Recurrence of Type 1 Diabetes After Simultaneous Pancreas-Kidney Transplantation in the Absence of GAD and IA-2 Autoantibodies
Recurrence of Type 1 Diabetes After Simultaneous Pancreas-Kidney Transplantation in the Absence of GAD and IA-2 Autoantibodies
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DOI：
10.1111/j.1600-6143.2011.03844.x
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发表时间：
2012-02-01
影响因子：
8.8
通讯作者：
Berney, T.
中科院分区：
文献类型：
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作者：
Assalino, M.;Genevay, M.;Berney, T.
我们在此报告了同时进行胰肾移植 (SPK) 的受者在没有排斥反应的情况下 1 型糖尿病复发的模式。一名 38 岁女性因 1 型糖尿病继发的终末期肾病接受了 SPK。在整个随访过程中监测空腹血糖、HbA1c、果糖胺、C 肽和自身抗体（GAD-65、IA-2）。 SPK 后 3.5 年，尽管 C 肽水平处于正常高范围，但 HbA1c 和果糖胺急剧增加，表明失去了完美的代谢控制。 4个月后重新开始外源胰岛素治疗。 C 肽水平突然下降，并在 5.5 岁时检测不到。自身抗体水平在 SPK 时无法检测到，但从未转为阳性。 6岁时进行了胰腺再移植。失败的胰腺移植物具有正常的宏观外观。在组织学上，肾脏或胰腺没有细胞或体液排斥的迹象。观察到选择性的胰岛周围淋巴细胞浸润，以及β细胞几乎完全破坏。再移植后2.5年，胰腺移植物功能完美。这一观察结果明确表明，在没有排斥反应的情况下，胰腺移植物可能会因 1 型糖尿病复发而丢失。 GAD-65 和 IA-2 自身抗体不是自身免疫复发的可靠标志。
We report herein the patterns of type 1 diabetes recurrence in a simultaneous pancreas-kidney transplant (SPK) recipient, in the absence of rejection. A 38-year-old female underwent SPK for end-stage nephropathy secondary to type 1 diabetes. Fasting blood glucose, HbA1c, fructosamine, C-peptide and autoantibodies (GAD-65, IA-2) were monitored throughout follow-up. At 3.5 years post-SPK, HbA1c and fructosamine increased sharply, indicating loss of perfect metabolic control, despite C-peptide levels in the normal-high range. Exogenous insulin was restarted 4 months later. C-peptide levels abruptly fell and became undetectable at 5.5 years. Autoantibody levels, which were undetectable at the time of SPK, never converted to positivity. Pancreas retranspantation was performed at 6 years. The failed pancreas graft had a normal macroscopic appearance. On histology, there were no signs of cellular or humoral rejection in the kidney or pancreas. A selective peri-islet lymphocytic infiltrate was observed, together with near-total destruction of beta cells. At 2.5 years post retransplantation, pancreatic graft function is perfect. This observation indicates unequivocally that pancreas graft can be lost to recurrence of type 1 diabetes in the absence of rejection. GAD-65 and IA-2 autoantibodies are not reliable markers of autoimmunity recurrence.