We considered she was well treated with glucocorticoids therapy, which is one of the treatments for antiinsulin antibodies, because her local redness disappeared

We considered she was well treated with glucocorticoids therapy, which is one of the treatments for antiinsulin antibodies, because her local redness disappeared. the insulin dose appropriately while monitoring pH, base excess and other factors. Keywords:Antiinsulin antibody, Diabetic ketoacidosis, Insulin allergy We showed a case with serious diabetic ketoacidosis induced by insulin allergy and antiinsulin antibody in a subject with type 2 diabetes mellitus. This case suggests that once we use exogenous human insulin and/or insulinanalog, multiple classes of antibodies against insulin, such as IgE and IgG antibodies, can be induced simultaneously. Moreover, this case showed that we should know that since insulin requirement may be very high under severe insulin resistance and serious DKA, we have to increase insulin dose without hesitation while monitoring pH, BE and other factors in order to save their lives. == INTRODUCTION == Diabetic ketoacidosis (DKA) is one of the most serious acute metabolic complications of diabetes mellitus, and is characterized by hyperglycemia, metabolic acidosis and increased total ketone body concentrations1. As the main mechanism of DKA is usually a lack of insulin in the body, DKA is usually often observed among patients with type 1 diabetes mellitus . It has been reported that some immunological response is usually associated with insulin therapy2. Insulin allergy is still sometimes observed in clinical practice3. In addition, it is possible that patients with insulin allergy show positive for immunoglobulin Gderived insulin antibodies4. Clindamycin In general, antiinsulin antibodies are mainly induced in diabetes mellitus patients treated with insulin preparations. Both insulin allergy and antiinsulin antibodies can cause instability in glycemic control. == CASE REPORT == A 56yearold Japanese woman was brought to the emergency room with coma. She was diagnosed as type 2 diabetes mellitus at the age of 47 years, and was taking antidiabetic drugs. Her history included spinal disc herniation at age 54 years, and she was treated with insulin preparations (insulin human and aspart). After then, she started taking antidiabetic drugs, but she was treated again with insulin degludec at age 55 years for half a year. After her interruption of therapy for 7 months, she restarted receiving insulin therapy. One week after starting insulin glargine, however, local redness was gradually observed at the injection site. Therefore, glargine was changed to degludec/aspart. One week after changing insulin preparation, local redness at the injection site was still observed. As shown in Table1, as she Clindamycin had hyperglycemia, metabolic acidosis and increased total ketone body concentrations, we finally diagnosed her as DKA. Two weeks after restarting insulin, DKA was induced together with general fatigue. == Table 1. == Laboratory data observed in the emergency room GTP, glutamyltranspeptidase; ALP, alkaline phosphatase; ALT, alanine aminotransferase; AntiGAD antibody, antiglutamic acid decarboxylase antibody; AntiIA2Ab, antiinsulinomaassociated protein2 antibody; AntiICAAb, antiislet cell antibody; AntiTgAb, antithyroglobulin Ab; AntiTPOAb, antithyroid peroxidase Ab; AntiZnT8Ab, antizinc transporter8Antibody; AST, aspartate aminotransferase; BE, base excess; BUN, blood urea nitrogen; CRP, Creactive Clindamycin protein; LDH, lactate dehydrogenase; PAmylase, pancreatic amylase; TRAb, antithyrotropin receptor antibody; TSH, Alas2 thyroidstimulating hormone. On admission, we started to treat her hyperglycemic crises with continuous insulin infusion using human insulin. We gradually increased the continuous insulin dose, and DKA was improved with 18 units/h of insulin infusion. As the result, a total insulin dose for 24 h reached >300 units (Physique1a). We decreased continuous insulin dose, but Clindamycin her blood glucose level increased again, together with metabolic acidosis. Therefore, we maintained the insulin infusion dose to treat metabolic acidosis and investigated the cause of insulin resistance. == Physique 1. == (a) Time course of clinical parameters and continuous insulin infusion rate in the present patient. On admission to a high care unit, we started to treat her hyperglycemic crises. Although we started continuous insulin infusion, her hyperglycemic condition and metabolic acidosis were not improved. After increasing dose of continuous insulin up to 18 units/h, hyperglycemia and metabolic acidosis were finally improved. As a result, the total insulin dose for 24 h reached >300 units. We gradually tapered the continuous insulin dose at once, but her glucose level increased again together with metabolic acidosis. (b) A Scatchard analysis of insulin antibody under the diabetic ketoacidosis condition. K1 and K2 show affinity constant.