This patient was a 71-year-old man who was admitted because of polydipsia and polyuria that had persisted for 8 years, as well as recurrent episodes of unconsciousness throughout this period. He was diagnosed with type 2 diabetes mellitus 8 years before admission. Acarbose was initially prescribed, but was switched to insulin aspart 30 (8–12 units twice a day) because of poor glucose control 5 years previously. Three months previously, the dose of insulin aspart 30 was gradually reduced to 4–10 units because of hypoglycemia. However, he had unexpected episodes of unconsciousness due to hypoglycemia 12 days before admission. Moreover, his symptoms were obviously relieved after food intake. He was subsequently treated with voglibose instead of insulin injections. However, the hypoglycemic symptoms continued to appear between 02:00 am and 03:00 am, despite the absence of other treatments. A laboratory examination showed the following: C-peptide values were 15.22/17.59/19.73/15.22 nmol/L at 0/1/2/3 h, and insulin concentrations were > 2089.5/> 2089.5/> 2089.5/> 2089.5 pmol/L at 0/1/2/3 h during the OGTT, respectively. The anti-insulin antibody test was also positive. His treatment regimen was changed to prednisone (5 mg three times a day), acarbose (50 mg three times a day), metformin (0.5 g twice a day), and glargine (12–18 units twice a day) for glucose control. Insulin injections were also gradually discontinued. Following this treatment, he showed improved glucose control. Laboratory tests during a recent follow-up showed the following: C-peptide levels of 0.77/2.40 nmol/L at 0/2 h and insulin levels of 430.13/1350.21 pmol/L at 0/2 h during the OGTT, respectively.
This patient was a 79-year-old man who presented with a 3-year history of hyperglycemia and a 1-year history of polydipsia. At the time of presentation, he had been in a hypodynamic state for 15 days. Three years previously, he was diagnosed with impaired glucose tolerance without any symptoms, but no treatment was provided. One year earlier, he developed polydipsia, hyperuresis, and cutaneous pruritus, and lost weight. His random plasma glucose concentrations increased to as high as 20 mmol/L. Consequently, he was started on aspart 30 (21 units before breakfast and 8 units before dinner) and metformin (0.5 g twice a day). One month previously, he visited our hospital because of complaints of recurrent midnight hypoglycemia, particularly at approximately 02:00 am. During that period, although an insulin injection was gradually reduced and subsequently discontinued, his glucose concentration still dropped to 3 mmol/L. Laboratory tests showed that C-peptide and insulin concentrations were above the normal range, and the insulin autoantibody test was positive. At that time, non-classical IAS was considered as the probable cause of repeated hypoglycemia, and treatment was changed to acarbose (50 mg three times a day). After 15 days, blood tests showed the following: fasting plasma glucose level, 3.71 mmol/L; anti-insulin antibody, > 45.4 U/mL; and insulin concentrations were 1567.44/1493.06/1370.20/1616.43/1812.01 pmol/L at 0/30/60/120/180 min and C-peptide concentrations were 3.41/3.68/3.95/4.56/4.51 nmol/L at 0/30/60/120/180 min during the OGTT, respectively. For treatment of IAS, prednisone therapy was started at 12 mg daily (4 mg per dose three time daily) then reduced to 8 mg daily after 2 weeks and to 4 mg per night 1 week later. The diabetes treatment plan was changed to human biosynthetic insulin injection (16 units per day), sitagliptin (50 mg per day), and voglibose (0.3–0.2 mg twice a day). Repeated laboratory tests showed the following: C-peptide concentrations were 0.73/1.67 nmol/L at 0/2 h, respectively, and the insulin concentration was 728.14 pmol/L at 0 h during the OGTT. The glucose concentration fluctuated between 7 and 12.9 mmol/L.