of prednisolone treatment, total and bioactive IGF-I were increased ( p < 0.001 and p < 0.05, respectively). Upon infliximab treatment, total IGF-I levels were augmented (p < 0.05), yet IGF bioactivity remained unaltered. Intact IGFBP-4 and the two IGFBP-4 fragments generated upon cleavage by PAPP-A were all decreased following treatment with either prednisolone or infliximab (all p < 0.05). PAPP-A levels were only increased by infliximab ( p = 0.005), whereas the inhibitor STC2 did not respond to any of the treatments. Conclusion IGF-I and IGFBP-4 concentrations were markedly altered in patients with IBD and near-normalized with disease remission following treatment with prednisolone or infliximab. Thus, IGFBP-4 may modulate IGF bioavailability in IBD. The effect of immunosuppression did not appear to extend beyond the regulation of IGF and IGFBP-4, as neither PAPP-A nor STC2 were discernibly affected. Trial registration ClinicalTrials.gov: NCT00955123 . Date of registration: August 7, 2009 (retrospectively registered). |
| ArticleNumber | 83 |
| Audience | Academic |
| Author | Agnholt, Jørgen Frystyk, Jan Hjortebjerg, Rikke Thomsen, Karen L. |
| Author_xml | – sequence: 1 givenname: Rikke orcidid: 0000-0001-8237-0889 surname: Hjortebjerg fullname: Hjortebjerg, Rikke email: rikke.hjortebjerg@clin.au.dk organization: Medical Research Laboratory, Department of Clinical Medicine, Faculty of Health, Aarhus University, The Danish Diabetes Academy – sequence: 2 givenname: Karen L. surname: Thomsen fullname: Thomsen, Karen L. organization: Department of Hepatology and Gastroenterology, Aarhus University Hospital – sequence: 3 givenname: Jørgen surname: Agnholt fullname: Agnholt, Jørgen organization: Department of Hepatology and Gastroenterology, Aarhus University Hospital – sequence: 4 givenname: Jan surname: Frystyk fullname: Frystyk, Jan organization: Medical Research Laboratory, Department of Clinical Medicine, Faculty of Health, Aarhus University, Department of Clinical Research, Faculty of Health, University of Southern Denmark, Department of Endocrinology, Odense University Hospital |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31159802$$D View this record in MEDLINE/PubMed |
| BookMark | eNp9kstu1DAUhiNURC_wAGyQJTZs0trOxQ4LpKGiZaRKzKJI7CzHlxlXSTzYnrbzOLwpJ01LOxWgLGId___nc-z_MNsb_GCy7C3Bx4Tw-iQSylmdY9LkBGOc1y-yA1IyktMC_9h7st7PDmO8wpgwTotX2X5BSNVwTA-yX5crg-bnZyhuYzI9cgNay-TMkCK6cWkFBdvJvpfJhy1q_Y3pkHbRyGhQCkYmoyfdOhg9uOg7aBH5cOdzt66X7Ue09gmATnYo-A52LUpwakxyGJxXslNuyCk6QYvZYpHPYAENfV7kJZK3Lr7OXlrZRfPm_n-UfT_7cnn6Nb_4dj4_nV3kqsZFyqlqVcWrttUVp401hFoqG9ZWlhlWa21tRW2riWWVKiwvGbaFJaXihNRa1aw4yuYTV3t5JdYBWg9b4aUTdwUflkKG5FRnRGm5okXZlLoqS4A1WivJLTZcG05oDaxPE2u9aXujFUwfZLcD3d0Z3Eos_bWoq5LVmAPgwz0g-J8bE5PoXVSm6-Rg_CYKSosK1xzjCqTvn0mv_CYMcFWgKguMm4bzR9VSwgDwOB7OVSNUzKoGM1oyNvZ9_BcVfNr0TsHLWgf1HcO7p4P-mfAhYCBgk0AFH2MwViiXIGB-nNt1gmAxRllMURYQZTFGWYxo8sz5AP-fh06eCNphacLjXfzb9Bs87QVB |
| CitedBy_id | crossref_primary_10_1210_clinem_dgaa617 crossref_primary_10_1038_s41421_022_00502_2 crossref_primary_10_3389_fendo_2024_1456195 crossref_primary_10_1016_j_ajoc_2021_101069 crossref_primary_10_1038_s41413_024_00381_1 crossref_primary_10_1210_clinem_dgad754 crossref_primary_10_3389_fendo_2020_00614 crossref_primary_10_3390_ijms25042014 crossref_primary_10_1016_j_biopha_2021_112239 crossref_primary_10_1186_s43042_024_00533_2 crossref_primary_10_3389_fendo_2023_1193742 |
