title: Insulin and islet autoantibodies after pancreas transplantation.
abstract: Autoimmune recurrence and subsequent diabetes after pancreas transplantation has been described. In this cross-sectional study 91 type 1 diabetic patients were examined after successful pancreas/kidney transplantation (SPK). We studied the prevalence of autoantibodies to insulin (IAA), glutamate decarboxylase (GAD) and tyrosine phosphatase (IA-2) as well as parameters of pancreas graft function. Graft recipients were grouped according to immunoreactivity: group 1: no immunoreactivity; group 2: immunoreactivity to one antigen; group 3: immunoreactivity to two or three antigens. Twenty-five percent of graft recipients displayed no immunoreactivity, 39% displayed positivity for one antigen and 36% were positive for two or three antigens. There were no significant differences concerning fasting glucose, HbA1(c), glucose tolerance and renal function between the groups. Patients with cyclosporine (n = 42) as first-line immunosuppression displayed more often immunoreactivity to IA-2 and IAA than patients treated with tacrolimus (n = 49) (31% vs. 14%, P = 0.04; 67% vs. 47%, P = 0.04). In addition methylprednisolone therapy was related to less immunoreactivity to IA-2. Immunological markers for type 1 diabetes can be determined in the majority of pancreas graft recipients despite adequate immunosuppression. However, immunoreactivity was not associated with impaired graft function. Patients with cyclosporine for immunosuppression and withdrawal of glucocorticoids therapy were more often immunoreactive to IAA and IA-2.
authors.affiliation: Diabetes Center, Medizinische Klinik, University of Munich, Munich, Germany. christoph.dieterle@med.uni-muenchen.de
authors.forename: Christoph D
authors.initials: CD
authors.lastname: Dieterle
authors.forename: Franz-Xaver
authors.initials: FX
authors.lastname: Hierl
authors.forename: Bodo
authors.initials: B
authors.lastname: Gutt
authors.forename: Helmut
authors.initials: H
authors.lastname: Arbogast
authors.forename: Georg R
authors.initials: GR
authors.lastname: Meier
authors.forename: Martin
authors.initials: M
authors.lastname: Veitenhansl
authors.forename: Johannes N
authors.initials: JN
authors.lastname: Hoffmann
authors.forename: Rüdiger
authors.initials: R
authors.lastname: Landgraf
mesh_terms: D000328:Adult; D001323:Autoantibodies / Q000737:chemistry*; D001327:Autoimmune Diseases / Q000175:diagnosis; D001786:Blood Glucose / Q000378:metabolism; D005260:Female; D005938:Glucocorticoids / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D005951:Glucose Tolerance Test; D005968:Glutamate Decarboxylase / Q000276:immunology; D006084:Graft Rejection; D006801:Humans; D007166:Immunosuppressive Agents / Q000494:pharmacology / Q000627:therapeutic use; D007328:Insulin / Q000378:metabolism; D007515:Islets of Langerhans / Q000276:immunology*; D008297:Male; D008775:Methylprednisolone / Q000627:therapeutic use; D008875:Middle Aged; D015233:Models, Statistical; D010179:Pancreas / Q000276:immunology; D016035:Pancreas Transplantation / Q000009:adverse effects / Q000379:methods*; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; D017027:Protein Tyrosine Phosphatases / Q000737:chemistry / Q000276:immunology; D012008:Recurrence; D016559:Tacrolimus / Q000494:pharmacology; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D001323:Autoantibodies; D001786:Blood Glucose; D005938:Glucocorticoids; D007166:Immunosuppressive Agents; D007328:Insulin; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; D017027:Protein Tyrosine Phosphatases; D005968:Glutamate Decarboxylase; D005947:Glucose; D016559:Tacrolimus; D008775:Methylprednisolone