谷氨酸脱羧酶65抗体(GAD65-Ab)是一些疾病如糖尿病或中枢神经系统的自身免疫性疾病如僵硬综合征中的自身免疫标志物。它可以与其他胰腺自身抗体一起出现,如胰岛素自身抗体(IAA),表现为胰岛β细胞受损的早期迹象,并在1型糖尿病(T1D)和成人隐匿性自身免疫性糖尿病(LADA)的发病机制中发挥作用。GAD65-Ab阳性很少见于患有其他获得性自身免疫性疾病的胰岛素依赖型糖尿病患者,如干燥综合征(SS)。此外,由胰岛自身抗体如GAD65-Ab显示的LADA也可并发桥本甲状腺炎(HT),另一种自身免疫性甲状腺疾病。迄今为止,自身免疫性疾病患者的GAD65-Ab阳性是否可预测T1D或LADA的发病或进展仍未知.在这里,描述了两例中国中年汉族女性三年无糖尿病的独特病例,尽管她们的血液检测GAD65-Ab或IAA持续呈阳性。两名患者均患有HT和SS。随访三年的OGTT(口服葡萄糖耐量试验)显示,患者的血糖水平控制良好,胰腺功能正常。然而,其中一名患者在短期失去饮食控制后出现餐后血糖暂时升高.这些患者中自身免疫抗体的存在在3年内对葡萄糖耐量或胰岛素分泌几乎没有影响。该研究假设血清GAD65-Ab阳性引起的原发性免疫损伤,一种自身免疫标志物,体重增加有助于LADA的进展。
The glutamic acid decarboxylase 65 antibody (GAD65-Ab) is an autoimmune marker in some diseases such as diabetes or autoimmune disorders of the central nervous system such as stiff-man syndrome. It can appear with other pancreatic autoantibodies, such as insulin autoantibodies (IAA), presenting as early signs of pancreatic islet β-cells impairing, and play roles in the pathogenesis of type1 diabetes (T1D) and latent autoimmune diabetes in adults (LADA). Positive GAD65-Ab is rarely observed in insulin-dependent diabetic patients with other acquired autoimmune diseases, such as Sjogren\'s syndrome (SS). Besides, LADA revealed by islet autoantibodies such as GAD65-Ab can also be complicated with Hashimoto\'s thyroiditis (
HT), another autoimmune thyroid disease. To date, whether GAD65-Ab positive in patients with autoimmune diseases predicts the onset or progression to T1D or LADA remains unknown. Herein, two unique cases of middle-aged Chinese Han women free from diabetes for three years are described despite their blood tests persistently testing positive for GAD65-Ab or IAA. Both patients suffered from
HT and SS. Follow-up OGTTs (oral glucose tolerance test) for three years revealed that the patients had a well-controlled glycemic level and normal pancreatic function. However, one of the patients had a temporary increase of postprandial glucose after a short-term loss of diet control. The presence of auto-immune antibodies in these patients had little impact on glucose tolerance or insulin secretion in 3 years. The study postulate that both the primary immune injury caused by serum GAD65-Ab positive, an autoimmune marker, and increased body weight contribute to the progression of LADA.