In a 56-year-old woman with
granulomas of
gold thioglucose in her hips, who developed
insulin autoimmune syndrome, the relationships among the frequency or severity of
hypoglycemic attacks, serum
insulin (IRI) concentration, and characteristics of
insulin antibodies were investigated during the
clinical course with
steroid treatment and two resection operations for the
gold-thioglucose granulomas. When
hypoglycemia was severe, the total IRI level was elevated, and Scatchard analysis showed that a high-affinity (k1), low-capacity (b1) population of
antibodies had a relatively low affinity constant and very high binding capacity compared with the same population of
antibodies in
insulin-treated diabetic patients. When the attacks were relieved by
steroid treatment and/or
granuloma resection operation, the total IRI level was decreased and the high-affinity (k1), low-capacity (b1) population of
antibodies showed a higher affinity constant and a lower binding capacity than those during the attacks. This indicated that the
antibodies changed their characteristics to release
insulin into the serum. The k1/b1 population of
insulin antibodies with the lower affinity constant and higher binding capacity may easily release human
insulin into the serum, leading to
hypoglycemia. The longitudinal change of the k1/b1 population suggests a clonal change of the B cells producing the
insulin antibody in
insulin autoimmune syndrome.