We investigated the effects of ultra-rapid acting insulin (URI). Thirty patients with type 2 diabetes were randomly classified into 3 groups. Upon admission during study period, the preprandial and bedtime glucose levels (PBGLs) were stabilized at 80-89 mg/dL by basal-bolus insulin therapy. Group 1: The PBGLs were stabilized. Then, the same dose of glulisine was administered. Next, patients wore a flash glucose monitoring device (FGM), and glycemic variability (GV) was evaluated on days 3 and 4; glulisine was switched to lispro (at the same dose) on day 5, and the GV was evaluated on days 8 and 9. Lispro was switched to aspart (at the same dose) on day 10, and the GV was evaluated on days 13 and 14. Following the same regimen, URI was administered in the order of lispro, aspart, and glulisine in Group 2 and aspart, glulisine, and lispro in Group 3. The highest postprandial GL, postprandial glucose gradient, coefficient of variation and area over the curve of glucose (<70 mg/dL) were all significantly lower in the patients who received glulisine, lispro, and aspart-in that order. Glulisine may be the most effective insulin analogues for reducing GV.
Nurses assigned to a ward observe the feet of diabetic patients on admission and provide medical support for the early detection and prevention of diabetic foot in our hospital. The relationship between the results obtained from a DPNCheck®, a simple nerve conduction measurement device that is useful for diagnosing diabetic neuropathy, and the risk of diabetic foot assessed by the nurses was examined in the present study. One hundred and eleven patients with type 2 diabetes (mean age: 64±14 years, duration of diabetes: 10±9 years) was studied. The abnormal group was defined as the patients with ≥2 abnormalities in 16 observation items for the feet. Assignment to the abnormal group was relatively frequent (n=54, 49 %), and the sensory nerve action potential amplitude (SNAP) was significantly lower in the abnormal group (7.1±4.2 μV) than in the normal group (9.5±5.1 μV). The total number of abnormalities in observation items showed a significantly negative correlation with the SNAP. In particular, the SNAP was significantly lower in the patients found to have an abnormality in their skin or blood flow than in those without such an abnormality. The DPNCheck® is considered useful for identifying patients who should receive educational guidance and/or medical support concerning foot care.
In addition to lowering glycated hemoglobin levels sodium-glucose cotransporter 2 (SGLT2) inhibitor treatment has been shown to have many other beneficial effects on the metabolic function of patients with type 2 diabetes. Furthermore, it was recently reported-based on the results of a 2-year clinical trial-that SGLT2 treatment improved the estimated glomerular filtration rate (eGFR) in type 2 diabetic patients with a normal renal function. We therefore retrospectively investigated the effects of SGLT2 inhibitors in 111 outpatients who had been treated with SGLT2 inhibitors for more than 3 years. At 3 years after the initiation of treatment, the patients' glycated hemoglobin levels, body weight, AST, ALT, γ-GTP, LDL-C, blood pressure, and serum uric acid levels were significantly decreased, and their HDL-C and hematocrit levels were significantly increased. Moreover, their eGFRs were found to have significantly increased at 2 years after the initiation of treatment. Consequently, we found that the many beneficial effects of SGLT2 inhibitors on the metabolic function continued for 3 years and we considered that SGLT2 inhibitor treatment might improve the renal function of type 2 diabetic patients with s normal renal function.
We herein report a 44-year-old man who presented with so-called euglycemic diabetic ketoacidosis. He was diagnosed with type 2 diabetes and administered canagliflozin 100 mg and metformin 500 mg at 4 days before admission. In addition, on the same day (4 days before admission), an extremely-low-carbohydrate diet was started of his own volition. Four days later, he visited our hospital complaining of strong physical weariness. His blood glucose level was 183 mg/dL, HbA1c was 12.1 %, and urinary ketone was 3+, and metabolic acidosis was observed. He was diagnosed with euglycemic diabetic ketoacidosis (euDKA) and admitted immediately. After hospitalization, continuous intravenous infusions of insulin and glucose was started. Insulin administration was changed to a subcutaneous injection on the second day. He was discharged from our hospital 10 days after admission. We suggest that the extremely-low-carbohydrate diet, in addition to the administration of an SGLT2 inhibitor, triggered euDKA. There have been several reports of euDKA in patients taking SGLT2 inhibitors. Approximately 60 % of cases had a reduction in their carbohydrate intake as a cause. When prescribing an SGLT2 inhibitor, attention should be paid to the patient's diet, such as encouraging the avoidance of extreme carbohydrate restriction.
A thirty-nine-year-old woman with a 20-year history of type 2 diabetes mellitus was admitted to our hospital because of her spontaneous pregnancy at 7 weeks of gestation. As she had severe diabetic nephropathy (serum creatinine, 1.66 mg/dL; estimated glomerular filtration rate, 29 mL/min/1.73 m2), she had been advised to avoid pregnancy. In spite of the high risk of perinatal complications, she strongly desired to continue the pregnancy. Her blood glucose and blood pressure were carefully controlled with hospitalization and outpatient care. At 34 weeks of gestation, her renal function deteriorated (serum creatinine, 2.35 mg/dL; estimated glomerular filtration rate, 20 mL/min/1.73 m2), she also complained blurred vision, and the fetus showed signs of growth retardation. A baby boy of 1712 g in body weight was delivered by caesarean section. The neonate was hypoglycemic, but free of deformation. Multidisciplinary treatment and management are necessary for pregnant women with severe diabetic nephropathy.