To investigate the influence of diabetes mellitus on mortality in Japanese individuals who are 80 years old in the general population, we compared 74 diabetic subjects with 592 non-diabetic subjects who received the general and dental health examinations in Fukuoka prefecture in 1998 and who were followed-up for 4 years and 12 years after the baseline examination to collect data and information on the cause of death. The cumulative survival rate during the 12-year follow-up period from all-cause mortality and pneumonia mortality in the diabetic group was lower than that in the non-diabetic group. A Multivariate Cox regression analysis revealed that the risk of mortality in the diabetic group was higher than that in the non-diabetic group (1.76-fold for 4 years and 1.84-fold for 12 years). Notably, the risk of pneumonia mortality in the diabetic group was 3.26-fold and 2.97-fold higher than that in the non-diabetic group at 4 years and 12 years, respectively. During the 12 year follow-up period, the cancer mortality in the diabetic group was 2.42-fold higher than that in the non-diabetic group. In the poor glycemic control group, all-cause mortality at 4 years and all-cause mortality, pneumonia mortality, and cardiovascular disease mortality at 12 years were higher in comparison to the non-diabetic group. Diabetes mellitus increased the risk of mortality, especially pneumonia mortality, even in people who are 80 years old.

A study was performed on patients with severe type 2 diabetes, including those with diabetic ketoacidosis (mean HbA1c of 13 %), whose glucose tolerance improved to normal or impaired status after short-term intensive insulin therapy. The clinical history and laboratory values were analyzed using medical records for 24 patients who achieved good glycemic control with oral hypoglycemic agents without insulin or a GLP-1 agonist after the intensive therapy and underwent a 75-g oral glucose tolerance test after receiving the therapy. Five patients showed normal glucose tolerance, 13 had impaired glucose tolerance, and 6 had a persistent diabetes pattern. Compared with the diabetic group, patients with normal or impaired glucose tolerance were more frequently newly diagnosed with diabetes and had a higher HOMA-β (86.0 [63.6] vs. 59.6 [25.2], p=0.02) after treatment. These results suggest that intensive insulin therapy is effective for the recovery of the beta cell function and improvement of glucose tolerance in patients with severe diabetes, including diabetic ketoacidosis, to a condition of normal or impaired tolerance.

We carried out a field survey on the carbohydrate intake of type-2 diabetes mellitus outpatients (male: 33 subjects, female: 39 subjects, age: 69±10 years, BMI: 24.4±4.1 kg/m², HbA1c: 8.2±0.8 %) who had an HbA1c concentration of ≥7.0 % in order to investigate the factors associated with following nutrition therapies that focus on an individual's carbohydrate intake. The mean energy intake was 1566±342 kcal, while the mean carbohydrate, protein, and fat intake was 215.1±49.0 g (percentage energy: 57.7±6.8 %), 58.8±14.7 g (percentage energy: 15.1±2.4 %), and 47.8±15.5 g (percentage energy: 27.2±5.3 %), respectively. The mean BMI of the patients with a carbohydrate energy percentage of <50 % was 26.9±7.5 kg/m², which was greater in comparison to the other two groups. The subjects with carbohydrate energy of ≥60 % were relatively older and their percentage of protein energy (12.9 %) was significantly lower in comparison to the other groups. The results suggested the importance of indicating the appropriate amount of carbohydrates for each patient (taking their age, gender, body type, and tastes into consideration, with an understanding of a patient's carbohydrate intake) to nutritional therapy that aims to control the glucose levels of patients with diabetes mellitus.

The number of elderly patients with type 2 diabetes Mellitus (T2DM) is increasing. Such patients show a high rate of renal dysfunction in connection with aging. The selection of appropriate medicines and dosage adjustment are needed to avoid serious hypoglycemia. This study aimed to evaluate the efficacy of Linagliptin, a DPP-4 inhibitor that is primarily excreted by bile. Thirty-nine T2DM patients who were 75 years of age or older and who were newly treated with Linagliptin, who were treated with Linagliptin as an add-on to conventional anti-diabetic therapy, or who were switched to Linagliptin from other DPP-4 inhibitors (i.e., Sitagliptin, or Vildagliptin), were included in the present study. The changes in their blood glucose, renal and liver function, and serum lipid levels were investigated. The patients' blood glucose and HbA1c levels of all patients improved for 3.6 months. The renal function was not affected by treatment and the patients showed no significant change in their body weight. No hypoglycemia or other side effects occurred. In conclusion, Linagliptin had beneficial effects and could be used safely in the treatment of elderly T2DM patients with functional disorders.

Dipeptidyl peptidase-4 (DPP-4) inhibitors were first approved in Japan in 2009, and are rapidly becoming a common treatment option for type 2 diabetes because of their safety and effectiveness, especially for Asians including Japanese. We recently encountered a patient with type 2 diabetes and fever that was possibly attributable to treatment with alogliptin, a DPP-4 inhibitor. The diagnosis of drug-induced fever due to alogliptin was based on the resolution of the patient's fever after the discontinuation of alogliptin, the recurrence of fever after re-exposure to alogliptin, relative bradycardia, and a positive drug lymphocyte stimulation test result. Physicians should consider the possibility of drug-induced fever when pyrexia of unknown origin occurs in patients who are being treated with DPP-4 inhibitors.

A 51-year-old man was admitted to our hospital with diabetic ketoacidosis of remarkably acute onset. The patient's plasma glucose concentration was 54.9 mmol/L, his HbA1c level was 6.2 %, and his fasting plasma C-peptide and urine C-peptide levels were undetectable. According to the diagnostic criteria for fulminant Type 1 Diabetes (FT1D), the patient was diagnosed with FT1D. The patient was positive for anti-GAD and anti-IA-2 antibodies, indicating an autoimmune etiology, despite the patient possessing the HLA DR-DQ haplotype, which protects against autoimmune Type 1 diabetes mellitus. This case was appropriate for discussing etiology of FT1D.