Ohara Nobumasa, Kaneko Masanori, Furukawa Tatsuo, Koike Tadashi, Sone Hirohito, Tanaka Shoichiro, Kaneko Kenzo, Kamoi Kyuzi
Department of Endocrinology and Metabolism, Nagaoka Red Cross Hospital, Japan.
Intern Med. 2016;55(5):485-9. doi: 10.2169/internalmedicine.55.5398. Epub 2016 Mar 1.
A 59-year-old Japanese woman developed diabetes mellitus without ketoacidosis in the presence of glutamic acid decarboxylase autoantibody (GADA) (24.7 U/mL). After the amelioration of her hyperglycemia, the patient had a relatively preserved serum C-peptide level. Her endogenous insulin secretion capacity remained almost unchanged during 5 years of insulin therapy. The patient's GADA titers normalized within 15 months. The islet-related autoantibodies, including GADA, are believed to be produced following the autoimmune destruction of pancreatic beta cells and are predictive markers of type 1 diabetes mellitus. Therefore, the transient appearance of GADA in our patient may have reflected pancreatic autoimmune processes that terminated without progression to insulin deficiency.
一名59岁的日本女性在存在谷氨酸脱羧酶自身抗体（GADA）（24.7 U/mL）的情况下发生了无酮症酸中毒的糖尿病。在她的高血糖得到改善后，患者的血清C肽水平相对保留。在胰岛素治疗的5年期间，她的内源性胰岛素分泌能力几乎保持不变。患者的GADA滴度在15个月内恢复正常。包括GADA在内的胰岛相关自身抗体被认为是在胰腺β细胞自身免疫性破坏后产生的，并且是1型糖尿病的预测标志物。因此，我们患者中GADA的短暂出现可能反映了胰腺自身免疫过程，该过程在未进展至胰岛素缺乏的情况下终止。
