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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 27 (1984), S. 149-153 
    ISSN: 1432-0428
    Keywords: Pancreas transplant ; cyclosporin ; azathioprine ; HLA-identical siblings ; glucose metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Of 89 pancreas transplants performed in 77 diabetic patients (43 with and 34 without previous kidney transplants), 53 were from cadaver and 36 from related donors. To date, 64 patients (83%) are alive and 27 (35%) have functioning grafts (14 〉 1 year), including 0 out of 3 duct-ligated, 3 out of 15 open-duct, 17 out of 32 enteric-drained, and 7 out of 39 duct-injected. Of technically successful allografts, 8 out of 16 (50%) in the azathioprine- and 17 out of 47 (36%) in the cyclosporin-treated recipients are functioning (eight cyclosporin patients also take azathioprine). Seven of the nine (78%) non-kidney-transplant recipients of technically successful pancreas allografts from HLA-identical siblings have functioning grafts. Causes of graft failure include allograft rejection, fibrosis secondary to duct injection, or selective β-cell destruction independent of rejection. Of the 24 recipients who are currently insulin-independent, 14 have normal or near-normal glucose tolerance test results, while 10 have abnormal results, even though they are otherwise euglycaemic. The patient population to whom pancreas transplantation is applied is gradually changing, and non-uraemic, non-kidney-transplant patients currently comprise the majority of our cases (17 out of 24 in 1983; nine of the 17 currently have functioning grafts). We now prefer the enteric drainage technique. Except for recipients of related grafts from a previous kidney donor, in which case it is necessary only to continue the current immunosuppressive regimen, we now administer cyclosporin and prednisone for immunosuppression in recipients of HLA-identical sibling grafts, and cyclosporin, azathioprine and prednisone (triple therapy) for recipients of HLA-mismatched grafts. The most interesting features in this series of cases are the variable patterns of glucose metabolism post-transplant, the finding that processes other than graft rejection, may lead to loss of β-cell function, preliminary observations on changes in morphology of kidneys following restoration of normoglycaemia, and the evolution of an immunosuppressive regimen that appears to prevent allograft rejection in non-uraemic, non-kidney-transplant patients.
    Type of Medium: Electronic Resource
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