| Cites_doi | 10.1097/01.MIB.0000437496.07181.4c 10.1210/jc.2015-2196 10.1016/S0140-6736(80)92767-1 10.1242/dev.00997 10.1530/EJE-12-0518 10.1210/en.2007-1219 10.1152/ajpgi.90576.2008 10.1210/en.2003-1313 10.1093/ndt/gfl276 10.1074/jbc.M114.611665 10.1046/j.1365-2265.1998.00562.x 10.1016/j.ghir.2012.09.004 10.1152/ajpendo.00405.2013 10.1152/ajpendo.00410.2002 10.1016/j.ghir.2006.10.003 10.1530/EJE-16-0940 10.1016/j.pharep.2016.03.006 10.1016/j.beem.2013.08.010 10.1016/j.ghir.2018.01.001 10.1016/j.ghir.2018.05.002 10.1016/j.clinbiochem.2014.11.022 10.1517/14728222.2014.858698 10.1530/EJE-16-0569 10.1152/ajpendo.00268.2004 10.1016/j.pharep.2016.04.016 10.1096/fj.04-2073fje 10.1007/s12079-015-0259-9 10.1530/JOE-13-0610 10.1016/j.ghir.2011.06.002 10.1111/j.1365-2036.2005.02449.x 10.1210/jcem-61-4-618 10.1161/JAHA.116.005358 10.1210/jc.2017-00696 10.3389/fendo.2018.00388 10.18632/oncotarget.5010 10.1530/EJE-13-0661 10.1210/jc.2017-00033 10.3109/03008207.2013.848200 10.1016/j.dld.2016.06.038 10.1677/joe.0.1360525 10.1210/en.2005-0908 10.1016/S0002-9270(01)04110-7 10.1136/bmj.j2505 10.1080/00365520601010115 10.1016/j.tem.2012.02.008 10.1054/ghir.2001.0248 10.1002/jnr.10512 10.1210/me.2005-0196 10.1152/ajpcell.00199.2005 10.1136/gut.43.1.29 10.1210/me.2007-0536 10.1530/EJE-13-0835 |
| ContentType | Journal Article |
| Copyright | The Author(s). 2019 COPYRIGHT 2019 BioMed Central Ltd. 2019. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
| Copyright_xml | – notice: The Author(s). 2019 – notice: COPYRIGHT 2019 BioMed Central Ltd. – notice: 2019. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
| DBID | C6C AAYXX CITATION CGR CUY CVF ECM EIF NPM 3V. 7QP 7QR 7T5 7X7 7XB 88E 8FD 8FI 8FJ 8FK ABUWG AFKRA AZQEC BENPR CCPQU DWQXO FR3 FYUFA GHDGH H94 K9. M0S M1P P64 PHGZM PHGZT PIMPY PJZUB PKEHL PPXIY PQEST PQQKQ PQUKI PRINS 7X8 5PM DOA |
| DOI | 10.1186/s12876-019-1000-6 |
| DatabaseName | Springer Nature OA Free Journals CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed ProQuest Central (Corporate) Calcium & Calcified Tissue Abstracts Chemoreception Abstracts Immunology Abstracts Health & Medical Collection ProQuest Central (purchase pre-March 2016) Medical Database (Alumni Edition) Technology Research Database Hospital Premium Collection Hospital Premium Collection (Alumni Edition) ProQuest Central (Alumni) (purchase pre-March 2016) ProQuest Central (Alumni) ProQuest Central UK/Ireland ProQuest Central Essentials ProQuest Central ProQuest One Community College ProQuest Central Korea Engineering Research Database Health Research Premium Collection Health Research Premium Collection (Alumni) AIDS and Cancer Research Abstracts ProQuest Health & Medical Complete (Alumni) ProQuest Health & Medical Collection Medical Database Biotechnology and BioEngineering Abstracts ProQuest Central Premium ProQuest One Academic (New) Publicly Available Content Database ProQuest Health & Medical Research Collection ProQuest One Academic Middle East (New) ProQuest One Health & Nursing ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Academic ProQuest One Academic UKI Edition ProQuest Central China MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ Directory of Open Access Journals |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) Publicly Available Content Database Technology Research Database ProQuest One Academic Middle East (New) ProQuest Central Essentials ProQuest Health & Medical Complete (Alumni) ProQuest Central (Alumni Edition) ProQuest One Community College ProQuest One Health & Nursing ProQuest Central China ProQuest Central ProQuest Health & Medical Research Collection Health Research Premium Collection Health and Medicine Complete (Alumni Edition) ProQuest Central Korea Health & Medical Research Collection AIDS and Cancer Research Abstracts Chemoreception Abstracts ProQuest Central (New) ProQuest Medical Library (Alumni) ProQuest One Academic Eastern Edition ProQuest Hospital Collection Health Research Premium Collection (Alumni) ProQuest Hospital Collection (Alumni) Biotechnology and BioEngineering Abstracts ProQuest Health & Medical Complete ProQuest Medical Library ProQuest One Academic UKI Edition Immunology Abstracts Engineering Research Database ProQuest One Academic Calcium & Calcified Tissue Abstracts ProQuest One Academic (New) ProQuest Central (Alumni) MEDLINE - Academic |
