Diabetes & metabolism journal · 2011
Autoimmune hypoglycemia in a patient with characterization of insulin receptor autoantibodies.
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Chon Suk, Choi Moon Chan, Lee Yun Jung, Hwang You Cheol, Jeong In-Kyung, Oh Seungjoon, Ahn Kyu Jeung, Chung Ho Yeon, Woo Jeong-Taek, Kim Sung-Woon, Kim Jin-Woo, Kim Young Seol
Аннотация
BACKGROUND: Type B insulin resistance syndrome is a manifestation of autoantibodies to the insulin receptor that results in severe hyperglycemia and acanthosis nigricans. However, the mechanisms by which these autoantibodies induce hypoglycemia are largely unknown. In this paper, we report the case of patient with type B insulin resistance syndrome who presented with frequent severe fasting hypoglycemia and acanthosis nigricans.
METHODS: To evaluate the mechanism of hypoglycemia, we measured the inhibition of insulin binding to erythrocytes and IM9 lymphocytes in a sample of the patient's dialyzed serum before and after immunosuppressive therapy.
RESULTS: In the patient's pre-treatment serum IgG, the binding of (125)I-insulin to erythrocytes was markedly inhibited in a dose-dependent manner until the cold insulin level reached 10(-9) mol/L. We also observed dose-dependent inhibition of insulin binding to IM9 lymphocytes, which reached approximately 82% inhibition and persisted even when diluted 1:20. After treatment with glucocorticoids, insulin-erythrocyte binding activity returned to between 70% and 80% of normal, while the inhibition of insulin-lymphocyte binding was reduced by 17%.
CONCLUSION: We treated a patient with type B insulin resistance syndrome showing recurrent fasting hypoglycemia with steroids and azathioprine. We characterized the patient's insulin receptor antibodies by measuring the inhibition of insulin binding.
METHODS: To evaluate the mechanism of hypoglycemia, we measured the inhibition of insulin binding to erythrocytes and IM9 lymphocytes in a sample of the patient's dialyzed serum before and after immunosuppressive therapy.
RESULTS: In the patient's pre-treatment serum IgG, the binding of (125)I-insulin to erythrocytes was markedly inhibited in a dose-dependent manner until the cold insulin level reached 10(-9) mol/L. We also observed dose-dependent inhibition of insulin binding to IM9 lymphocytes, which reached approximately 82% inhibition and persisted even when diluted 1:20. After treatment with glucocorticoids, insulin-erythrocyte binding activity returned to between 70% and 80% of normal, while the inhibition of insulin-lymphocyte binding was reduced by 17%.
CONCLUSION: We treated a patient with type B insulin resistance syndrome showing recurrent fasting hypoglycemia with steroids and azathioprine. We characterized the patient's insulin receptor antibodies by measuring the inhibition of insulin binding.