Poor glycemic control attributable to insulin antibody in a fulminant type 1 diabetes patient under hemodialysis: successful treatment with double filtration plasmapheresis and prednisolone

• Main Authors: Kentaro Wada, Haruhito A. Uchida, Yuko Wada
• Format: Article
• Language: English
• Published: BMC 2017-04-01
• Series: Renal Replacement Therapy
• Subjects: Insulin antibody; Insulin antibody binding capacity; Fulminant type 1 diabetes; Hemodialysis; Double filtration plasmapheresis; Prednisolone
• Online Access: http://link.springer.com/article/10.1186/s41100-017-0096-9

Abstract Background Insulin antibody appears in approximately 40% of insulin users using human insulin and insulin analog formulations. Insulin antibody, characterized by high affinity and low insulin antibody binding capacity (% bound), rarely causes clinical problems including poor glycemic control. Recently, the insulin antibody against human insulin causing deterioration of glycemic control, characterized by low affinity and high insulin antibody binding capacity similar to those observed in insulin autoimmune syndrome, has been reported. Case presentation A 62-year-old male developing fulminant type 1 diabetes showing rapid hyperglycemia (602 mg/dL) and normal range of glycoalbumin (GA) (18.4%) in the introductory stage of hemodialysis (HD) was transferred to our hospital 3 weeks after the onset of diabetes. He had been administered insulin intensification therapy in other medical clinic; however, his glycemic control remained poor, showing ketoacidosis. After hospitalization, he was initially administered intravenous insulin for 2 days and then switched to subcutaneous intensification therapy (24 U/day); the dose was gradually increased maximum of 72 U/day within 2 months. His glycemic control deteriorated despite high-dose insulin administration and change in the insulin type. Insulin antibody was detected, insulin antibody binding capacity (% bound) was of a high value (89.5%), GA was 32.9%, and casual blood glucose widely changed in continuous glucose monitor, suggesting that unstable blood glucose fluctuations caused by insulin antibody; therefore, treatment with double filtration plasmapheresis (DFPP) and prednisolone (PSL) was performed. The insulin dose reduced, and glycemic control improved from 1 month after the commencement of treatment. Subsequently, insulin antibody level remained high; however, after 6 months, % bound declined (20.9%), and glycemic control improved (GA 23.7%) by PSL (gradually reduced to 5 mg/day). The Scatchard plots also indicated the effectiveness with DFPP and PSL therapy. Conclusions The authors present a unique case of fulminant type 1 diabetes developing during the HD introduction period. Although this is a rare complication, physicians specializing in dialysis therapy should also keep in mind that this is a life-threatening complication if the treatment is delayed and that concomitant therapy with apheresis such as DFPP and long-term steroids is effective in some cases when glycemic control deteriorates attributable to insulin antibody.