| DatabaseTitleList | MEDLINE MEDLINE - Academic Publicly Available Content Database |
| Database_xml | – sequence: 1 dbid: C6C name: Springer Nature OA Free Journals url: http://www.springeropen.com/ sourceTypes: Publisher – sequence: 2 dbid: DOA name: DOAJ Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 3 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 4 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database – sequence: 5 dbid: BENPR name: ProQuest Central url: http://www.proquest.com/pqcentral?accountid=15518 sourceTypes: Aggregation Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine |
| EISSN | 1471-230X |
| EndPage | 11 |
| ExternalDocumentID | oai_doaj_org_article_4f8c23494d5443f89ddca8f0e8de8126 PMC6547608 A590724776 31159802 10_1186_s12876_019_1000_6 |
| Genre | Evaluation Study Journal Article |
| GrantInformation_xml | – fundername: Aarhus Universitets Forskningsfond funderid: http://dx.doi.org/10.13039/501100002739 – fundername: Colitis-Crohn Foreningen funderid: http://dx.doi.org/10.13039/501100006483 – fundername: Beckett-Fonden funderid: http://dx.doi.org/10.13039/501100009898 – fundername: Danish Diabetes Academy supported by the Novo Nordisk Foundation – fundername: Novo Nordisk Fonden funderid: http://dx.doi.org/10.13039/501100009708 – fundername: Strategiske Forskningsråd funderid: http://dx.doi.org/10.13039/100007398 – fundername: ; |
| GroupedDBID | --- 0R~ 23N 2WC 53G 5VS 6J9 6PF 7X7 88E 8FI 8FJ AAFWJ AAJSJ AASML AAWTL ABDBF ABUWG ACGFO ACGFS ACIHN ACIWK ACPRK ACUHS ADBBV ADRAZ ADUKV AEAQA AENEX AFKRA AFPKN AHBYD AHMBA AHYZX ALMA_UNASSIGNED_HOLDINGS AMKLP AMTXH AOIJS BAPOH BAWUL BCNDV BENPR BFQNJ BMC BPHCQ BVXVI C6C CCPQU CS3 DIK E3Z EAD EAP EAS EBD EBLON EBS EJD EMB EMK EMOBN ESX F5P FYUFA GROUPED_DOAJ GX1 HMCUK HYE IAO IHR INH INR ITC KQ8 M1P M48 M~E O5R O5S OK1 OVT P2P PHGZM PHGZT PIMPY PJZUB PPXIY PQQKQ PROAC PSQYO PUEGO RBZ RNS ROL RPM RSV SMD SOJ SV3 TR2 TUS UKHRP W2D WOQ WOW XSB AAYXX ALIPV CITATION CGR CUY CVF ECM EIF NPM PMFND 3V. 7QP 7QR 7T5 7XB 8FD 8FK AZQEC DWQXO FR3 H94 K9. P64 PKEHL PQEST PQUKI PRINS 7X8 5PM |
| ID | FETCH-LOGICAL-c603t-2cbc585bbd5829fe12f2a97b5f7e76ddff52fbd1f75c3f8470f3f14c8116dc673 |
| IEDL.DBID | 7X7 |
| ISSN | 1471-230X |
| IngestDate | Wed Aug 27 01:30:22 EDT 2025 Thu Aug 21 18:21:10 EDT 2025 Fri Sep 05 10:00:42 EDT 2025 Fri Jul 25 11:01:08 EDT 2025 Tue Jun 17 21:06:51 EDT 2025 Tue Jun 10 20:42:28 EDT 2025 Thu Apr 03 07:07:12 EDT 2025 Thu Apr 24 23:04:03 EDT 2025 Tue Jul 01 04:12:03 EDT 2025 Sat Sep 06 07:35:48 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 1 |
| Keywords | Inflammatory bowel disease Stanniocalcin-2 Infliximab IGF binding protein-4 Prednisolone Pregnancy-associated plasma protein-a |
| Language | English |
| License | Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c603t-2cbc585bbd5829fe12f2a97b5f7e76ddff52fbd1f75c3f8470f3f14c8116dc673 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Article-2 ObjectType-Undefined-1 ObjectType-Feature-3 content type line 23 |
| ORCID | 0000-0001-8237-0889 |
| OpenAccessLink | https://www.proquest.com/docview/2243009988?pq-origsite=%requestingapplication% |
| PMID | 31159802 |
| PQID | 2243009988 |
| PQPubID | 44673 |
| PageCount | 11 |
| ParticipantIDs | doaj_primary_oai_doaj_org_article_4f8c23494d5443f89ddca8f0e8de8126 pubmedcentral_primary_oai_pubmedcentral_nih_gov_6547608 proquest_miscellaneous_2235068005 proquest_journals_2243009988 gale_infotracmisc_A590724776 gale_infotracacademiconefile_A590724776 pubmed_primary_31159802 crossref_citationtrail_10_1186_s12876_019_1000_6 crossref_primary_10_1186_s12876_019_1000_6 springer_journals_10_1186_s12876_019_1000_6 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 2019-06-03 |
