Post-transplant diabetes with anti-glutamic acid decarboxylase antibody during tacrolimus therapy.
A 54-year-old man undergoing hemodialysis because of end-stage renal failure was transplanted with a cadaver kidney in November 1997. He had no history of diabetes. Tacrolimus was used as the primary immunosuppressant. Three weeks after transplantation, he developed insulin-requiring diabetes mellitus. Anti-glutamic acid decarboxylase antibody was not detected on the third post-operative day, but appeared 4 weeks after transplantation. The recipient had DNA haplotypes that indicated susceptibility to Type 1 diabetes in Japanese subjects. Immunosuppressive therapy was changed from tacrolimus to cyclosporin. Thereafter, titer of anti-glutamic acid decarboxylase antibody disappeared and the patient's insulin requirement was notably reduced. The mechanism underlying the development of diabetes in this case appears to be, in part, direct beta-cell toxicity due to tacrolimus therapy, resulting in secondary beta-cell autoimmunity. This case suggests that tacrolimus therapy after transplantation should be used with caution in patients with genetic susceptibility to Type 1 diabetes.
Yoshioka
K
K
Department of Internal Medicine, Osaka City General Hospital, Osaka, Japan.
Sato
T
T
Okada
N
N
Ishii
T
T
Imanishi
M
M
Tanaka
S
S
Kim
T
T
Sugimoto
T
T
Fujii
S
S
D000906:Antibodies / Q000097:blood*; D005968:Glutamate Decarboxylase / Q000276:immunology*; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use*; D016030:Kidney Transplantation / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D016559:Tacrolimus / Q000627:therapeutic use*
D000906:Antibodies; D007166:Immunosuppressive Agents; D005968:Glutamate Decarboxylase; D016559:Tacrolimus