内源性高胰岛素血症引起低血糖时葡萄糖反调节激素反应

J. Chung, D. Cho, D. Chung, M. Chung
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引用次数: 2

摘要

背景:在内源性高胰岛素血症(如胰岛素瘤或胰岛素自身免疫性综合征)引起的低血糖患者中,对自发性低血糖的反调节激素反应知之甚少。因此,我们比较了内源性高胰岛素血症引起的自发性低血糖和72小时禁食结束时的激素反应。方法:我们测量了8例胰岛素瘤患者和18例胰岛素自身免疫性综合征患者自发性低血糖时胰高血糖素、肾上腺素、皮质醇和生长激素的反应。我们还评估了13名进行72小时禁食的正常对照者的这些反应。结果:在胰岛素瘤患者(中位血清葡萄糖水平,35.0 mg/dL),血浆胰高血糖素水平(中位,42.9 vs. 76.2 pg/mL;P < 0.05)均低于对照组(血清葡萄糖62.5 mg/dL),而两组其他激素反应差异无统计学意义。相比之下,胰岛素自身免疫性综合征患者(血清葡萄糖水平中位数为34.5 mg/dL),血浆胰高血糖素水平(中位数分别为73.7 vs 76.2 pg/mL)低于对照组,但两组间差异无统计学意义。胰岛素瘤患者与胰岛素自身免疫综合征患者自发性低血糖时的反调节激素反应无统计学差异。结论:我们的研究结果表明,除了高胰岛素血症外,胰岛素瘤患者胰高血糖素分泌缺陷可能导致低血糖,而不是胰岛素自身免疫性综合征。(J韩国
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Glucose Counterregulatory Hormone Response During Hypoglycemia due to Endogenous Hyperinsulinemia
Background: In patients with hypoglycemia due to endogenous hyperinsulinemia such as insulinoma or insulin autoimmune syndrome, little is known about the counterregulatory hormone response to spontaneous hypoglycemia. We therefore compared hormone responses during spontaneous hypoglycemia due to endogenous hyperinsulinemia with those at the end of a 72-hour fast. Methods: We measured glucagon, epinephrine, cortisol, and growth hormone responses during spontaneous hypoglycemia in 8 patients with insulinoma and 18 patients with insulin autoimmune syndrome. We also assessed these responses in 13 normal control subjects who underwent a 72-hour fast. Results: In patients with insulinoma (median serum glucose level, 35.0 mg/dL), plasma glucagon levels (median, 42.9 vs. 76.2 pg/mL, respectively; P < 0.05) were lower than those in control subjects (serum glucose level, 62.5 mg/dL), whereas, there were no statistically significant differences in the other hormone responses between the two groups. In contrast, in the patients with insulin autoimmune syndrome (median serum glucose level, 34.5 mg/dL), plasma glucagon levels (median, 73.7 vs. 76.2 pg/mL, respectively) were lower than those in the control subjects, but there was no statistically significant difference between the two groups. There were no statistically significant differences in counterregulatory hormone responses during spontaneous hypoglycemia between patients with insulinoma and patients with insulin autoimmune syndrome. Conclusion: Our results suggest that defective glucagon secretion in patients with insulinoma rather than insulin autoimmune syndrome may contribute to hypoglycemia in addition to hyperinsulinemia. (J Korean
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