| PublicationDateYYYYMMDD | 2019-06-03 |
| PublicationDate_xml | – month: 06 year: 2019 text: 2019-06-03 day: 03 |
| PublicationDecade | 2010 |
| PublicationPlace | London |
| PublicationPlace_xml | – name: London – name: England |
| PublicationTitle | BMC gastroenterology |
| PublicationTitleAbbrev | BMC Gastroenterol |
| PublicationTitleAlternate | BMC Gastroenterol |
| PublicationYear | 2019 |
| Publisher | BioMed Central BioMed Central Ltd BMC |
| Publisher_xml | – name: BioMed Central – name: BioMed Central Ltd – name: BMC |
| References | J Thomsen (1000_CR16) 2015; 6 Y Ning (1000_CR49) 2006; 20 AC Chang (1000_CR46) 2008; 149 KH Katsanos (1000_CR4) 2001; 11 RM Beattie (1000_CR37) 1998; 49 H Gronbaek (1000_CR5) 2002; 97 A Hoeflich (1000_CR24) 2018; 9 R Hjortebjerg (1000_CR21) 2015; 100 LS Unterman (1000_CR11) 1985; 61 M Eivindson (1000_CR41) 2007; 17 ZT Resch (1000_CR52) 2004; 145 J Frystyk (1000_CR32) 1995; 5 R Hjortebjerg (1000_CR36) 2018; 39 Y Ning (1000_CR45) 2008; 22 R Hjortebjerg (1000_CR14) 2015; 48 KL Thomsen (1000_CR27) 2014; 20 JP Miell (1000_CR13) 1993; 136 CA Conover (1000_CR15) 2012; 23 RS Walmsley (1000_CR29) 1998; 43 RF Harvey (1000_CR28) 1980; 1 P Eder (1000_CR38) 2016; 48 R Hjortebjerg (1000_CR56) 2018; 41 Claus Oxvig (1000_CR18) 2015; 9 A Michalak (1000_CR2) 2016; 68 EJ Mason (1000_CR48) 2011; 21 PF Vestergaard (1000_CR30) 2013; 170 US Espelund (1000_CR25) 2017; 102 JW Chen (1000_CR34) 2003; 284 Z Hochberg (1000_CR43) 2002; 58 C Davidge-Pitts (1000_CR26) 2014; 222 CA Conover (1000_CR44) 2004; 131 P Ye (1000_CR51) 2003; 71 ZT Resch (1000_CR55) 2006; 147 EC Ebert (1000_CR39) 2009; 296 N Ramshanker (1000_CR10) 2017; 102 H Zatorski (1000_CR6) 2016; 68 HE Gruber (1000_CR50) 2013; 54 R Hjortebjerg (1000_CR8) 2014; 18 MF Gude (1000_CR35) 2012; 22 R Hjortebjerg (1000_CR9) 2014; 27 RA Frost (1000_CR42) 2004; 82 E-Suppl MR Jepsen (1000_CR17) 2015; 290 CA Conover (1000_CR53) 2006; 290 BL Cohen (1000_CR1) 2017; 357 M Eivindson (1000_CR7) 2007; 42 CA Conover (1000_CR20) 2013; 305 V Birzniece (1000_CR33) 2014; 170 GH Waetzig (1000_CR40) 2005; 19 MF Gude (1000_CR19) 2016; 175 1000_CR23 G Vervoort (1000_CR31) 2006; 21 R Hjortebjerg (1000_CR22) 2017; 176 W Li (1000_CR54) 2012; 2012 UV Gentilucci (1000_CR3) 2005; 21 J Frystyk (1000_CR12) 2013; 168 AD Gagliardi (1000_CR47) 2005; 288 |
| References_xml | – volume: 20 start-page: 7 issue: 1 year: 2014 ident: 1000_CR27 publication-title: Inflamm Bowel Dis doi: 10.1097/01.MIB.0000437496.07181.4c – volume: 100 start-page: 3032 issue: 8 year: 2015 ident: 1000_CR21 publication-title: J Clin Endocrinol Metab doi: 10.1210/jc.2015-2196 – volume: 1 start-page: 514 issue: 8167 year: 1980 ident: 1000_CR28 publication-title: Lancet. doi: 10.1016/S0140-6736(80)92767-1 – volume: 131 start-page: 1187 issue: 5 year: 2004 ident: 1000_CR44 publication-title: Development. doi: 10.1242/dev.00997 – volume: 168 start-page: 1 issue: 1 year: 2013 ident: 1000_CR12 publication-title: Eur J Endocrinol doi: 10.1530/EJE-12-0518 – volume: 149 start-page: 2403 issue: 5 year: 2008 ident: 1000_CR46 publication-title: Endocrinology doi: 10.1210/en.2007-1219 – volume: 296 start-page: G612 issue: 3 year: 2009 ident: 1000_CR39 publication-title: Am J Physiol Gastrointest Liver Physiol doi: 10.1152/ajpgi.90576.2008 – volume: 145 start-page: 1124 issue: 3 year: 2004 ident: 1000_CR52 publication-title: Endocrinology. doi: 10.1210/en.2003-1313 – volume: 21 start-page: 2998 issue: 10 year: 2006 ident: 1000_CR31 publication-title: Nephrology Dialysis Transplantation doi: 10.1093/ndt/gfl276 – volume: 290 start-page: 3430 issue: 6 year: 2015 ident: 1000_CR17 publication-title: J Biol Chem doi: 10.1074/jbc.M114.611665 – volume: 49 start-page: 483 issue: 4 year: 1998 ident: 1000_CR37 