Self-injection formulations such as insulin or GLP-1 analog are often contaminated with the patient's blood. This problem is mainly ascribed to the patients' lack of knowledge regarding self-injection. However, little is known about the influence of blood contamination on self-injection formulations. In this report we examined the influence of blood contamination on the active component in several commercially available self-injection formulations. We found that GLP-1 analog formulations did not show visible changes upon contamination with blood, while most insulin formulations exhibited a time-dependent increase in turbidity. Fast-acting insulin formulations, such as humalog, tended to form deposits easily. The deposits were found to be composed of insulin and hemoglobin, and eventually the concentration of insulin in the formulation decreased. From these results, we propose that it is necessary for patients to use a correct injection procedure in order to prevent blood backflow and to avoid the blood vessels during injection. The use of an injection device that prevents blood backflow would also be desirable.

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The factors affecting changes in outpatient medical costs were studied in 318 patients with type 2 diabetes who had regularly visited our department since 2008. Over a 5-year period, the medical costs significantly increased from 316,000±167,000 yen per year to 379,000±209,000 yen per year in 204 cases (64 %). The change in medical costs showed a significant positive correlation with the body mass index (BMI) and the HbA1c value, and a significant negative correlation with the medical cost, serum HDL-cholesterol concentration and the hemoglobin level at the beginning of the observation period. A multivariate analysis revealed that the medical cost, BMI and HbA1c value at the start of the observation period were significant independent factors that were associated with the change in medical costs over the five-year period. There have been no previous reports investigating the changes in medical costs among patients with type 2 diabetes. Intervention trials are considered to be necessary to determine whether the correction of body weight may suppress the increase in the medical costs of patients with type 2 diabetes.

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A 35-year-old man was admitted to the hospital with symptoms of excessive thirst, polyuria, and nausea that had persisted for one month. He was diagnosed with type 2 diabetes and treatment was initiated with metformin (750 mg/day) and empagliflozin (10 mg/day). Immediately after the administration of these drugs, he became unable to eat or take his medication due to severe nausea and vomiting and was subsequently admitted to our emergency room. The patient was diagnosed with diabetic ketoacidosis (DKA) based on his history and clinical data, and was treated with continuous intravenous insulin infusion. However, his ketosis persisted until day 6. His serum concentration of empagliflozin was detectable on both the fourth and fifth days, suggesting that a pharmacological effect of empagliflozin may have caused the delayed recovery from ketosis. It is necessary to consider the possibility that, in addition to inducing DKA, SGLT2 inhibitors may also cause a delay in recovery from ketosis.

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An 88-year-old woman, with a diabetic history of at least 6 years, was admitted to another hospital at 85 years of age, with involuntary movement and hyperglycemia. She was subsequently treated with insulin injections once per day. In consideration of her advanced age, an attempt was made to decrease the dose of insulin by administering a DPP-4 inhibitor. However, the patient's HbA1c level had been elevated (8.9-15.0 %) for two months and choreiform movement began to affect her left upper limb. She was therefore admitted to our hospital to undergo further examinations and treatment. The chorea rapidly disappeared after the correction of dehydration and hyperglycemia by fluid replacement and insulin therapy, respectively. Her involuntary movement was definitely diagnosed as diabetic chorea (DC) based on her clinical course and the cranial diagnostic imaging findings. To prevent other involuntary actions, ¹²³I-Ioflupane SPECT was performed, which showed a decreased level of dopamine transporters in the corpus striatum on the affected (right) side. We found no reports evaluating the mechanisms of DC based on neurophysiological findings. The findings in the present case could therefore be considered to be important in further investigations to elucidate the etiology of DC.

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A 48-year-old man presented to a local hospital with a 3-week history of low-grade fever, a 4-day history of epigastralgia and a 6-day history of diarrhea. Acute pancreatitis was initially suspected based on the patient's elevated serum amylase level. Three days before admission, the patient developed severe thirst and polydipsia. On admission to our hospital, his plasma glucose level was 494 mg/dl, his HbA1c concentration was 6.2 %, and ketoacidosis was noted. On the 35th day of hospitalization, the patient's serum C-peptide level was undetectable after intravenous glucagon loading. According to these results and the clinical course, he was diagnosed with fulminant type 1 diabetes. Intensive insulin therapy was administered with CSII. His glucose, CPR and IRI levels in preserved serum samples that were taken at the local hospital (6 days prior to his admission to our hospital) were 61 mg/dl, 1.6 ng/ml and 5.8 μU/ml, respectively. These values were considered to indicate a state of hyperinsulinemic hypoglycemia. There have been nine reports, including own of case, in which patients experienced hypoglycemia before the onset of fulminant type 1 diabetes. These cases illustrate the rapid destruction of beta-cells followed by hyperinsulinemic hypoglycemia before the onset of fulminant type 1 diabetes and may provide valuable insight into a new etiology of hypoglycemia.

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