Erik Zimmermann-Nielsen

Publications (5)10.85 Total impact

• Article: The insulin-like growth factor (IGF)-system in active ulcerative colitis and Crohn's disease: relations to disease activity and corticosteroid treatment.

  Martin Eivindson, Henning Grønbaek, Allan Flyvbjerg, Jan Frystyk, Erik Zimmermann-Nielsen, Jens Frederik Dahlerup
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  ABSTRACT: Metabolic bone disease (MBD) and muscle wasting (MW) are serious complications in adults suffering from inflammatory bowel disease (IBD). The inflammatory process and corticosteroid treatment may lead to changes in the IGF-system associated with MBD and MW. To assess changes in the IGF-system and clinical and biochemical markers in ulcerative colitis (UC) and Crohn's disease (CD). We studied 37 IBD patients with severe clinical exacerbation (20 with UC, 17 with CD) before and during high dose corticosteroid treatment and tapering (8-12 weeks). Total IGF-I was reduced in CD (36% p<0.01) and UC (41% p<0.001) before treatment and normalized completely. Free IGF-I baseline levels were unchanged compared to controls. In UC, free IGF-I levels increased significantly at week 1 and week 4 (p<0.01, respectively). In CD, no changes in free IGF-I levels were observed. IGFBP-2 baseline levels were increased by a factor 2.3 in UC and CD compared to controls (p<0.01 respectively) and normalized during treatment. IGFBP-3 was reduced by 38% (p<0.01) in CD and 32% (p<0.01) in UC with only partial normalization. Harvey-Bradshaw index, C - reactive protein and albumin normalized during treatment. Significant changes in total and free IGF-I and IGFBP-2 and IGFBP-3 were demonstrated in CD and UC patients in exacerbation with only partial normalization during high dose corticosteroid treatment and tapering without differences between UC and CD. These changes may be part of MBD and MW in active IBD.
  Growth Hormone & IGF Research 03/2007; 17(1):33-40. · 2.16 Impact Factor
• Source

  Available from: Jens Frederik Dahlerup

  Article: Complement activation capacity in plasma before and during high-dose prednisolone treatment and tapering in exacerbations of Crohn's disease and ulcerative colitis.

  Erik Zimmermann-Nielsen, Henning Grønbaek, Jens Frederik Dahlerup, Gunnar Baatrup, Ole Thorlacius-Ussing
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  ABSTRACT: Ulcerative colitis (UC) and Crohn's disease (CD) are characterized by intestinal inflammation mainly caused by a disturbance in the balance between cytokines and increased complement (C) activation. Our aim was to evaluate possible associations between C activation capacity and prednisolone treatment. Plasma from patients with exacerbations of UC (n = 18) or CD (n = 18) were collected before and during high dose prednisolone treatment (1 mg/kg body weight) and tapering. Friedman's two way analysis of variance, Mann-Whitney U test and Wilcoxon signed-rank sum test were used Before treatment, plasma from CD patients showed significant elevations in all C-mediated analyses compared to the values obtained from 38 healthy controls (p < 0.02), and in mannan binding lectin (MBL)-concentration and MBL-C4-activation capacity (AC) values compared to UC patients (p < 0.02). Before treatment, plasma from UC patients showed significant elevations only in the classical pathway-mediated C3-AC compared to values obtained from healthy controls (p < 0.01). After treatment was initiated, significant reductions, which persisted during follow-up, were observed in the classical pathway-mediated C3-AC and MBL-C4-AC in plasma from CD patients (p < 0.05). Our findings indicate that C activation capacity is up-regulated significantly in plasma from CD patients. The decreases observed after prednisolone treatment reflect a general down-regulation in immune activation.
  BMC Gastroenterology 01/2005; 5:31. · 2.42 Impact Factor
• Article: Complement activation capacity in plasma before and during high-dose prednisolone treatment and tapering in exacerbations of Crohn's disease and ulcerative colitis