publication-title: Clin Endocrinol doi: 10.1046/j.1365-2265.1998.00562.x – volume: 22 start-page: 200 issue: 6 year: 2012 ident: 1000_CR35 publication-title: Growth Hormon IGF Res doi: 10.1016/j.ghir.2012.09.004 – volume: 305 start-page: E1145 issue: 9 year: 2013 ident: 1000_CR20 publication-title: Am J Physiol Endocrinol Metab doi: 10.1152/ajpendo.00405.2013 – volume: 284 start-page: E1149 issue: 6 year: 2003 ident: 1000_CR34 publication-title: Am J Physiol Endocrinol Metab doi: 10.1152/ajpendo.00410.2002 – volume: 17 start-page: 33 issue: 1 year: 2007 ident: 1000_CR41 publication-title: Growth Hormon IGF Res doi: 10.1016/j.ghir.2006.10.003 – volume: 176 start-page: 521 issue: 5 year: 2017 ident: 1000_CR22 publication-title: Eur J Endocrinol doi: 10.1530/EJE-16-0940 – volume: 5 start-page: 169 issue: 4 year: 1995 ident: 1000_CR32 publication-title: Growth Regul – volume: 68 start-page: 809 issue: 4 year: 2016 ident: 1000_CR6 publication-title: Pharmacol Rep doi: 10.1016/j.pharep.2016.03.006 – volume: 27 start-page: 771 issue: 6 year: 2014 ident: 1000_CR9 publication-title: Best Pract Res Clin Endocrinol Metab doi: 10.1016/j.beem.2013.08.010 – volume: 2012 start-page: 9 year: 2012 ident: 1000_CR54 publication-title: Mediat Inflamm – volume: 39 start-page: 54 year: 2018 ident: 1000_CR36 publication-title: Growth Hormon IGF Res doi: 10.1016/j.ghir.2018.01.001 – volume: 41 start-page: 7 year: 2018 ident: 1000_CR56 publication-title: Growth Hormon IGF Res doi: 10.1016/j.ghir.2018.05.002 – volume: 48 start-page: 322 issue: 4–5 year: 2015 ident: 1000_CR14 publication-title: Clin Biochem doi: 10.1016/j.clinbiochem.2014.11.022 – volume: 18 start-page: 209 issue: 2 year: 2014 ident: 1000_CR8 publication-title: Expert Opin Ther Targets doi: 10.1517/14728222.2014.858698 – volume: 175 start-page: 509 issue: 6 year: 2016 ident: 1000_CR19 publication-title: Eur J Endocrinol doi: 10.1530/EJE-16-0569 – volume: 288 start-page: E92 issue: 1 year: 2005 ident: 1000_CR47 publication-title: Am J Physiol Endocrinol Metab doi: 10.1152/ajpendo.00268.2004 – volume: 68 start-page: 837 issue: 4 year: 2016 ident: 1000_CR2 publication-title: Pharmacol Rep doi: 10.1016/j.pharep.2016.04.016 – volume: 19 start-page: 91 issue: 1 year: 2005 ident: 1000_CR40 publication-title: FASEB journal : official publication of the Federation of American Societies for Experimental Biology doi: 10.1096/fj.04-2073fje – volume: 58 start-page: 33 issue: Suppl 1 year: 2002 ident: 1000_CR43 publication-title: Horm Res – volume: 9 start-page: 177 issue: 2 year: 2015 ident: 1000_CR18 publication-title: Journal of Cell Communication and Signaling doi: 10.1007/s12079-015-0259-9 – volume: 222 start-page: 87 issue: 1 year: 2014 ident: 1000_CR26 publication-title: J Endocrinol doi: 10.1530/JOE-13-0610 – volume: 21 start-page: 243 issue: 5 year: 2011 ident: 1000_CR48 publication-title: Growth Hormon IGF Res doi: 10.1016/j.ghir.2011.06.002 – volume: 21 start-page: 1063 issue: 9 year: 2005 ident: 1000_CR3 publication-title: Aliment Pharmacol Ther doi: 10.1111/j.1365-2036.2005.02449.x – volume: 61 start-page: 618 issue: 4 year: 1985 ident: 1000_CR11 publication-title: J Clin Endocrinol Metab doi: 10.1210/jcem-61-4-618 – ident: 1000_CR23 doi: 10.1161/JAHA.116.005358 – volume: 102 start-page: 4031 issue: 11 year: 2017 ident: 1000_CR10 publication-title: J Clin Endocrinol Metab doi: 10.1210/jc.2017-00696 – volume: 9 start-page: 388 year: 2018 ident: 1000_CR24 publication-title: Front Endocrinol doi: 10.3389/fendo.2018.00388 – volume: 6 start-page: 32266 issue: 31 year: 2015 ident: 1000_CR16 publication-title: Oncotarget. doi: 10.18632/oncotarget.5010 – volume: 170 start-page: 229 issue: 2 year: 2013 ident: 1000_CR30 publication-title: Eur J Endocrinol doi: 10.1530/EJE-13-0661 – volume: 102 start-page: 3526 issue: 9 year: 