Cho B Y, Lee H K, Koh C S, Min H K
Diabetes Res Clin Pract. 1987 May-Jun;3(3):119-24. doi: 10.1016/s0168-8227(87)80017-7.
A 31-year-old woman with Graves' disease developed fasting hypoglycemia after treatment for 3 weeks with methimazole. Although the patient had not received exogenous insulin, high titers of insulin autoantibodies were found in serum and large amounts of total and free insulin (1550 and 82 microU/ml, respectively) and C-peptide reactivity (CPR, 22 ng/ml) were detected in serum. After glucose loading, blood glucose and total insulin levels increased abnormally. The immunoglobulin class of the autoantibodies was IgG and the light chains were of the kappa type. The titers of insulin autoantibodies, elevated serum total and free insulin, and CPR levels decreased gradually, but insulin autoantibodies and elevated insulin levels were still present in the serum 8 months after the episode of hypoglycemia. These findings suggest that the patient's fasting hypoglycemia was due to excess free insulin released from antibody-bound insulin, and that methimazole might play a role in the initiation of production of insulin autoantibodies.
一名31岁的格雷夫斯病女性在接受甲巯咪唑治疗3周后出现空腹低血糖。尽管该患者未接受外源性胰岛素治疗，但血清中发现了高滴度的胰岛素自身抗体，且血清中检测到大量的总胰岛素和游离胰岛素（分别为1550和82微单位/毫升）以及C肽反应性（CPR，22纳克/毫升）。葡萄糖负荷后，血糖和总胰岛素水平异常升高。自身抗体的免疫球蛋白类别为IgG，轻链为κ型。胰岛素自身抗体滴度、血清总胰岛素和游离胰岛素升高以及CPR水平逐渐下降，但低血糖发作8个月后血清中仍存在胰岛素自身抗体和升高的胰岛素水平。这些发现表明，患者的空腹低血糖是由于抗体结合的胰岛素释放出过量游离胰岛素所致，且甲巯咪唑可能在胰岛素自身抗体产生的起始过程中起作用。