  Erik Zimmermann-Nielsen, Henning Grønbæk, Jens Dahlerup, Gunnar Baatrup, Ole Thorlacius-Ussing
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  ABSTRACT: Abstract Background Ulcerative colitis (UC) and Crohn's disease (CD) are characterized by intestinal inflammation mainly caused by a disturbance in the balance between cytokines and increased complement (C) activation. Our aim was to evaluate possible associations between C activation capacity and prednisolone treatment. Methods Plasma from patients with exacerbations of UC (n = 18) or CD (n = 18) were collected before and during high dose prednisolone treatment (1 mg/kg body weight) and tapering. Friedman's two way analysis of variance, Mann-Whitney U test and Wilcoxon signed-rank sum test were used Results Before treatment, plasma from CD patients showed significant elevations in all C-mediated analyses compared to the values obtained from 38 healthy controls (p < 0.02), and in mannan binding lectin (MBL)-concentration and MBL-C4-activation capacity (AC) values compared to UC patients (p < 0.02). Before treatment, plasma from UC patients showed significant elevations only in the classical pathway-mediated C3-AC compared to values obtained from healthy controls (p < 0.01). After treatment was initiated, significant reductions, which persisted during follow-up, were observed in the classical pathway-mediated C3-AC and MBL-C4-AC in plasma from CD patients (p < 0.05). Conclusion Our findings indicate that C activation capacity is up-regulated significantly in plasma from CD patients. The decreases observed after prednisolone treatment reflect a general down-regulation in immune activation.
  BMC Gastroenterology. 01/2005;
• Article: Activation capacity of the alternative and classic complement pathways in patients operated on for colorectal cancer.

  Erik Zimmermann-Nielsen, Lene H Iversen, Sven-Erik Svehag, Ole Thorlacius-Ussing, Gunnar Baatrup
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  ABSTRACT: Tumor cells may suppress activation of the host's complement system, and the functional state of the complement system may be a prognostic marker of outcome in patients with malignancies. Serial plasma samples from patients undergoing intended curative surgery for colorectal cancer were analyzed for complement factor C3 activation capacity. Samples were collected from 91 patients with colorectal cancer and 13 with benign colorectal diseases before surgery and 1, 2, and 7 days after surgery, between 8 and 13 days after surgery, and 3, 6, 12, 18, 24, 36, 48, and 60 months after surgery. The samples were analyzed with an enzyme-linked immunosorbent assay that measured C3 activation capacity by the alternative and classic complement pathways. Cancer patients were compared according to Dukes stage, type of surgery performed, transfusion of blood, development of infection, venous thromboembolism, and cancer recurrence. Plasma samples obtained from cancer patients before surgery showed C3 activation capacities corresponding to those of samples from patients with benign disease. For both patient groups, C3 activation capacity decreased after surgery and normalized within seven days. Significant differences in C3 activation capacities were observed between cancer patients that were related to Dukes stage and in patients with and without buffy coat-depleted red cells suspended in saline, adenine, glucose, and mannitol transfusion, infectious events, and deep venous thromboembolism. Measurement of C3 activation capacity was of predictive value in patients who developed infection. Serial measurements of C3 activation capacity in plasma from patients who had undergone surgery for colorectal cancer revealed significant differences related to Dukes staging after surgery and to the development of infections but not to cancer recurrence.
  Diseases of the Colon & Rectum 05/2002; 45(4):544-53. · 3.13 Impact Factor
• Article: Activation Capacity of the Alternative and Classic Complement Pathways in Patients Operated on for Colorectal Cancer

  Erik Zimmermann-Nielsen, LeneH. Iversen, Sven-Erik Svehag, Ole Thorlacius-Ussing, Gunnar Baatrup
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  ABSTRACT: PURPOSE: Tumor cells may suppress activation of the hosts complement system, and the functional state of the complement system may be a prognostic marker of outcome in patients with malignancies. Serial plasma samples from patients undergoing intended curative surgery for colorectal cancer were analyzed for complement factor C3 activation capacity. METHODS: Samples were collected from 91 patients with colorectal cancer and 13 with benign colorectal diseases before surgery and 1, 2, and 7 days after surgery, between 8 and 13 days after surgery, and 3, 6, 12, 18, 24, 36, 48, and 60 months after surgery. The samples were analyzed with an enzyme-linked immunosorbent assay that measured C3 activation capacity by the alternative and classic complement pathways. Cancer patients were compared according to Dukes stage, type of surgery performed, transfusion of blood, development of infection, venous thromboembolism, and cancer recurrence. RESULTS: Plasma samples obtained from cancer patients before surgery showed C3 activation capacities corresponding to those of samples from patients with benign disease. For both patient groups, C3 activation capacity decreased after surgery and normalized within seven days. Significant differences in C3 activation capacities were observed between cancer patients that were related to Dukes stage and in patients with and without buffy coat-depleted red cells suspended in saline, adenine, glucose, and mannitol transfusion, infectious events, and deep venous thromboembolism. Measurement of C3 activation capacity was of predictive value in patients who developed infection. CONCLUSION: Serial measurements of C3 activation capacity in plasma from patients who had undergone surgery for colorectal cancer revealed significant differences related to Dukes staging after surgery and to the development of infections but not to cancer recurrence.
  Diseases of the Colon & Rectum 01/2002; 45(4):544-553. · 3.13 Impact Factor