2017 ident: 1000_CR25 publication-title: J Clin Endocrinol Metab doi: 10.1210/jc.2017-00033 – volume: 54 start-page: 432 issue: 6 year: 2013 ident: 1000_CR50 publication-title: Connect Tissue Res doi: 10.3109/03008207.2013.848200 – volume: 48 start-page: 1168 issue: 10 year: 2016 ident: 1000_CR38 publication-title: Dig Liver Dis doi: 10.1016/j.dld.2016.06.038 – volume: 136 start-page: 525 issue: 3 year: 1993 ident: 1000_CR13 publication-title: J Endocrinol doi: 10.1677/joe.0.1360525 – volume: 147 start-page: 885 issue: 2 year: 2006 ident: 1000_CR55 publication-title: Endocrinology. doi: 10.1210/en.2005-0908 – volume: 97 start-page: 673 issue: 3 year: 2002 ident: 1000_CR5 publication-title: Am J Gastroenterol doi: 10.1016/S0002-9270(01)04110-7 – volume: 82 E-Suppl start-page: E100 year: 2004 ident: 1000_CR42 publication-title: J Anim Sci – volume: 357 start-page: j2505r year: 2017 ident: 1000_CR1 publication-title: BMJ doi: 10.1136/bmj.j2505 – volume: 42 start-page: 464 issue: 4 year: 2007 ident: 1000_CR7 publication-title: Scand J Gastroenterol doi: 10.1080/00365520601010115 – volume: 23 start-page: 242 issue: 5 year: 2012 ident: 1000_CR15 publication-title: Trends in Endocrinology & Metabolism doi: 10.1016/j.tem.2012.02.008 – volume: 11 start-page: 364 issue: 6 year: 2001 ident: 1000_CR4 publication-title: Growth Hormon IGF Res doi: 10.1054/ghir.2001.0248 – volume: 71 start-page: 721 issue: 5 year: 2003 ident: 1000_CR51 publication-title: J Neurosci Res doi: 10.1002/jnr.10512 – volume: 20 start-page: 2173 issue: 9 year: 2006 ident: 1000_CR49 publication-title: Mol Endocrinol doi: 10.1210/me.2005-0196 – volume: 290 start-page: C183 issue: 1 year: 2006 ident: 1000_CR53 publication-title: Am J Physiol Cell Physiol doi: 10.1152/ajpcell.00199.2005 – volume: 43 start-page: 29 issue: 1 year: 1998 ident: 1000_CR29 publication-title: Gut doi: 10.1136/gut.43.1.29 – volume: 22 start-page: 1213 issue: 5 year: 2008 ident: 1000_CR45 publication-title: Mol Endocrinol doi: 10.1210/me.2007-0536 – volume: 170 start-page: 375 issue: 3 year: 2014 ident: 1000_CR33 publication-title: Eur J Endocrinol doi: 10.1530/EJE-13-0835 |
| SSID | ssj0017823 |
| Score | 2.2736146 |
| Snippet | Background
Patients with inflammatory bowel disease (IBD) present with reduced serum insulin-like growth factor I (IGF-I). Anti-inflammatory treatment with... Patients with inflammatory bowel disease (IBD) present with reduced serum insulin-like growth factor I (IGF-I). Anti-inflammatory treatment with prednisolone... Background Patients with inflammatory bowel disease (IBD) present with reduced serum insulin-like growth factor I (IGF-I). Anti-inflammatory treatment with... Thirty-eight patients with active IBD treated with either prednisolone (n = 17) or infliximab (n = 21) were examined before and after 7 days of treatment.... Abstract Background Patients with inflammatory bowel disease (IBD) present with reduced serum insulin-like growth factor I (IGF-I). Anti-inflammatory treatment... |
| SourceID | doaj pubmedcentral proquest gale pubmed crossref springer |
| SourceType | Open Website Open Access Repository Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 83 |
| SubjectTerms | Adult Anti-inflammatory agents Biological activity Biological Availability Blood proteins Cell activation Diabetes therapy Dosage and administration Drug therapy Enzymes Female Gastroenterology Gastrointestinal diseases Genetic aspects Glucocorticoids Glycoproteins - blood Health aspects Hepatology Humans IGF binding protein-4 Immunosuppression Immunotherapy Induction Chemotherapy Inflammatory bowel disease Inflammatory bowel diseases Inflammatory Bowel Diseases - blood Inflammatory Bowel Diseases - drug therapy Infliximab Infliximab - pharmacokinetics Insulin Insulin-Like Growth Factor Binding Protein 4 - drug