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  • pancreatic hormones  (2)
  • Antilympocyte Globulin  (1)
  • Pancreas transplantation  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Determinants of a normal (versus impaired) oral glucose tolerance after combined pancreas-kidney transplantation in IDDM patients (1996)
    Springer
    Diabetologia 39 (1996), S. 462-468 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Pancreas transplantation ; insulin secretion ; pancreatic hormones ; oral glucose tolerance ; glucagon stimulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary After successful pancreas transplantation, insulin-dependent diabetic patients are characterized by a normal or at worst impaired oral glucose tolerance (World Health Organisation criteria). It is not known which pathophysiological mechanisms cause the difference between normal and impaired oral glucose tolerance. Therefore, we studied 41 patients after successful combined pancreas-kidney transplantation using stimulation in the fasting state with oral glucose (75 g), intravenous glucose (0.33 g/kg) and glucagon bolus injection (1 mg i. v.). Glucose (glucose oxidase), insulin and C-peptide (immunoassay) were measured. Repeated-measures analysis of variance and multiple regression analysis were used to analyse the results which showed: 28 patients had a normal, and 13 patients had an impaired oral glucose tolerance. Impaired oral glucose tolerance was associated with a greatly reduced early phase insulin secretory response (insulin p 〈 0.0001; C-peptide p = 0.037). Age (p = 0.65), body mass index (p = 0.94), immunosuppressive therapy (cyclosporin A p = 0.84; predniso(lo)ne p = 0.91; azathioprine p = 0.60) and additional clinical parameters were not different. Reduced insulin secretory responses in patients with impaired oral glucose tolerance were also found with intravenous glucose or glucagon stimulations. Exocrine secretion (α-amylase in 24-h urine collections) also demonstrated reduced pancreatic function in these patients (–46 %; p = 0.04). Multiple regression analysis showed a significant correlation of 120-min glucose with ischaemia time (p = 0.003) and the number of HLA-DR mismatches (p = 0.026), but not with HLA-AB-mismatches (p = 0.084). In conclusion, the pathophysiological basis of impaired oral glucose tolerance after pancreas transplantation is a reduced insulin secretory capacity. Transplant damage is most likely caused by perioperative influences (ischaemia) and by the extent of rejection damage related, for example, to DR-mismatches. [Diabetologia (1996) 39: 462–468]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400678
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Determinants of a normal (versus impaired) oral glucose tolerance after combined pancreas-kidney transplantation in IDDM patients (1996)
    Springer
    Diabetologia 39 (1996), S. 462-468 
    Details
    ISSN: 1432-0428
    Keywords: Pancreas transplantation ; insulin secretion ; pancreatic hormones ; oral glucose tolerance ; glucagon stimulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary After successful pancreas transplantation, insulin-dependent diabetic patients are characterized by a normal or at worst impaired oral glucose tolerance (World Health Organisation criteria). It is not known which pathophysiological mechanisms cause the difference between normal and impaired oral glucose tolerance. Therefore, we studied 41 patients after successful combined pancreas-kidney transplantation using stimulation in the fasting state with oral glucose (75 g), intravenous glucose (0.33 g/kg) and glucagon bolus injection (1 mg i.v.). Glucose (glucose oxidase), insulin and C-peptide (immunoassay) were measured. Repeated-measures analysis of variance and multiple regression analysis were used to analyse the results which showed: 28 patients had a normal, and 13 patients had an impaired oral glucose tolerance. Impaired oral glucose tolerance was associated with a greatly reduced early phase insulin secretory response (insulin p〈0.0001; C-peptide p=0.037). Age (p=0.65), body mass index (p=0.94), immunosuppressive therapy (cyclosporin A p=0.84; predniso(lo)ne p=0.91; azathioprine p=0.60) and additional clinical parameters were not different. Reduced insulin secretory responses in patients with impaired oral glucose tolerance were also found with intravenous glucose or glucagon stimulations. Exocrine secretion (α-amylase in 24-h urine collections) also demonstrated reduced pancreatic function in these patients (−46%; p=0.04). Multiple regression analysis showed a significant correlation of 120-min glucose with ischaemia time (p=0.003) and the number of HLA-DR mismatches (p=0.026), but not with HLA-AB-mismatches (p=0.084). In conclusion, the pathophysiological basis of impaired oral glucose tolerance after pancreas transplantation is a reduced insulin secretory capacity. Transplant damage is most likely caused by perioperative influences (ischaemia) and by the extent of rejection damage related, for example, to DR-mismatches.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400678
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Cumulation and elimination of horse-anti-dog lymphocyte and normal horse gammaglobulin in dogs (1976)
    Springer
    Research in experimental medicine 167 (1976), S. 231-238 
    Details
    ISSN: 1433-8580
    Keywords: Antilympocyte Globulin ; Immunosuppression ; Elimination of Gamma-Globulin ; Antilymphozytenglobulin ; Immunsuppression ; Gammglobulinelimination
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Zwei Gruppen von Hunden wurden elf Tage lang mit 20 mg/kg 131-I-markiertem Pferde-anti-human-Lymphozyten-Globulin bzw. Normal-Pferde-Gammaglobulin i.v. behandelt. Pferde-anti-human-Lymphozyten-Globulin wurde signifikant schneller eliminiert als Normal-Pferde-Gammaglobulin. Im Gegensatz zu dem kontinuierlichen Anstieg der Serum-Radioaktivität unter Normal-Pferde-Gammaglobulin-Behandlung war in der Pferde-anti-human-Lymphozyten-Globulin-Gruppe ab dem 5. Tag eine Plateaubildung zu beobachten. Zum Behandlungsende betrug die Serumkonzentration des xenogenen Proteins 165 ± 8 mg/1 in der Pferde-anti-human-Lymphozyten-Globulin- und 498 ± 15 mg/1 in der Normal-Pferde-Gammaglobulin-Gruppe. Die Pferde-anti-human-Lymphozyten-Globulin-behandelten Tiere zeigten einen signifikant höheren Anstieg agglutinierender Antikörper gegen Pferde-Erythrozyten als Normal-Pferde-Gammaglobulin-behandelte Tiere. Diese starke Immunogenizität von antilymphozytärem Pferde-Gammaglobulin muß bei der Applikation von Pferde-anti-human-Lymphozyten-Globulin berücksichtigt werden.
    Notes: Summary Two groups of dogs received daily intravenous doses of 20 mg/kg 131-I-labelled horse-anti-dog lymphcyte globulin or normal horse gammaglobulin respectively over a period of 11 days. Horse-anti-dog lymphocyte globulin showed a significantly higher eleimination rate than normal horse gammaglobulin. In contrary to the continuous increase in serum radioactivity during normal horse gammaglobulin treatment, there was a plateau after the 5th day in the horse-anti-dog lymphocyte globulin group. The xenogeneic protein concentration, measured with the single radial immunodiffusion technique, at the end of treatment was 165 ± 8 mg/1 in the horse-anti-dog lymphocyte globulin, compared to 498 ± 15 mg/1 in the normal horse gammaglobulin group. After treatment horse-anti-dog-lymphcyte globulin treated animals showed a significantly higher increase in active hemagglutination titer against horse erythrocytes with an average of 2−8.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01851647
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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