Department of Endocrinology and Metabolism, Peking University People's Hospital, Beijing 100044, China.
Department of Endocrinology and Metabolism, Guiyang Hospital of Guizhou Aviation Industry Group, Guiyang, Guizhou 550009, China.
Chin Med J (Engl). 2020 Nov 5;133(21):2595-2598. doi: 10.1097/CM9.0000000000000972.
With the increasing use of immune checkpoint inhibitors (ICI) including anti-cytotoxic T lymphocyte associated antigen-4 (CTLA-4) and anti-programmed cell death-1 (PD-1) in cancers, ICI-induced type 1 diabetes has been reported throughout the world. In this review, we aim to summarize the characteristics of this disease and discuss the mechanism of it. As an immune-related adverse event, type 1 diabetes developed after the administration of anti-PD-1 or anti-PD-ligand 1 (PD-L1) in the combination with or without anti-CTLA-4. It usually presented with acute onset, and 62.1% of the reported cases had diabetic ketoacidosis. Only a third of them had positive autoantibodies associated with type 1 diabetes. Susceptible HLA genotypes might be associated. T-cell-stimulation by blocking of the interaction of PD-1 and PD-L1 in pancreatic β cells was the main mechanism involved in the pathology. Insulin was the only effective treatment of ICI-induced type 1 diabetes. In conclusions, ICI-induced type 1 diabetes is a potentially life-threating adverse event after the immunotherapy of cancers. Screening and early recognition is important. Further investigation of the mechanism may help to better understand the pathology of type 1 diabetes.
随着免疫检查点抑制剂(ICI)的广泛应用,包括抗细胞毒性 T 淋巴细胞相关抗原 4(CTLA-4)和抗程序性细胞死亡蛋白 1(PD-1)在癌症中的应用,ICI 诱导的 1 型糖尿病在全球范围内都有报道。在这篇综述中,我们旨在总结这种疾病的特征,并讨论其发病机制。作为一种免疫相关的不良反应,1 型糖尿病发生在抗 PD-1 或抗 PD-配体 1(PD-L1)与或不与抗 CTLA-4 联合使用后。它通常表现为急性发作,报告的病例中有 62.1%有糖尿病酮症酸中毒。只有三分之一的病例有与 1 型糖尿病相关的阳性自身抗体。易感 HLA 基因型可能与之相关。阻断 PD-1 和 PD-L1 在胰腺β细胞中的相互作用导致 T 细胞的刺激是该疾病发病机制中的主要机制。胰岛素是治疗 ICI 诱导的 1 型糖尿病的唯一有效方法。总之,ICI 诱导的 1 型糖尿病是癌症免疫治疗后一种潜在危及生命的不良反应。筛查和早期识别很重要。对发病机制的进一步研究可能有助于更好地理解 1 型糖尿病的发病机制。