effects Insulin-like growth factor I Insulin-Like Growth Factor I - drug effects Insulin-like growth factor II Insulin-like growth factor-binding protein 3 Insulin-like growth factor-binding protein 4 Insulin-like growth factors Intercellular Signaling Peptides and Proteins - blood Internal Medicine Intestinal disorders Intestine Male Medical research Medicine Medicine & Public Health Monoclonal antibodies Novels Physical growth Prednisolone Prednisolone - pharmacokinetics Pregnancy Pregnancy-associated plasma protein-a Pregnancy-Associated Plasma Protein-A - drug effects Protein binding Protein biosynthesis Protein synthesis Receptor mechanisms Remission Research Article Stanniocalcin Stanniocalcin-2 TNF inhibitors Tumor necrosis factor-TNF Tumor necrosis factor-α |
| SummonAdditionalLinks | – databaseName: DOAJ Directory of Open Access Journals dbid: DOA link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Lb9QwELZQD4gL4k1KQUZCQgJZdZz4EW5bxFKQivZApd6i-CUitclqdyv6d_inzCTepSkCLtyieKyMPWPP2DP5hpBXeW4D-AGSBRMtK43ImbWWMxllIa2wJnj83_nkizo-LT-fybNrpb4wJ2yEBx4n7rCMxgnEUPGI1BZN5b1rTOTB-ADGaQDb5hXfHqZS_ADsXpFimLlRh2vYhTWenCuG99lMTazQANb_-5Z8zSbdzJe8ETQdbNH8HrmbnEg6G5m_T26F7gG5fZLC5A_JDxA-_fRxTkecZtp2NOGnrilevMKLCJpwMUTYqe2_h3OaIjV0yDwPfqRbroLvWlDPvgu0Xw392qv2orHv6LLfYKYR8IEZirSPFHxJis5m16KBBFaYoId0MVss2AwegKGjBStpc9WuH5HT-Yev749ZqsXAnOLFhglnHZwsrPXSiCqGXETRVNrKqINW3scoRbQ-j1o6kFKpeSxiXjqT58o7pYvHZK8DXp8SWjiLkNgNeIIK5BobbmwRuaqEh81BlxnhW9nULgGVY72M83o4sBhVj-KsQZwIucxrlZE3uy7LEaXjb8RHKPAdIQJsDy9A7eqkdvW_1C4jr1FdatwGgDnXpL8ZYIgIqFXPZMW1KLUGyoMJJSxfN23eKlydto91DX5Vgb67MRl5uWvGnpgS14X-EmkKiYVTuMzIk1E_d0NCCKXKcJERPdHcyZinLV37bQAXx2LUisN33251_Bdbf5zS_f8xpc_IHYErFK-4igOyt1ldhufg8W3si2Fx_wRQTFEN priority: 102 providerName: Directory of Open Access Journals – databaseName: Scholars Portal Journals: Open Access dbid: M48 link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV3di9QwEA_nCeKL-G31lAiCoMRL0yZNBZE9cT2Fk31w4d5K83UW9tp1dw_XP8f_1Jm2u2fP895KM2knzUxmkpn-hpAXcWw8-AGSeR0MS7WImTGGMxlkIo0w2jv83_noqzqcpl-O5fEO2ZS36j_g8tKtHdaTmi5mb9Y_fr0HhX_XKrxW-0tYYzPcF-cMT6uZukaut-EizORLz4MKYAyTPrB5abeBaWoR_P9dp_8yVBeTKC9EUlsDNb5NbvWeJR11onCH7Pj6Lrlx1MfO75HfIBH086cx7cCbaVXTHlR1SfE0Fm4EEI_TNuxOTfPTz2gfvqFtOrp3Hd184V1dgcw2tafNou1XravT0ryl82aF6UfAB6Yt0iZQcDApeqB1hVYTWGGC7tPJaDJhI7gAhg4mLKXlulreJ9Pxx28fDllfoIFZxZMVE9ZY2G4Y46QWefCxCKLMMyND5jPlXAhSBOPikEmbBLCDPCQhTq2OY-WsypIHZLcGXh8RmliDONkluIcqzdNQcm2SwFUuHKwYWRoRvpmbwvbo5VhEY1a0uxitim46C5hOxGHmhYrIq22XeQfdcRXxAU74lhBRt9sbzeKk6JW4SIO2AvF8HKIGBp07Z0sduNfOg6MED3mJ4lKgtAJztux_cYAhIspWMZI5z0SaZUC5N6AEnbbD5o3AFRuVKMDZStCh1zoiz7fN2BPz5GrfnCFNIrGaCpcRedjJ53ZIiKuUay4ikg0kdzDmYUtdfW8Rx7FCteLw3tcbGT9n67-f9PHVg3hCbgrUPTzRSvbI7mpx5p-Cg7cyz1q1_QOhIEs_ priority: 102 providerName: Scholars Portal – databaseName: Springer Nature OA Free Journals dbid: C6C link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV1bi9QwFA66gvgi3h1dJYIgKGHTpElT32YHx1VYmQcX9i00NyzstsPMLO7f8Z96TtsZt-sFfBuak85JzzU5yRdCXmeZi5AHKBZNciw3ImPOOc5UUlI54UwMeN75-Is-Osk_n6rTASwaz8Jcrd9nRh-swX8WOOctGa5EM32T3FLgd1GZZ3q2KxhAoJND0fKP3UZhp0Pn_90HXwlC1zdIXquSdsFnfo_cHbJGOu3FfJ_ciM0Dcvt4qIs_JD9A2vTTxzntgZlp3dABMHVNcaUVHiQQ_XlXUqeu_R7P6FCaod1W8xh6uuUqhqYGfWybSNtV16--rM8r954u2w1uLQI-cEsibROF5JFidtnUGBGBFSboAV1MFws2hR_A0OGC5bS6rNePyMn8w9fZERsuX2Bec7lhwjsPUwnngjKiTDETSVRl4VQqYqFDSEmJ5EKWCuVlghjHk0xZ7k2W6eB1IR-TvQZ4fUqo9A4xsCtI_XRe5qnixsnEdSkCeIMinxC-lY31AzI5XpBxZrsZitG2F6cFcSLGMrd6Qt7uuix7WI5_ER-iwHeEiKjdPQBFs4OB2jwZLxCrJyAiYDJlCL4yiUcTIiRB8JI3qC4W7R6Y89VwfAGGiAhadqpKXoi8KIByf0QJ9urHzVuFs4O_WFtIpCQm68ZMyKtdM_bEPXBNbC-QRiq8KYWrCXnS6-duSIiZVBouJqQYae5ozOOWpv7WoYnj7dOaw_--2-r4L7b--kmf_Rf1c3JHoCni4pXcJ3ub1UV8Abncxr3srPgnd2xAuA priority: 102 providerName: Springer Nature |
| Title | The IGF system in patients with inflammatory bowel disease treated with prednisolone or infliximab: potential role of the stanniocalcin-2 / PAPP-A / IGFBP-4 axis |
