Two Cases of Insulin Autoimmune Syndrome

Inomata Shigeki, Arakawa Hiromichi, Yamasuda Takeshi, Ito Masuo, Inoue Masanori, Osawa Yoshiyuki, Inoue Shuichi, Masuda Hisayuki

doi:10.11213/tonyobyo1958.25.985

Two patients with “insulin autoimmune syndrome” are presented.<BR>Case 1, a 52-year-old woman, was admitted to our hospital because of recurrent hypoglycemic attacks. She had been given a-mercaptopropionyl glycine for skin eruptions over a 4-day period. Three weeks after drug administration, hypoglycemic coma occurred abruptly in August 1980. A 100 g glucose tolerance test (100 g GTT) on admission showed a diabetic pattern. The total immunoreactive insulin (total IRI), free immunoreactive insulin (free IRI), and free C-peptide inununoreactivity (free CPR) during 100 gGTT were 800-3, 760 μUlml, 14-96 μU/m/, and 0-22.5 ng/ml, respectively. The ¹²⁵I-insulin binding capacity was 75%. Prednisolone administration was begun from October 1980. After normalization of the fasting plasma glucose value, associated with a decline of the total IRI and CPR, the hypoglycemic attacks disappeared. Remarkable clinical improvement was attained by the administration of prednisolone.<BR>Case 2, a 72-year-old woman, was admitted to our hospital because of repeated hypoglycemic attacks. She had undergone total gastrectomy and revealed posttransfusion hepatitis in 1979. Administration of glutathione for the hepatitis was continued for one and half years. She suffered from hypoglycemic coma in October 1980. A 100 g GTT showed oxyhyperglycemia. The total IRI, free IRI, and free CPR during 100 gGTT were 140-1, 065 μU/m/, 2-72 μUlml, and 0.91-10.7 nemi, respectively. The ¹²⁵I-insulin binding capacity was 80%. The patient showed spontaneous remission without special therapy in December 1980.<BR>Anti-insulin antibodies which belonged to IgG were found in the present cases by using the specific precipitation method, and its light chain types consisted of the Kappa type in Case 1, and of the Kappa-Lambda type in Case 2. It is suggested that anti-insulin antibody production due to altered insulin antigeneity, which can be affected by some drugs with an SH group in their molecular structure, under pancreatic B cell hyperfunction, could have caused the hypoglycemia in the present cases. Estimation of the HLA typing revealed A 11, B 15, Cw 3 and Cw 4 in both cases.

Two Cases of Insulin Autoimmune Syndrome

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