This patient was a 52-year-old man diagnosed with type 2 diabetes mellitus at the local hospital according to a fasting glucose test that showed a concentration of 16 mmol/L. His postprandial glucose concentration was 27 mmol/L. However, the patient was asymptomatic. He was then treated with a 50/50 Mixture Recombinant Human Insulin Injection (Gansulin 50R) of 12–16 units twice a day, and the dose had been adjusted to 6–10 units 2 months previously. During this period, his glucose was well controlled. One month previously, he developed dizziness and was flustered again. He also started sweating excessively, and at that time, his fasting plasma glucose concentration was 2.8 mmol/L. One week previously, the treatment was changed to acarbose 0.1 mg three times a day because of repeated occurrence of hypoglycemic symptoms. His insulin concentrations were 1294.01/1303.77/1456.7/2057.11/2032.41 pmol/L at 0/30/60/120/180 min and C-peptide concentrations were 1.30/1.80/2.21/2.87/2.55 nmol/L at 0/30/60/120/180 min during the OGTT, respectively. The anti-insulin antibody test was positive. He was prescribed metformin (0.5 g twice a day), acarbose (0.05 g three times a day), aspart (6–5-5 units three times a day), and methylprednisolone (4 mg three times a day) for glucose control. After these changes, hypoglycemia syndrome did not recur (Table ).
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.