| URI | https://link.springer.com/article/10.1186/s12876-019-1000-6 https://www.ncbi.nlm.nih.gov/pubmed/31159802 https://www.proquest.com/docview/2243009988 https://www.proquest.com/docview/2235068005 https://pubmed.ncbi.nlm.nih.gov/PMC6547608 https://doaj.org/article/4f8c23494d5443f89ddca8f0e8de8126 |
| Volume | 19 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV3db9MwELdgkxAviG8KozISEhLIauLEjsMLaquVgdSpmphU8RLFXyPSlpS2E_t3-E-5S92ODLGXqI3t9Fyf7853l98R8jaOtQM7QDCnvGap4jHTWkdMeJEIzbVyFt93nh7Lo9P061zMg8NtFdIqtzKxFdS2MegjH4CqSdCcUerT4ifDqlEYXQ0lNO6S_RgsESzdkM13B64YtF8SIpmxkoMVyOIMz885Q682kx1d1EL2_yuY_9JMN7Mmb4ROW400eUgeBFOSDjdr_4jccfVjcm8aguVPyG9gAfrl84Ru0JppVdOAorqi6H6FGx744aKNs1Pd_HLnNMRraJt_7uym32LpbF0Bkza1o82yHVddVRel_kgXzRrzjYAOzFOkjadgUVI0OesK1SSQwjgd0NlwNmND-AAEjWYspeVVtXpKTieH38ZHLFRkYEZGyZpxow2cL7S2QvHcu5h7XuaZFj5zmbTWe8G9trHPhEk8KL7IJz5OjYpjaY3MkmdkrwZaXxCaGI3A2CXYgzLNU19GSic-kjm3ICKytEei7doUJsCVY9WM86I9tihZbJazgOVE4OWokD3yfjdkscHquK3zCBd81xFhttsbzfKsCLu2SL0yHAF8LMIEepVba0rlI6esA8sIHvIO2aVAYQDEmTK80wBTRFitYijyKONplkHPg05P2MSm27xluCIIkVVxzfI98mbXjCMxMa52zSX2SQSWT4lEjzzf8OduSgiklKuI90jW4dzOnLstdfWjhRjHktQygt_9sOXxa7L--5e-vH0Sr8h9jnsPXVjJAdlbLy_da7Do1rrfbts-2R8dHs9O4NtYjvutdwSu01TB9WT0_Q9TaE2g |
| linkProvider | ProQuest |
| linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1tb9MwELZGJwFfEO8UBhgJhASymjhvDtKEWlhp2VpVaJP2LcRvEGlLSttp4-fwR_ht3CVuR4fYt32r4nNq5853Z9_5OUJe-r404AdEzAgrWSi4z6SUHotsFESSS2E03ncejePBQfj5MDrcIL-Xd2EwrXKpE2tFrSuFZ-QdMDUBujNCvJ_-YFg1CqOryxIauSutoLdriDF3sWPX_DyFLdx8e_gR-P2K8_7O_ocBc1UGmIq9YMG4kgp8Zil1JHhqjc8tz9NERjYxSay1tRG3Uvs2iVRgQZl7NrB-qITvx1rFSQDvvUY2QzxAaZHN3s548mUVxwD7G7hYqi_izhysQYI7-JThuTqL16xhXTTgX9Pwl228mLd5IXhb28T-bXLLObO020jfHbJhyrvk-siF6--RXyCEdPipTxu8aFqU1OG4zikeAMMDCxJ5XEf6qaxOzRF1ESNaZ8Ab3dBNZ0aXBSyTqjS0mtX9irPiOJfv6LRaYMYTjAMzJWllKfi0FJ3eskBDDUNhnHbopDuZsC78gAH1Jiyk-Vkxv08OroRbD0irhLE-IjRQEqG5c_BI4zANbe4JGVgvTrkGJZWEbeIteZMpB5iOdTuOsnrjJOKsYWcG7EToZy-L2-TNqsu0QQu5jLiHDF8RItB3_aCafcuc3shCKxRHCCGNQIVWpFqrXFjPCG3AN4OXvEZxyVAdweBU7m5VwBQR2CvrRqmX8DBJgHJrjRLUiFpvXgpc5tTYPDtfdG3yYtWMPTE1rzTVCdIEERZw8aI2edjI52pKCOWUCo-3SbImuWtzXm8pi-81yDkWxY49-N-3Sxk_H9Z_P-njyyfxnNwY7I_2sr3hePcJuclxHeKBWrBFWovZiXkK_uVCPnOLmJKvV603_gDbr403 |
| linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV1bb9MwFLZgkyZeEPcVBhgJCQlkNXFix-EtA8pW2FQJJu0tim8QaUuqthP7O_xTzkncQsZF4q2Kj1M752of-zuEPI9j7SAOEMwpr1mqeMy01hETXiRCc62cxfvOR8fy4CSdnorTUOd0uT7tvk5J9ncaEKWpWY3n1vcqruR4CVY1w5VwznB_msnrZFuJPIfV13ZRTD9NN4kEcIBJSGb-sePAHXWo_b_b5l-c09WDk1eyp51TmtwiN0M0SYue_bfJNdfcITtHIV9-l3wHKaCH7ye0B2ymdUMDkOqS4g4sPPAgEuddqp3q9ps7oyFlQ7sj6M72dPOFs00Ncto2jraLrl99WZ9X-jWdt_jlQI4pHlWkracQVFKMOpsaPSUMhXE6prNiNmMF_IAB7c9YSqvLenmPnEzefX5zwEJRBmZklKwYN9rAEkNrKxTPvYu551WeaeEzl0lrvRfcaxv7TJjEg--LfOLj1Kg4ltbILLlPthoY6y6hidGIjV1BSCjTPPVVpHTiI5lzC1YiS0ckWvOmNAGxHAtnnJXdykXJsmdnCexE7OWolCPyctNl3sN1_It4Hxm-IUSk7e5Bu_hSBsUtU68MRwwfi0iBXuXWmkr5yCnrIDiCl7xAcSnRHsDgTBWuNcAUEVmrLEQeZTzNMqDcG1CCHpth81rgymBHliUEWAkG8UqNyLNNM_bEs3GNay-QJhFYQSUSI_Kgl8_NlBBLKVcRH5FsILmDOQ9bmvprhzKOVallBP_7ai3jP4f110_68L-on5Kd2dtJ-fHw-MMjcoOjVuL-VrJHtlaLC_cYwr2VfhJU-geY4E1l |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=The+IGF+system+in+patients+with+inflammatory+bowel+disease+treated+with+prednisolone+or+infliximab%3A+potential+role+of+the+stanniocalcin-2+%2F+PAPP-A+%2F+IGFBP-4+axis&rft.jtitle=BMC+gastroenterology&rft.au=Hjortebjerg%2C+Rikke&rft.au=Thomsen%2C+Karen+L&rft.au=Agnholt%2C+J%C3%B8rgen&rft.au=Frystyk%2C+Jan&rft.date=2019-06-03&rft.pub=BioMed+Central&rft.eissn=1471-230X&rft.volume=19&rft_id=info:doi/10.1186%2Fs12876-019-1000-6 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1471-230X&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1471-230X&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1471-230X&client=summon |